HSV-2 Herpes Topical Curcumin holds Promise
“Curcumin can stop the genital herpes virus, it helps in reducing the inflammation and makes it less susceptible to HIV and other STIs,” Prof Garg says.
#hsv2 #curcumin #herpes
Danielle Vitali, Puja Bagri, Jocelyn M. Wessels, Meenakshi Arora, Raghu Ganugula, Ankit Parikh, Talveer Mandur, Allison Felker, Sanjay Garg, M.N.V. Ravi Kumar, Charu Kaushic. Curcumin Can Decrease Tissue Inflammation and the Severity of HSV-2 Infection in the Female Reproductive Mucosa. International Journal of Molecular Sciences, 2020; 21 (1): 337 DOI: 10.3390/ijms21010337
Herpes Virus Cleared from Cells BX795
From a completely accidental discovery: “BX795 is known as an inhibitor of TBK1, an enzyme involved in innate immunity and neuroinflammation. When TBK1 is suppressed in cells, infection is actually promoted. But when the researchers added higher concentrations of BX795 to cultured human corneal cells infected with HSV-1, the infection was quickly cleared.”
Citation: An off-target effect of BX795 blocks herpes simplex virus type 1 infection of the eye. Science Translational Medicine, 2018; 10 (428): eaan5861 DOI: 10.1126/scitranslmed.aan5861
Long-term (24-month) supplementation with multivitamins plus selenium for human immunodeficiency virus (HIV)-infected patients in Botswana in the early stages of disease who had not received antiretroviral therapy delayed time to HIV disease progression, was safe and reduced the risk of immune decline and illness, according to a study appearing in the November 27 issue of JAMA.
“Micronutrient deficiencies, known to influence immune function, are prevalent even before the development of symptoms of HIV disease and are associated with accelerated HIV disease progression. Micronutrient supplementation has improved markers of HIV disease progression (CD4 cell count, HIV viral load) and mortality in clinical trials; however, these studies were conducted either in the late stages of HIV disease or in pregnant women,” according to background information in the article.
Marianna K. Baum, Ph.D., of Florida International University, Miami, and colleagues examined whether specific supplemental micronutrients enhance the immune system and slow HIV disease progression during the early stages of the disease in antiretroviral therapy (ART)-naive adults. They randomized 878 HIV patients to supplementation with daily multivitamins (B vitamins and vitamins C and E), selenium alone, multivitamins with selenium, or placebo for 24 months. The vitamins (vitamins B, C and E, and the trace element selenium) are nutrients essential for maintaining a responsive immune system. Selenium may also have an important role in preventing HIV replication.
Participants receiving the combined supplement of multivitamins plus selenium had a lower risk compared to placebo of reaching a CD4 cell count 250/µL or less (a measure that is consistent with the standard of care in Botswana for initiation of ART at the time of the study). This supplement also reduced the risk of a combination of measures of disease progression (CD4 cell count ≤ 250/µL, AIDS-defining conditions, or AIDS-related death, whichever occurred earlier).
“This evidence supports the use of specific micronutrient supplementation as an effective intervention in HIV-infected adults in early stages of HIV disease, significantly reducing the risk for disease progression in asymptomatic, ART-naive, HIV-infected adults. This reduced risk may translate into delay in the time when the HIV-infected patients experience immune dysfunction and into broader access to HIV treatment in developing countries,” the authors conclude.
The researchers add that their “findings are generalizable to other HIV subtype C-infected cohorts in resource-limited settings where the provision of ART is being scaled up, rolled out, or not yet available to all in conditions similar to those in Botswana at the time of this study.”
(doi:10.l001/jama.2013.280923; Available pre-embargo to the media at http://media.jamanetwork.com)
Editor’s Note: This study was funded by the National Institute on Drug Abuse. All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported
Posted By Caroline May On 1:30 PM 11/25/2013 In |
A case study contained within a lengthy World Health Organization report reviewing the health inequities among European countries says Greeks may be contracting HIV intentionally in order to go on public assistance.
According to the “case study” contained in the report “Review of social determinants and the health divide in the WHO European Region: final report,” while suicides, homicide, and thefts increased during the Greek economic crisis, so too did the rate of HIV infection — about half of which the report says were likely self-inflicted to obtain benefits.
“Suicides rose by 17% between 2007 and 2009 and to 25% in 2010, according to unofficial 2010 data (398),” the case study reads. “The Minister of Health reported a further 40% rise in the first half of 2011 compared with the same period in 2010. Suicide attempts have also increased, particularly among people reporting economic distress (610). Homicide and theft rates have doubled.
DURHAM, N.C. – A substance in breast milk that neutralizes HIV and may protect babies from acquiring HIV from their infected mothers has been identified for the first time by researchers at Duke Medicine.
The protein, called Tenascin-C or TNC, had previously been recognized as playing a role in wound healing, but had not been known to have antimicrobial properties. The discovery could lead to potential new HIV-prevention strategies.
Reporting in the journal Proceedings of the National Academy of Sciences during the week of Oct. 21, 2013, the researchers describe how the TNC protein in breast milk binds to and neutralizes the HIV virus, potentially protecting exposed infants who might otherwise become infected from repeated exposures to the virus.
“Even though we have antiretroviral drugs that can work to prevent mother-to-child transmission, not every pregnant woman is being tested for HIV, and less than 60 percent are receiving the prevention drugs, particularly in countries with few resources,” said senior author Sallie Permar, M.D., Ph.D., assistant professor of pediatrics, immunology and molecular genetics and microbiology at Duke. “So there is still a need for alternative strategies to prevent mother-to-child transmission, which is why this work is important.”
Worldwide in 2011, an estimated 330,000 children acquired HIV from their mothers during pregnancy or birth, or through breastfeeding according to UNICEF. As international health organizations have set a goal of eliminating mother-to-child infections, researchers have worked to develop safe and affordable alternatives to antiretroviral therapy that can be used to block HIV transmission to infants.
Permar and colleagues focused on breast milk, which has long been recognized as having some protective quality that inhibits mother-to-child transmission despite multiple daily exposures over months and even years of nursing. Earlier studies had identified some antiviral properties in breast milk, but the majority of the HIV-neutralizing activity of breast milk remained unexplained. More recent studies pointed to a large protein that had yet to be identified.
In their study, the Duke team screened mature milk samples from uninfected women for neutralizing activity against a panel of HIV strains, confirming that all of the detectable HIV-neutralization activity was contained in the high molecular weight portion. Using a multi-step protein separation process, the researchers narrowed the detectable HIV-neutralization activity to a single protein, and identified it as TNC.
“TNC is a component of the extracellular matrix that is integral to how tissues hold themselves together,” Permar said, noting that co-author Harold Erickson, Ph.D., professor of cell biology at Duke, was among the first to identify and describe TNC in the 1980s. “This is a protein involved during wound healing, playing a role in tissue repair. It is also known to be important in fetal development, but its reason for being a component of breast milk or its antiviral properties had never been described.”
Further analysis described how TNC works against HIV by blocking virus entry. The protein is uniquely effective in capturing virus particles and neutralizes the virus, specifically binding to the HIV envelope. These properties provide widespread protection against infection.
“It’s likely that TNC is acting in concert with other anti-HIV factors in breast milk, and further research should explore this,” Permar said. “But given TNC’s broad-spectrum HIV-1-binding and neutralizing activity, it could be developed as an HIV-prevention therapy, given orally to infants prior to breastfeeding, similar to the way oral rehydration salts are routinely administered to infants in developing regions.”
Permar said TNC would also appear to be inherently safe, since it is a naturally occurring component of breast milk, and it may avoid the problem of HIV resistance to antiretroviral regimens that complicate maternal/infant applications.
“The discovery of the HIV inhibiting effect of this common protein in breast milk provides a potential explanation for why nursing infants born to HIV-infected mothers do not become infected more often than they do,” said Barton F. Haynes, M.D., director of the Duke Human Vaccine Institute. “It also provides support for inducing inhibitory factors in breast milk that might be even more protective, such as antibodies, that would completely protect babies from HIV infection in this setting.”
In addition to Permar, co-senior author was S. Munir Alam. Other authors include Genevieve G. Fouda, Frederick H. Jaeger, Joshua D. Amos, Carrie Ho, Erika L. Kunz, Kara Anasti, Lisa W. Stamper, Brooke E. Liebl; Kimberly H. Barbas, Tomoo Ohashi, M. Arthur Moseley, Hua-Xin Liao and Harold P. Erickson.
The study was funded by the Doris Duke Charitable Foundation Clinical Scientist Development Award; Duke University School of Medicine; Center for HIV/AIDS Vaccine Immunology; and the National Institute of Allergic and Immunologic Diseases (U19 AI067854) (K08AI087992) (CA047056).
- The HIV subtype 02_AG/A is spreading rapidly and is now thought to account for more than 50 per cent of new HIV infections in Siberia
- It is thought to be the most virulent subtype of the virus in Russia
- Infections have also been reported in Chechnya, Kyrgyzstan and Kazakhstan
By Emma Innes
PUBLISHED: 06:42 EST, 17 October 2013 | UPDATED: 06:51 EST, 17 October 2013
Russian scientists believe they have identified a new and more virulent strain of HIV.
The subtype, known as 02_AG/A, is spreading rapidly and is now thought to account for more than 50 per cent of new HIV infections in Siberia.
The virus was first seen in the city of Novosibirsk in 2006 and is thought to be the most virulent subtype of the virus in Russia.
Russian scientists believe they have identified a new and more virulent strain of HIV. The subtype, known as 02_AG/A, is spreading rapidly. Image shows mature HIV virus infection
It was discovered by scientists at the State Research Center of Virology and Biotechnology VECTOR in Siberia, The Moscow News reports.
Natalya Gashnikova, head of the retroviruses department at Vektor, said 02_AG/A could spread through the population much more quickly than the current main HIV strain found in Russia.
The number of HIV positive people in Novosibirsk has jumped from 2,000 in 2007 to 15,000 in 2012, according to Russia’s Federal AIDS Centre and 50 per cent of the new cases have been caused by 02_AG/A.
The newly identified subtype is not confined to Siberia – cases have also been reported in Chechnya, in the south of Russia, and Kyrgyzstan and Kazakhstan.
HIV can be divided into two main types – HIV-1 and HIV-2. HIV-1 is the more virulent of the two and is, therefore, responsible for the majority of cases.
HIV-1 can also be divided into subgroups and the newly discovered 02_AG/A is a subgroup of HIV-1.
All of the subgroups are transmitted from person to person through the same transmission methods – including unprotected sex and sharing needles – but some are easier to pass on than others.
02_AG/A is thought to be easier to transmit than some other subtypes.
The virus was first seen in the city of Novosibirsk in 2006 and is thought to be the most virulent subtype of the virus in Russia. It is now thought to account for more than 50 per cent of new HIV infections in Siberia
UN figures show that the only regions where the number of HIV infections is increasing are Eastern Europe and Central Asia – 52 per cent of people with HIV in this area live in Russia.
This is believed to be partly because there is little awareness of HIV in many parts of Russia and because Russian school offer very little sex education.
The number of new HIV infections globally has plummeted by a third since 2001 and more than halved among children, the United Nations recently revealed.
Globally, 2.3 million people contracted the AIDS virus last year – down 33 per cent from 2001, while 260,000 children became infected – 52 per cent less than in 2001.
‘The annual number of new HIV infections continues to decline with especially sharp reductions in the number of children newly infected with HIV,’ UNAIDS executive director Michel Sidibe said.
Last year, 1.6 million people died of AIDS-related deaths, down from 1.8 million in 2011 and 2.3 million in 2005.
The report showed that 9.7 million people in low and middle-income countries, the bulk of those infected, had access to HIV drugs last year, compared to only 1.3 million seven years earlier.
While the hike is impressive, it falls short of a UN target announced two years ago to reach 15 million people by 2015.
Some 35.3 million people were living with the virus last year – about 70 per cent of them in sub-Saharan Africa – up from 30 million in 2001.
Read more: http://www.dailymail.co.uk/health/article-2464403/New-virulent-strain-HIV-spreading-rapidly-Russia-claim-scientists.html#ixzz2hzqsBz5g Follow us: @MailOnline on Twitter | DailyMail on Facebook
Posted: July 19, 2013 at 5:00 am, Last Updated: July 23, 2013 at 6:49 am
Yuntao Wu. Creative Services photo
A compound found in soybeans may become an effective HIV treatment without the drug resistance issues faced by current therapies, according to new research by George Mason University researchers.
It’s in the early stages, but genistein, derived from soybeans and other plants, shows promise in inhibiting the HIV infection, says Yuntao Wu, a professor with the George Mason-based National Center for Biodefense and Infectious Diseases and the Department of Molecular and Microbiology.
Still, that doesn’t mean people should begin eating large amounts of soy products. “Although genistein is rich in several plants such as soybeans, it is still uncertain whether the amount of genistein we consume from eating soy is sufficient to inhibit HIV,” Wu says.
Genistein is a “tyrosine kinase inhibitor” that works by blocking the communication from a cell’s surface sensors to its interior. Found on a cell’s surface, these sensors tell the cell about its environment and also communicate with other cells. HIV uses some of these surface sensors to trick the cell to send signals inside. These signals change cell structure so that the virus can get inside and spread infection.
But genistein blocks the signal and stops HIV from finding a way inside the cell. It takes a different approach than the standard antiretroviral drug used to inhibit HIV.
“Instead of directly acting on the virus, genistein interferes with the cellular processes that are necessary for the virus to infect cells,” Wu says. “Thus, it makes the virus more difficult to become resistant to the drug. Our study is currently it its early stage. If clinically proven effective, genistein may be used as a complement treatment for HIV infection.”
Wu and researcher Jia Guo in the lab. Creative Services photo
Wu sees possibilities in this plant-based approach, which may address drug toxicity issues as well. Because genistein is plant-derived, it may be able to sidestep drug toxicity, a common byproduct of the daily and lifelong pharmaceutical regimen faced by patients with HIV to keep the disease at bay, Wu says. Typically, patients take a combination of multiple drugs to inhibit the virus. The frequency can lead to drug toxicity. Plus, HIV mutates and becomes drug-resistant.
Wu and his team are working at finding out how much genistein is needed to inhibit HIV. It’s possible that plants may not have high enough levels, so drugs would need to be developed, Wu says.
Wu’s research is feeling the financial squeeze these days due to sequestration and budget cuts within the National Institutes of Health, he says. His lab has turned to novel ways to fund the HIV research, including the genistein project. A bicycle ride dubbed NYC DC AIDS Research Ride raised money for Wu’s lab a few years ago and has stepped up its efforts with a new fundraiser.
Other George Mason researchers on the genistein project include Jia Guo, Taban Rasheed, Alyson Yoder, Dongyang Yu, Huizhi Liang, Fei Yi and Todd Hawley.Xuehua Xu and Tian Jin from the National Institute of Allergy and Infectious Diseases in Rockville, Md., and Binhua Ling from Tulane University Health Sciences Center are also working on the research.
HIV vaccine study halted by US government over unsuccessful shots
Associated Press in Washington
guardian.co.uk, Thursday 25 April 2013 17.52 EDT
The US government halted a large HIV vaccine study on Thursday, saying the experimental shots were not successful in preventing infection.
Nor did the shots reduce the amount of the Aids virus in the blood when people who had been vaccinated later became infected, the National Institutes of Health said.
“It’s disappointing,” said Dr Anthony Fauci, head of NIH’s National Institute of Allergy and Infectious Diseases. But he said there was “important information” gained from the study that will help determine what to try next.
The study had enrolled 2,504 volunteers, mostly gay men, in 19 cities since 2009. Half received dummy shots, and half received a two-part experimental vaccine developed by the NIH. All were provided free condoms and given extensive counseling about the risks of HIV.
It’s a strategy known as “prime-boost”. A DNA-based vaccine made with genetically engineered HIV material is given to prime the immune system to attack the Aids virus. Then a different vaccine, encasing the same material inside a shell made of a disabled cold virus, acts as a booster shot to strengthen that response. Neither vaccine could cause HIV.
The idea was to train immune cells known as T cells to spot and attack the very earliest HIV-infected cells in someone’s body. The hope was that the vaccine could either prevent HIV infection, or help those infected anyway to fight it.
A safety review this week found that slightly more study participants who had received the vaccine later became infected with HIV. It’s not clear why. But the difference wasn’t statistically significant, meaning it may be due to chance. Overall, there were 41 HIV infections in the vaccinated group and 30 among placebo recipients. When researchers examined only participants diagnosed after being in the study for at least 28 weeks – long enough for the shots to have done their job – there were 27 HIV infections among the vaccinated and 21 among the placebo recipients.
The NIH said Thursday that it is stopping vaccinations in the study, known as HVTN 505, but that researchers will continue to study the volunteers’ health.
Josh Robbins, 30, of Nashville, Tennessee, was one of the participants who became infected with HIV. He said he was glad he had taken part because its close monitoring meant he was diagnosed and treated much sooner than most people.
“We’ve got to keep moving forward,” Robbins said. The study “certainly can lead us down a new direction to hopefully find something that might work.”
Multiple attempts at creating an Aids vaccine have failed over the years. A 2009 study in Thailand is the only one ever to show a modest success, using a somewhat different prime-boost approach. Newer research suggests another approach – to try creating powerful antibodies that could work a step earlier than the T-cell attack, before HIV gets inside the first cell.
Both approaches need continued research funding, said Mitchell Warren of the international Aids Vaccine Advocacy Coalition. “Clearly an Aids vaccine remains critical,” he said.
Testing helps catch the disease early, but experts caution that aggressive use of antiretroviral drugs in asymptomatic patients could breed more resistant HIV
One of the most widely advocated strategies for dealing with HIV/AIDS could double the number of multi-drug-resistant HIV cases in the population of men who have sex with men (MSM) in LA County over the next 10 years, cautions a new study.
In the United States, LA County has the largest incident population of HIV positive individuals.
The so-called “test and treat” policy — which calls for universal testing for HIV as well as treatment with antiretroviral drugs for even those at the earliest stages of the disease — is popular because it has been shown to decrease the number of new HIV cases and deaths due to AIDS.
The problem, according to the study, is that such aggressive and widespread use of antiretroviral drugs would also rapidly and dramatically increase the prevalence of multiple-drug-resistant HIV (MDR).
“We’re not saying that testing everybody and treating everybody is bad. All we’re saying is that you should proceed with caution and closely monitor the prevalence of multi-drug-resistant HIV as you scale up the test and treat model,” said lead author Neeraj Sood, associate professor at the USC Schaeffer Center for Health Policy and Economics.
Sood collaborated with Zachary Wagner, also of the USC Schaeffer Center; USC Ph.D. student Emmanuel Drabo; and Raffaele Vardavas and Amber Jaycocks of the RAND Corporation. Their study received advance online publication by Clinical Infectious Diseases on March 13.
Sood and his colleagues studied the MSM population in LA County, which accounts for 82 percent of people living with HIV/AIDS countywide. They tracked how the disease was treated from 2000 to 2009 and how the virus responded.
Using data from the Centers for Disease Control and their own data, the researchers then generated a model of how the disease would respond under a more aggressive “test and treat” policy over the next 10 years.
The model showed the prevalence of MDR jumping from 4.79 percent to 9.06 percent by 2023.
A more cautious approach, Sood suggested, would be simply to aggressively test for the disease but to avoid prescribing antiretroviral drugs to asymptomatic patients. The modeling shows that strategy still making significant gains against HIV/AIDS, without the increase in MDR HIV.
“Prior studies show a dramatic reduction in risk-taking behavior by individuals once they know their HIV-positive status,” Sood said.
This work was supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development, grant # R01HD054877.
Two weeks after the revelation that a baby has been “cured” of HIV, reports suggest that a similar treatment can cure some adults too. Early treatment seems crucial, but does not guarantee success.
Asier Sáez-Cirión of the Pasteur Institute’s unit for regulation of retroviral infections in Paris analysed 70 people with HIV who had been treated with antiretroviral drugs (ARVs) between 35 days and 10 weeks after infection – much sooner than people are normally treated.
All of the participants’ drug regimes had been interrupted for one reason or another. For example, some people had made a personal choice to stop taking the drugs, others had been part of a trial of different drug protocols.
Most of the 70 people relapsed when their treatment was interrupted, with the virus rebounding rapidly to pre-treatment levels. But 14 of them – four women and 10 men – were able to stay off of ARVs without relapsing, having taken the drugs for an average of three years.
The 14 adults still have traces of HIV in their blood, but at such low levels that their body can naturally keep it in check without drugs.
On average, the 14 adults have been off medication for seven years. One has gone 10-and-a-half years without drugs. “It’s not eradication, but they can clearly live without pills for a very long period of time,” says Sáez-Cirión.
Last week, a baby was reported to have been “functionally cured” of HIV after receiving a three-drug regime of ARVs almost immediately after birth. Sáez-Cirión warns that rapid treatment doesn’t work for everyone, but the new study reinforces the conclusion that early intervention is important.
“There are three benefits to early treatment,” says Sáez-Cirión. “It limits the reservoir of HIV that can persist, limits the diversity of the virus and preserves the immune response to the virus that keeps it in check.”
Further analysis confirmed that the 14 adults were not “super-controllers” – the 1 per cent of the population that are naturally resistant to HIV – since they lack the necessary protective genes. Also, natural controllers rapidly suppress their infections, whereas these 14 mostly had severe symptoms which led to their early treatment. “Paradoxically, doing badly helped them do better later,” says Sáez-Cirión.
The researchers are trying to identify additional factors that could explain why early intervention only works on some people, hopefully extending the scope for more functional cures.
“This whole area is fascinating, and we’ve been looking very closely at issues of early initiation of treatment, and the potential for functional cures,” says Andrew Ball, senior adviser on HIV/AIDS strategy at the World Health Organization in Geneva.
“The big challenge is identifying people very early in their infection,” says Ball, adding that many people resist testing because of the stigma and potential discrimination. “There’s a good rationale for being tested early, and the latest results may give some encouragement to do that,” he says.
Journal reference: PLoS Pathogens, DOI: 10.1371/journal.ppat.1003211
Joshua L. Hood, MD, PhD
Nanoparticles (purple) carrying melittin (green) fuse with HIV (small circles with spiked outer ring), destroying the virus’s protective envelope. Molecular bumpers (small red ovals) prevent the nanoparticles from harming the body’s normal cells, which are much larger in size.
Nanoparticles carrying a toxin found in bee venom can destroy human immunodeficiency virus (HIV) while leaving surrounding cells unharmed, researchers at Washington University School of Medicine in St. Louis have shown. The finding is an important step toward developing a vaginal gel that may prevent the spread of HIV, the virus that causes AIDS.
“Our hope is that in places where HIV is running rampant, people could use this gel as a preventive measure to stop the initial infection,” says Joshua L. Hood, MD, PhD, a research instructor in medicine.
The study appears in the current issue of Antiviral Therapy.
Bee venom contains a potent toxin called melittin that can poke holes in the protective envelope that surrounds HIV, and other viruses. Large amounts of free melittin can cause a lot of damage. Indeed, in addition to anti-viral therapy, the paper’s senior author, Samuel A. Wickline, MD, the J. Russell Hornsby Professor of Biomedical Sciences, has shown melittin-loaded nanoparticles to be effective in killing tumor cells.
The new study shows that melittin loaded onto these nanoparticles does not harm normal cells. That’s because Hood added protective bumpers to the nanoparticle surface. When the nanoparticles come into contact with normal cells, which are much larger in size, the particles simply bounce off. HIV, on the other hand, is even smaller than the nanoparticle, so HIV fits between the bumpers and makes contact with the surface of the nanoparticle, where the bee toxin awaits.
“Melittin on the nanoparticles fuses with the viral envelope,” Hood says. “The melittin forms little pore-like attack complexes and ruptures the envelope, stripping it off the virus.”
According to Hood, an advantage of this approach is that the nanoparticle attacks an essential part of the virus’ structure. In contrast, most anti-HIV drugs inhibit the virus’s ability to replicate. But this anti-replication strategy does nothing to stop initial infection, and some strains of the virus have found ways around these drugs and reproduce anyway.
“We are attacking an inherent physical property of HIV,” Hood says. “Theoretically, there isn’t any way for the virus to adapt to that. The virus has to have a protective coat, a double-layered membrane that covers the virus.”
Beyond prevention in the form of a vaginal gel, Hood also sees potential for using nanoparticles with melittin as therapy for existing HIV infections, especially those that are drug-resistant. The nanoparticles could be injected intravenously and, in theory, would be able to clear HIV from the blood stream.
“The basic particle that we are using in these experiments was developed many years ago as an artificial blood product,” Hood says. “It didn’t work very well for delivering oxygen, but it circulates safely in the body and gives us a nice platform that we can adapt to fight different kinds of infections.”
Since melittin attacks double-layered membranes indiscriminately, this concept is not limited to HIV. Many viruses, including hepatitis B and C, rely on the same kind of protective envelope and would be vulnerable to melittin-loaded nanoparticles.
While this particular paper does not address contraception, Hood says the gel easily could be adapted to target sperm as well as HIV. But in some cases people may only want the HIV protection.
“We also are looking at this for couples where only one of the partners has HIV, and they want to have a baby,” Hood says. “These particles by themselves are actually very safe for sperm, for the same reason they are safe for vaginal cells.”
While this work was done in cells in a laboratory environment, Hood and his colleagues say the nanoparticles are easy to manufacture in large enough quantities to supply them for future clinical trials.
Hood JL, Jallouck AP, Campbell N, Ratner L, Wickline SA. Cytolytic nanoparticles attenuate HIV-1 infectivity. Antiviral Therapy. Vol. 19: 95 – 103. 2013
This work was supported by the Bill & Melinda Gates Foundation Grand Challenges Explorations grant number OPP1024642 ‘Fusogenic nanoparticles for combined anti-HIV/contraception.’
Washington University School of Medicine’s 2,100 employed and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children’s hospitals. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked sixth in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children’s hospitals, the School of Medicine is linked to BJC HealthCare.
Sun, 3 Mar 2013 21:29 GMT
* Mississippi girl’s case is the first account of an HIV cure in an infant
* Doctors started treatment within 30 hours of the child’s birth
By Julie Steenhuysen
CHICAGO, March 3 (Reuters) – A baby girl in Mississippi who was born with HIV has been cured after very early treatment with standard drug therapy, U.S. researchers reported on Sunday, in a potentially ground-breaking case that could offer insights on how to eradicate HIV infection in its youngest victims.
The child’s story is the first account of an infant achieving a so-called functional cure, a rare event in which a person achieves remission without the need for drugs and standard blood tests show no signs that the virus is making copies of itself.
More testing needs to be done to see if the treatment would have the same effect on other children, but the results could change the way high-risk babies are treated and possibly lead to a cure for children with HIV, the virus that causes AIDS.
“This is a proof of concept that HIV can be potentially curable in infants,” said Dr. Deborah Persaud, a virologist at Johns Hopkins University in Baltimore, who presented the findings at the Conference on Retroviruses and Opportunistic Infections in Atlanta.
The child’s story is different from the now famous case of Timothy Ray Brown, the so-called “Berlin patient,” whose HIV infection was completely eradicated through an elaborate treatment for leukemia in 2007 that involved the destruction of his immune system and a stem cell transplant from a donor with a rare genetic mutation that resists HIV infection.
Instead of Brown’s costly treatment, the Mississippi baby’s case involved the use of a cocktail of widely available drugs already used to treat HIV infection in infants.
When the baby girl was born in a rural hospital, her mother had just tested positive for HIV infection. Because her mother had not received any prenatal HIV treatment, doctors knew the child was born at high risk of being infected. So they transferred the baby to the University of Mississippi Medical Center in Jackson, where she came under the care of Dr. Hannah Gay, a pediatric HIV specialist.
Because of her high infection risk, Dr. Gay put the infant on a cocktail of three standard HIV-fighting drugs when she was just 30 hours old, even before lab tests came back confirming her infection. In more typical pregnancies when an HIV-infected mother has been given drugs to reduce the risk of transmission to her child, the baby would only have been given a single drug to reduce her infection risk.
Researchers believe this early use of antiviral treatment likely resulted in the infant’s cure by keeping the virus from forming hard-to-treat pools of cells known as viral reservoirs, which lie dormant and out of the reach of standard medications. These reservoirs rekindle HIV infection in patients who stop therapy, and they are the reason most HIV-infected individuals need lifelong treatment to keep the infection at bay.
After starting on treatment, the baby’s immune system responded and tests showed levels of the virus were diminishing until it was undetectable 29 days after birth. The baby received regular treatment for 18 months, but then stopped coming to appointments for a period of about 10 months, when her mother said she was not given any treatment. The doctors did not say why the mother stopped coming.
When the child came back under the care of Dr. Gay, she ordered standard blood tests to see how the child was faring before resuming antiviral therapy.
What she found was surprising. The first blood test did not turn up any detectible levels of HIV. Neither did the second. And tests for HIV-specific antibodies – the standard clinical indicator of HIV infection – also remained negative.
“At that point, I knew I was dealing with a very unusual case,” Dr. Gay said.
Baffled, Dr. Gay turned to her friend and longtime colleague, Dr. Katherine Luzuriaga of the University of Massachusetts, and she and Persaud did a series of sophisticated lab tests on the child’s blood.
The first looked for silent reservoirs of the virus where it remains dormant but can replicate if activated. That is detected in a type of immune cell known as a CD4 T-cell. After culturing the child’s cells, they found no sign of the virus.
Then, the team looked for HIV DNA, which indicates that the virus has integrated itself into the genetic material of the infected person. This test turned up such low levels that it was just above the limit of the test’s ability to detect it.
The third test looked for bits of genetic material known as viral RNA. They only found a single copy of viral RNA in one of the two tests they ran.
Because there is no detectible virus in the child’s blood, the team has advised that she not be given antiretroviral therapy (ART), whose goal is to block the virus from replicating in the blood. Instead, she will be monitored closely.
Dr. Rowena Johnston, vice president and director of research for the Foundation for AIDS Research, which helped fund the study, said the fact that the cure was achieved by antiretroviral therapy alone makes it “imperative that we learn more about a newborn’s immune system, how it differs from an adult’s and what factors made it possible for the child to be cured.”
Because the child’s treatment was stopped, the doctors were able to identify that this child had been cured, raising questions about whether other children who received early treatment and have undetectable viral loads may also be cured without knowing it.
But the doctors warned parents not to be tempted to take their children off treatment to see if the virus comes back. Normally, when patients stop taking their medications, the virus comes roaring back, and treatment interruptions increase the risk that the virus will develop drug resistance.
“We don’t want that,” Dr. Gay said. “Patients who are on successful therapy need to stay on their successful therapy until we figure out a whole lot more about what was going on with this child and what we can do for others in the future.”
The researchers are trying to find biomarkers that would offer a rationale to consider stopping therapy within the context of a clinical trial. If they can learn what caused the child to clear her virus, they hope to replicate that in other babies, and eventually learn to routinely prevent infections. (Reporting by Julie Steenhuysen; Editing by Jilian Mincer and Sandra Maler)
People with HIV are less able to recognise facial emotion than non-infected people finds a study published in the launch edition of BioMed Central’s open access journal BMC Psychology. Reduction in their ability to recognise fear in others is linked to a similar loss in immediate recall, while those with a lower general neurocognitive performance also had a reduced ability to recognise happiness.
The mechanism behind recognition of facial emotion is complex, involving many different areas of the brain, including the frontostriatal pathway and amygdala. The frontostriatal pathway is essential for learning and behavioural adaption, while the amygdale is involved in memory and emotion. The loss of this ability can be debilitating, impacting daily life and personal interactions.
Comparing people with HIV to a control group without HIV, researchers from the Catholic University of the Sacred Heart in Rome discovered that from the six basic expressions of emotion (disgust, anger, fear, happiness, surprise, sadness) that fear is the most difficult emotion to recognise. People with HIV were less accurate in identifying fearful expressions than the controls and also tended to have difficulties in immediate recall of words indicating a link between the two.
People with a higher number of AIDS-related events, such as pneumonia, Kaposi’s sarcoma, or tuberculosis, and people with neurocognitive problems in memory, attention and decision making, language and speed of mental processing, were less able to recognise happiness in others.
Dr Eleonora Baldonero, who led the study commented, “The severity of HIV-associated neurocognitive disorders has been significantly reduced thanks to combination antiretroviral therapy. Nevertheless our research highlights a link between cognition and facial recognition and that AIDS-related events affect both. Understanding this on a individual level can help the long-term personal management of HIV.”
Open access publisher BioMed Central is proud to announce the launch of BMC Psychology, the newest addition to the BMC-series portfolio. This marks a significant milestone for the BMC-series family of open access journals, as it is the first new journal since 2008 and will lead the way for other new launches within the series.
In recognition of the need to keep the community up to date with the latest research in psychology the BMC series developed BMC Psychology as the first solely dedicated open access psychology journal of its kind, covering all aspects of psychology. It will also practice open peer review in keeping with all the medical journals currently published in the BMC series.
Dr Hilary Glover Scientific Press Officer, BioMed Central Tel: +44 (0) 20 3192 2370 Mob: +44 (0) 778 698 1967 Email: firstname.lastname@example.org
1. Evaluation of emotion processing in HIV-infected patients and correlation with cognitive performance Eleonora Baldonero, Nicoletta Ciccarelli, Massimiliano Fabbiani, Manuela Colafigli, Erika Improta, Alessandro D’Avino, Annalisa Mondi, Roberto Cauda, Simona Di Giambenedetto and Maria Caterina Silveri BMC Psychology (in press)
Please name the journal in any story you write. If you are writing for the web, please link to the article. All articles are available free of charge, according to BioMed Central’s open access policy.
Article citation and URL available on request on the day of publication.
2. BMC Psychology is an open access, peer-reviewed journal that considers manuscripts on all aspects of psychology, human behavior and the mind, including developmental, clinical, cognitive, experimental, social, evolutionary and educational psychology, as well as personality and individual differences. The journal welcomes quantitative and qualitative research methods, including animal studies.
3. The BMC series is a group of open access, peer-reviewed journals that spans most areas of biological and clinical research. There are currently 65 journals in the series (see complete list). BMC Biology and BMC Medicine are highly selective journals, publishing articles of broad interest; the other journals in the series focus on specific disciplines. @BMCSeries
4. BioMed Central (http://www.biomedcentral.com/) is an STM (Science, Technology and Medicine) publisher which has pioneered the open access publishing model. All peer-reviewed research articles published by BioMed Central are made immediately and freely accessible online, and are licensed to allow redistribution and reuse. BioMed Central is part of Springer Science+Business Media, a leading global publisher in the STM sector. @BioMedCentral
Contact: Enrique Rivero email@example.com 310-794-2273 University of California – Los Angeles Health Sciences
A team of UCLA-led researchers has identified a protein with broad virus-fighting properties that potentially could be used as a weapon against deadly human pathogenic viruses such as HIV, Ebola, Rift Valley Fever, Nipah and others designated “priority pathogens” for national biosecurity purposes by the National Institute of Allergy and Infectious Disease.
In a study published in the January issue of the journal Immunity, the researchers describe the novel antiviral property of the protein, cholesterol-25-hydroxylase (CH25H), an enzyme that converts cholesterol to an oxysterol called 25-hydroxycholesterol (25HC), which can permeate a cell’s wall and block a virus from getting in.
Interestingly, the CH25H enzyme is activated by interferon, an essential antiviral cell-signaling protein produced in the body, said lead author Su-Yang Liu, a student in the department of microbiology, immunology and molecular genetics at the David Geffen School of Medicine at UCLA.
“Antiviral genes have been hard to apply for therapeutic purposes because it is difficult to express genes in cells,” said Liu, who performed the study with principal investigator Genhong Cheng, a professor of microbiology, immunology and molecular genetics. “CH25H, however, produces a natural, soluble oxysterol that can be synthesized and administered.
“Also, our initial studies showing that 25HC can inhibit HIV growth in vivo should prompt further study into membrane-modifying cholesterols that inhibit viruses,” he added.
The discovery is particularly relevant to efforts to develop broad-spectrum antivirals against an increasing number of merging viral pathogens, Liu said.
Working with Jerome Zack, a professor of microbiology, immunology and molecular genetics and an associate director of the UCLA AIDS Institute, the researchers initially found that 25HC dramatically inhibited HIV in cell cultures. Next, they administered 25HC in mice implanted with human tissues and found that it significantly reduced their HIV load within seven days. The 25HC also reversed the T-cell depletion caused by HIV.
By contrast, mice that had the CH25H gene knocked out were more susceptible to a mouse gammaherpes virus, the researchers found.
In collaboration with Dr. Benhur Lee, a professor of pathology and laboratory medicine and a member of the UCLA AIDS Institute, they discovered that 25HC inhibited HIV entry into the cell. Furthermore, in cell cultures, it was found to inhibit the growth of other deadly viruses, such as Ebola, Nipah and the Rift Valley Fever virus.
Intriguingly, CH25H expression in cells requires interferon. While interferon has been known for more than 60 years to be a critical part of the body’s natural defense mechanism against viruses, the protein itself does not have any antiviral properties. Rather, it triggers the expression of many antiviral genes. While other studies have identified some antiviral genes that are activated by interferon, this research gives the first description of an interferon-induced antiviral oxysterol through the activation of the enzyme CH25H. It provides a link to how interferon can cause inhibition of viral membrane fusion, Liu said.
He noted some weaknesses in the research. For instance, 25HC is difficult to deliver in large doses, and its antiviral effect against Ebola, Nipah and other highly pathogenic viruses have yet to be tested in vivo. Also, the researchers still need to compare 25HC’s antiviral effect against other HIV antivirals.
Additional study co-authors were Roghiyh Aliyari, Kelechi Chikere, Matthew D. Marsden and Olivier Pernet, of UCLA; Jennifer K. Smith, Rebecca Nusbaum and Alexander N. Frieberg, of the University of Texas–Galveston; and Guangming Li, Haitao Guo and Lishan Su, of the University of North Carolina–Chapel Hill.
The National Institutes of Health (grants R01 AI078389, AI069120, AI080432, AI095097, AI077454, AI070010 and AI028697), the Warsaw Fellowship, the UCLA Center for AIDS Research (CFAR), the UCLA AIDS Institute, the UCLA Clinical and Translational Science Institute (CTSI), and the Pacific Southwest Regional Center of Excellence (PSWRCE) for Biodefense and Emerging Infectious Diseases funded this study.
The UCLA AIDS Institute, established in 1992, is a multidisciplinary think tank drawing on the skills of top-flight researchers in the worldwide fight against HIV and AIDS, the first cases of which were reported in 1981 by UCLA physicians. Institute members include researchers in virology and immunology, genetics, cancer, neurology, ophthalmology, epidemiology, social sciences, public health, nursing and disease prevention. Their findings have led to advances in treating HIV, as well as other diseases, such as hepatitis B and C, influenza and cancer.
For more news, visit the UCLA Newsroom and follow us on Twitter.
Special edition to mark World TB day maps new issues and approaches to curbing spread of infection
During the 1930s, dedicated sanitaria and invasive surgery were commonly prescribed for those with the infection – usually caused by Mycobacterium tuberculosis, which the editors describe as “the most successful human pathogen of all time.”
TB often lies dormant with no symptoms, but in a proportion of cases, becomes active, predominantly attacking the lungs. But it can also affect the bones and nervous system, and if left untreated can be fatal.
The infection is developing increasing resistance around the world to the powerful drugs currently used to treat it.
“Whatever we may have once optimistically thought, TB remains with death, taxes and political chicanery as being inevitable, unavoidable and deeply unpleasant,” write the joint editors, Andy Bush and Ian Pavord.
“It shows every sign of weathering the storm and superb randomised controlled trials, to emerge in ever-increasingly drug-resistant forms, potentially turning the clock back to the 1930s,” they say.
“This edition of Thorax, coinciding with world TB day, is themed to recognise the ongoing sinister successes of Mycobacterium tuberculosis, unarguably the most successful human pathogen of all time,” they conclude.
The issue contains international research papers, looking at a broad range of issues, from the risk of TB after seroconversion to HIV infection, to the impact of ethnicity on the pattern of disease.
Contact: Cody Mooneyhan firstname.lastname@example.org 301-634-7104 Federation of American Societies for Experimental Biology
New research in The FASEB Journal suggests that a network of steroid molecules found in the brain is disrupted during HIV infection, and treatment with the steroid DHEA-S prevents brain damage
Bethesda, MD—A team of scientists from Canada, Thailand and Morocco have found that DHEA-S may prevent neurocognitive impairment that affects a significant percentage of AIDS patients. In a report appearing in the February 2013 issue of The FASEB Journal, they describe how a network of steroid molecules found in the brain, termed “neurosteroids,” is disrupted during HIV infection leading to brain damage. This suggests that treatment with one of these steroid molecules, called DHEA-S, may offset the disruption caused by the virus to prevent or reduce brain damage.
“From these studies, we have gained a better understanding of how HIV injures the brain during AIDS, together with developing a new treatment approach for the resulting neurological disabilities arising from HIV/AIDS,” said Christopher Power, M.D., co-author of this study from the Department of Medicine at the Medical Research Centre at the University of Alberta in Edmonton, Canada.
To make their discovery, Power and colleagues initially found that neurosteroid enzyme levels were suppressed in the brains of people with HIV/AIDS and that a neurosteroid molecule, DHEA-S, prevented damage to cultured brain cells (neurons) caused by HIV. Then, using an animal model of AIDS, they showed that treatment with DHEA-S prevented neuronal damage in the brain by reducing the adverse effects of HIV. Neurosteroids have already been proposed as treatments for epilepsy, head injury, post-traumatic stress disorder and depression, and these findings extend the potential treatment applications for neurosteroid-related molecules.
“Most people know that AIDS wreaks total havoc on our immune systems,” said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal, “but far fewer people know that the disease can also lead to noticeable brain damage. This research study offers an explanation why this occurs as well as a possible solution for preventing it. The next steps, of course, involve looking into whether or not people will benefit from some form of DHEA-S treatment.”
Receive monthly highlights from The FASEB Journal by e-mail. Sign up at http://www.faseb.org/fjupdate.aspx.
The FASEB Journal is published by the Federation of the American Societies for Experimental Biology (FASEB). It is among the most cited biology journals worldwide according to the Institute for Scientific Information and has been recognized by the Special Libraries Association as one of the top 100 most influential biomedical journals of the past century. FASEB is composed of 26 societies with more than 100,000 members, making it the largest coalition of biomedical research associations in the United States. Its mission is to advance health and welfare by promoting progress and education in biological and biomedical sciences through service to its member societies and through collaborative advocacy.
Details: Ferdinand G. Maingat, Maria J. Polyak, Amber M. Paul, Pornpun Vivithanaporn, Farshid Noorbakhsh, Samir Ahboucha, Glen B. Baker, Keir Pearson, and Christopher Power. Neurosteroid-mediated regulation of brain innate immunity in HIV/AIDS: DHEA-S suppresses neurovirulence. FASEB J February 2013 27:725-737; doi:10.1096/fj.12-215079; http://www.fasebj.org/content/27/2/725.abstract.
Antiretroviral (ARV) drugs are the first line therapy for patients with HIV; however, ARV-treated, HIV-infected individuals still have a higher mortality rate than uninfected individuals. During the course of infection, HIV patients develop inflammation that damages the walls of the intestines, known as the gut mucosa, allowing intestinal microbes to escape and enter the blood stream to cause a life-threatening systemic infection. The health of the gut mucosa is significantly influenced by the complement of bacteria in the gut and there is mounting evidence that probiotic supplements benefit patients intestinal disorders, such as irritable bowel syndrome, C. difficile infection, and inflammatory bowel disease.
In this issue of the Journal of Clinical Investigation, researchers led by Jason Brenchley at the National Institute of Allergy and Infectious Disease, demonstrated that probiotic supplementation may also be beneficial for ARV-treated HIV patients. Brenchley and colleagues treated SIV-infected macaques (a model of human HIV-infection) with either ARV alone or ARV in combination with a mixture of probiotics. Macaques treated with probiotics had enhanced gastrointestinal immune function and decreased inflammation compared to macaques treated with ARV alone. In a companion article, Judith Aberg and colleagues at New York University School of Medicine discuss how these findings could benefit HIV patients.
TITLE: Probiotic/prebiotic supplementation of antiretrovirals improves gastrointestinal immunity in SIV-infected macaques
AUTHOR CONTACT: Jason M. Brenchley NIAID NIH, Bethesda, MD, USA Phone: 301-496-1498; E-mail: email@example.com
View this article at: http://www.jci.org/articles/view/66227?key=1cff041937d9040dfed7
ACCOMPANYING THE ATTENDING PHYSICIAN
TITLE: Clash of the microbes: let’s bring back the good guys
AUTHOR CONTACT: Judith Aberg New York University School of Medicine, New York, NY, USA Phone: 2122637300; Fax: ; E-mail: firstname.lastname@example.org
View this article at: http://www.jci.org/articles/view/66736?key=64b158b04e2a168811a3
- 17:40 13 December 2012 by Jessica Hamzelou
The largest ever study into the state of the world’s health has revealed that, for the first time, the number of years of healthy living lost as a result of people eating too much outweigh the number lost by people eating too little.
The Global Burden of Disease report – a massive research effort involving almost 500 scientists in 50 countries – also concludes that we have finally got a handle on some common infectious diseases, helping to save millions of children from early deaths. But collectively we are spending more of our lives living in poor health and with disability.
“The Global Burden of Disease 2010 is the most comprehensive assessment of human health in the history of medicine,” says Richard Horton, editor of The Lancet, in which the report will be published. “It provides insights into human health that are comparable in scope and depth to the sequencing of the human genome.”
The report assessed the prevalence of diseases and causes of death across the globe in 2010, and compared these to data collected in 1990 to identify any trends.
For the first time on a global scale, being overweight has become more of a health problem than lack of nutrition. In 1990, undernutrition was the leading cause of disease burden, measured as the number of years of healthy life an average person could expect to lose as a result of illness or early death. Back then, a high body-mass index, or BMI, was ranked tenth. Now, undernutrition has dropped to eighth place, while BMI has risen to become the sixth leading cause of disease burden.
Too much to eat
“A greater amount of disease burden has occurred because people are fat and have too much to eat, as opposed to having too little to eat,” says Alan Lopez at the University of Queensland in Brisbane, Australia, who worked on the study.
Being overweight can hike a person’s blood pressure and cause stroke and heart disease; together, these two conditions are responsible for a quarter of all deaths. And the problem isn’t limited to the west – the Middle East is one region that is seeing significant increases in BMI.
But while more of us may be overweight, we are also living longer. In some countries, the change has been huge – the Maldives, for example, has seen an increase in life expectancy of almost 30 years since the 1970s. Rural health programmes have also contributed to big improvements in countries including Bangladesh and Iran.
“There has been a lot of progress,” says Majid Ezzati at Imperial College London, who led part of the study investigating the risk factors of disease. “These are countries that have implemented programmes in large regions and nationwide to get interventions to the people that really need them.”
Progress in eliminating the causes of early childhood death – mainly infections, diarrhoea and birth problems – has been astounding. The rate of death in the under-5s has dropped by 60 per cent since 1990.
Sub-Saharan Africa is still experiencing high levels of mortality from infectious diseases such as HIV and malaria, yet globally deaths from infectious diseases have dropped. In fact, we are more likely to die from non-infectious diseases – especially those caused by being overweight.
Looking forward, obesity and the use of tobacco and alcohol are obvious targets for health policy change. But it is also important to focus on healthy ageing.
“The large burden [of disease] related to disability was a surprise,” says Christopher Murray at the University of Washington in Seattle. “There’s been a focus on mortality, but there’s a huge volume [of disease burden] related to things that don’t really kill you.”
Musculoskeletal disorders – such as neck and back pain – dominate this category, as do mental disorders and substance abuse.
There’s a need to improve awareness of these chronic conditions in the developing world, says Irene Agyepong at the University of Ghana in Accra, who was not involved in the study. “The kind of awareness we have in the western world is not there in the south,” she says. “We have to focus on it now rather than wait until it is upon us, like the HIV AIDS epidemic is on us.”
Tuesday, Nov. 27, 2012
Writer: James E. Hataway, 706/542-5222, email@example.com Contact: Biao He, 706/542-2855, firstname.lastname@example.org
Athens, Ga. – Researchers at the University of Georgia have discovered that a virus commonly found in dogs may serve as the foundation for the next great breakthrough in human vaccine development.
Although harmless in humans, parainfluenza virus 5, or PIV5, is thought to contribute to upper respiratory infections in dogs, and it is a common target for canine vaccines designed to prevent kennel cough. In a paper published recently in PLOS ONE, researchers describe how this virus could be used in humans to protect against diseases that have eluded vaccine efforts for decades.
“We can use this virus as a vector for all kinds of pathogens that are difficult to vaccinate against,” said Biao He, the study’s principal investigator and professor of infectious diseases in UGA’s College of Veterinary Medicine. “We have developed a very strong H5N1 flu vaccine with this technique, but we are also working on vaccines for HIV, tuberculosis and malaria.”
PIV5 does not cause disease in humans, as our immune system is able to recognize and destroy it. By placing antigens from other viruses or parasites inside PIV5, it effectively becomes a delivery vehicle that exposes the human immune system to important pathogens and allows it to create the antibodies that will protect against future infection.
This approach not only ensures full exposure to the vaccine but also is much safer because it does not require the use of attenuated, or weakened, pathogens. For example, an HIV vaccine delivered by PIV5 would contain only those parts of the HIV virus necessary to create immunity, making it impossible to contract the disease from the vaccine.
“Safety is always our number one concern,” said He, who is also a Georgia Research Alliance distinguished investigator and member of the Faculty of Infectious Diseases. “PIV5 makes it much easier to vaccinate without having to use live pathogens.”
Using viruses as a delivery mechanism for vaccines is not a new technique, but previous efforts have been fraught with difficulty. If humans or animals already possess a strong immunity to the virus used for delivery, the vaccine is unlikely to work, as it will be destroyed by the immune system too quickly.
“Pre-existing immunity to viruses is the main reason most of these vaccines fail,” He said.
But in this latest study, He and his colleagues demonstrate that immunity to PIV5 does not limit its effectiveness as a vaccine delivery mechanism, even though many animals-including humans- already carry antibodies against it.
In their experiments, the researchers found that a single dose inoculation using PIV5 protected mice from the influenza strain that causes seasonal flu. Another single dose experimental vaccine also protected mice from the highly pathogenic and deadly H5N1 virus commonly known as bird flu.
This recent work is a culmination of more than fifteen years of research and experimentation with the PIV5 virus, and He has confidence that it will serve as an excellent foundation for vaccines to treat diseases in both animals and humans.
“I believe we have the best H5N1 vaccine candidate in existence,” He said. “But we have also opened up a big field for a host of new vaccines.”
UGA Faculty of Infectious Diseases The University of Georgia Faculty of Infectious Diseases was created in 2007 to address existing and emerging infectious disease threats more effectively by integrating multidisciplinary research in animal, human and ecosystem health. Researchers from across the university focus on epidemiology, host-pathogen interactions, the evolution of infectious diseases, disease surveillance and predictors and the development of countermeasures such as vaccines, therapeutics and diagnostics. For more information about the Faculty of Infectious Diseases, see fid.ovpr.uga.edu.
UGA College of Veterinary Medicine The UGA College of Veterinary Medicine, founded in 1946, is dedicated to training future veterinarians, to conducting research related to animal and human diseases, and to providing veterinary services for animals and their owners. Research efforts are aimed at enhancing the quality of life for animals and people, improving the productivity of poultry and livestock, and preserving a healthy interface between wildlife and people in the environment they share. The college enrolls 102 students each fall out of more than 800 who apply.
Researchers coated condoms in microscopic particles of silver — which has long been known to have disinfectant …University of Manitoba medical microbiologist Dr Xiaojian Yao, who specializes in researching the HIV virus, has discovered a potential new way to protect ourselves against HIV and the Herpes virus: silver nanoparticles.
He and his team coated condoms in microscopic particles of silver — which has long been known to have disinfectant properties — and they found that when they brought the silver-coated condoms into contact with HIV and Herpes, both viruses were completely inactivated. Additionally, they discovered that both the T-cell and macrophage strains of HIV, as well as drug-resistant strains, were highly susceptible to the silver nanoparticles, and they also acted to prevent the growth of bacteria and fungi.
Nanoparticle research is being pursued in a number of fields, due to their potential as a bridge between larger, bulk substances and the structures of atoms and molecules.
“At such nanoscale, the extremely small size of silver particles exhibits remarkable, unusual physio-chemical properties and biological activity,” said Yao, according to the National Post.
It’s still unclear exactly how the silver nanoparticles are deactivating the viruses, but the research is still in its beginning stages. According to Yao, the nanoparticles themselves, or silver ions released by them, could be bonding to the viruses or altering ‘key proteins’ on the surface of the virus, preventing them from attaching to their host.
Current efforts to make condoms more effective in preventing STDs has included the use of Nonoxynol-9, which recent studies have shown can actually make infection more likely, due to causing genital inflammation and ulceration. Silver nanoparticles, on the other hand, do not cause inflammation and are, in fact, anti-inflammatory, according to the study. Although some silver ions are toxic, the silver nanoparticles themselves are relatively non-toxic, and since the condoms would be discarded quickly after use, exposure would be limited.
Furthermore, since the mere presence of the nanoparticles inhibits the viruses, bacteria and fungi, and the particles do no wash off, anyone who may handle the condom after use would also likely be protected from any potential infection.
Dr Julio Montaner, the director of the B.C. Centre for Excellence in HIV/AIDS called the research “promising”, according to the National Post, but the major issue with condoms is still whether or not they are used.
“Unfortunately, at the most critical moment when these decisions are so important, people’s judgment may be impaired,” said Dr. Montaner. “At the end of the day, if they stay in the pocket, it’s not going to do the job.”
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- Cows can’t catch HIV but they can produce antibodies against the virus
- Scientists injected cows with HIV protein, and collected resulting antibodies from the milk
- They plan to create a cream for women to prevent HIV transmission
PUBLISHED:05:24 EST, 24 October 2012| UPDATED:05:48 EST, 24 October 2012
Cows cannot contract HIV but their immune systems develop antibodies against the foreign protein
Love it or hate it, cow’s milk is an excellent source of calcium and vitamin D. Now scientists think they can harness it to protect people from HIV.
Researchers found that cows could be used to produce antibodies that defend against the human immunodeficiency virus (HIV). The animals can’t contract the disease themselves.
The next step will be to develop it into a cream which women can apply to protect themselves from contracting HIV from sexual partners.
A team from Melbourne University worked with Australian biotechnology company Immuron Ltd to develop the milk.
The scientists, led by Dr Marti Kramski, vaccinated pregnant cows with an HIV protein and studied the first milk that cows produced after giving birth.
The first milk, called the colostrum, is naturally packed with antibodies to protect the newborn calf from infections. The vaccinated cows produced HIV antibodies in their milk.
‘We were able to harvest antibodies specific to the HIV surface protein from the milk,’ said Dr Kramski.
‘We have tested these antibodies and found in our laboratory experiments that they bind to HIV and that this inhibits the virus from infecting and entering human cells.’
The HIV-inhibiting antibodies from cows’ milk will be developed into a cream called a microbicide that is applied into the vagina before and/or after sex to protect women from contracting sexually transmitted infections.
Other microbicides are being developed around the world but the antibodies in this research are easier and cheaper to produce, providing a new HIV-prevention strategy.
‘We hope that our anti-HIV milk antibodies will provide a user-friendly, female-controlled, safe and effective tool for the prevention of sexually acquired HIV infection,’ Dr Kramski said.
‘If proven effective in humans, it will empower women to protect themselves against HIV.’
Marti Kramski, left, at the University of Melbourne with frozen milk containing HIV antibodies. Pictured with colleagues Behnaz Heydarchi, middle, and Rob Center
About 30 million people are living with HIV globally and there is presently no effective vaccine for humans.The research was supported by the Australian Centre for HIV and Hepatitis Virology Research and the NHMRC.
Dr Kramski and her colleagues are now developing plans for animal and human studies.
The work was being sponsored by Fresh Science, a national program sponsored by the Australian Government. It is published in the journal Antimicrobial Agents and Chemotherapy.
2009 study posted for filing
(AFP)–May 19, 2009
WASHINGTON (AFP) – A chemical found in green tea helps inhibit sexual transmission of the virus which causes AIDS, said a study Tuesday that recommends using the compound in vaginal creams to supplement antiretrovirals.
Medical experts at Germany’s University of Heidelberg said the compound could be a low-cost arrow in the quiver of medical weapons to fight the spread of HIV in research-poor countries.
The researchers said they determined that the green tea polyphenol, or vegetable tannin, called epigallocatechin-3-gallate (EGCG) is capable of neutralizing a protein in sperm which serves as a vector for viral transmission during sex.
EGCG degrades what is known as a semen-derived enhancer of virus infection, or SEVI, described in the study as “an important infectivity factor of HIV.”
Writing in the online edition of the Proceedings of the National Academy of Sciences, the researchers said they “recently identified a peptide fraction in human semen that consistently enhanced HIV-1 infection.”
SEVIs capture viral elements and attach them to the surface of target cells, enhancing cell fusion and decreasing a cell’s ability to repel viral threats.
EGCG “targets SEVI for degradation” and “abrogates semen-mediated enhancement of HIV-1 infection in the absence of cellular toxicity,” said the researchers, some of whom work at the university’s Heinrich-Pette-Institute for Experimental Virology and Immunology.
Because of its effects on semen-based HIV transmission threats, the study’s authors said “EGCG appears to be a promising supplement to antiretroviral microbicides to reduce sexual transmission of HIV-1.”
With the vast majority of the world’s 33 million people with HIV infected through heterosexual sex, and as 96 percent of new infections occur in poor and developing nations, researchers said the use of green tea EGCG in topical creams would “provide a simple and affordable prevention method” to guard against HIV transmission.
Green tea, which originated in China and is widely consumed in Asia, the Middle East and growing numbers of western countries, is already popular for its antioxidant qualities.
2008 study posted for filing
Increasing the production of naturally occurring proteins that contain selenium in human blood cells slows down multiplication of the AIDS virus, according to biochemists.
“We have found that increasing the expression of proteins that contain selenium negatively affects the replication of HIV,” said K. Sandeep Prabhu, Penn State assistant professor of immunology and molecular toxicology. “Our results suggest a reduction in viral replication by at least 10-fold.”
Selenium is a micronutrient that the body needs to maintain normal metabolism. Unlike other nutrients, which bind to certain proteins and modulate the protein’s activity, selenium gets incorporated into proteins in the form of an amino acid called selenocysteine.
These proteins – selenoproteins – are especially important in reducing the stress caused by an infection, thereby slowing its spread.
Upon infecting a person, the virus quickly degrades selenoproteins so that it can replicate efficiently. It is unclear just how the virus is able to silence these proteins but Prabhu and his colleagues believe that stress inflicted on cells by the rapidly dividing virus, which produces a key protein known as Tat, is the likely culprit.
Tat is one of about 14 odd proteins produced by HIV during the first stage of infection. The job of these proteins is to trigger the expression of all the other genes that the virus needs to sustain itself. In addition, Tat also plays a key role in helping the virus replicate.
One of the proteins that targets Tat is a selenoprotein known as TR1.
“Since HIV targets the selenoproteins, we thought that the logical way to deal with the virus is to increase the expression of such proteins in the body,” explained Prabhu, whose team’s findings are outlined this week (Nov. 28) in the Journal of Biological Chemistry.
Researchers first isolated blood cells from healthy human volunteers who did not have HIV, and infected those cells with the virus. Next, they added tiny amounts of a selenium compound – sodium selenite – into the cell culture to see the effect on viral replication.
Results from the tests indicate that the addition of selenium inhibits the replication of HIV at least 10-fold, compared to cell cultures in which no selenium is added. When the researchers selectively reduced production of the selenium containing TR1 protein, they observed a 3.5-fold increase in viral replication.
“This confirms that while increasing the expression of TR1 has a negative impact on the replication of HIV, reducing it helps the virus replicate more efficiently,” explained Prabhu. He believes that TR1 works by upsetting the chemical structure of Tat, which in turn reduces the virus’ ability to replicate.
“Once we fully understand the function of these selenium proteins, it will give us a handle to come up with more effective drugs,” said Prabhu, whose work is partly funded by the National Institutes of Health.
Other researchers on the paper include Parisa Kalantari, post-doctoral scholar; Vivek Narayan, graduate student; Kambadur Muralidhar, visiting faculty; Ujjawal H. Gandhi, graduate student; and Hema Vunta, graduate student, all at Penn State; Satish K. Natarajan, research associate, University of Nebraska; and Andrew J. Henderson, associate professor of medicine and microbiology, Boston University.
Public release date: 30-Sep-2012
Researchers track the spread of human invasive non-Typhoidal Salmonella in sub-Saharan Africa
A new study out today (Sunday 30 September) reveals that the emergence and spread of a rapidly evolving invasive intestinal disease, that has a significant mortality rate (up to 45%) in infected people in sub-Saharan Africa, seems to have been potentiated by the HIV epidemic in Africa.
The team found that invasive non-Typhoidal Salmonella (iNTS) disease is caused by a new form of the bacteria Salmonella Typhimurium that has spread from two different focal hubs in Southern and Central Africa beginning 52 and 35 years ago, respectively. They also found that one of the major contributing factors for the successful spread of iNTS was the acquisition of genes that afford resistance to several front line drugs used to treat blood-borne infection such as iNTS.
iNTS is a blood-borne infection that kills approximately one of four people in sub-Saharan Africa who catch it. Yet, in the rest of the world, NTS is a leading cause of acute inflammatory diarrhoea that is self-limiting and tends to be fatal in less than 1 per cent of people infected. The disease is more severe in sub-Saharan Africa than the rest of the world because of factors such as malnutrition, co-infection with malaria or HIV and potentially the novel genotype of the Salmonella bacteria.
“The immune system susceptibility provided by HIV, malaria and malnutrition at a young age, may provide a population in sub-Saharan Africa that is large enough for this detrimental pathogen to enter, adapt, circulate and thrive,” says Chinyere Okoro, joint first author from the Wellcome Trust Sanger Institute. “We used whole genome sequencing to define a novel lineage of Salmonella Typhimurium that is causing a previously unrecognised epidemic across the region. Its genetic makeup is evolving into a more typhoid like bacteria, able to efficiently spread around the human body”
From sequenced samples, the team created a phylogenetic or ‘family tree’, depicting the pathogen’s evolution, dating when each sample first emerged and overlaying this with geographical information about where these samples came from. They found that this invasive disease comprises of two very closely related waves; the first wave originated from a possible south-eastern hub, about 52 years ago and the second originated about 35 years ago, possibly from the Congo Basin.
“The HIV epidemic in sub-Saharan Africa is thought to have begun in a central region and underwent expansion eastwards, a strikingly similar dynamic to that observed for second iNTS wave,” says Dr Robert Kingsley, joint first author from the Wellcome Trust Sanger Institute. “Our findings suggest the current epidemic of iNTS and its transmission across sub-Saharan Africa may have been potentiated by an increase in the critical population of susceptible, immune-compromised people.”
The team identified that the vast majority of samples from the second wave of iNTS contains a gene that makes them resistant to chloramphenicol, a frontline antibiotic in the treatment of Salmonella. This gene was not present in the samples from the first wave of iNTS. This observation suggests that iNTS acquired this gene early on in the evolution of the second wave, probably around the time of its spread from the Congo basin.
“Because it acquired resistance to chloramphenicol, this pathogen has much greater opportunity to survive and spread across the region,” says Professor Gordon Dougan, lead author from the Wellcome Trust Sanger Institute. “This is the first time that the power of whole-genome sequencing has been used to track the spread of iNTS. Our research highlights the power this approach has to monitor the emergence and spread of dangerous pathogens both locally and globally over time.”
“There has been some evidence that this disease can be passed from human to human. Now the race is on to discover how NTS is actually transmitted in sub-Saharan Africa so that effective intervention strategies can be implemented.”
Notes to Editors
Chinyere K. Okoro, Robert A. Kingsley, Thomas R. Connor et al. ‘Intra-continental spread of human invasive Salmonella Typhimurium pathovariants in sub-Saharan Africa’
Published in Nature Genetics 30 September 2012. DOI: 10.1038/ng.2423
This work was funded by the Wellcome Trust and Tropical Research Fellowship from the Wellcome Trust and Clinical Research Fellowship from GlaxoSmithKline.
Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton Cambridge, UK. CB10 1SA
Mahidol-Oxford Tropical Medicine Research Unit, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand
Department of Clinical Infection, Microbiology and Immunology, Institute for Infection and Global Health, University of Liverpool, Liverpool, UK
Centre for Microbiology Research, Kenya Medical Research Institute, Nairobi, Kenya
Malawi-Liverpool-Wellcome Trust Clinical Research Program, University of Malawi College of Medicine, Blantyre, Malawi
Department of Microbiology, College of Medicine, University of Malawi, Blantyre, Malawi
Department of Gastroenterology, Institute of Translational Medicine, Liverpool University, Liverpool, UK. L69 3GE
Health Protection Agency, Laboratory for Gastrointestinal Infections, Centre for Infections, London, United Kingdom
Norwich Medical School, University of East Anglia, Norwich, United Kingdom
Cellular and Molecular Medicine, School of Medical Sciences, University of Bristol, Bristol, United Kingdom
Division of Paediatric Infectious Diseases, Department of Paediatrics and Human Development, Michigan State University, East Lansing, MI 48824, USA
National Hospital Abuja, Plot 132 Central District (Phase II), Garki Abuja, Nigeria
Barcelona Centre for International Health Research (CRESIB, Hospital Clínic-Universitat de Barcelona), Barcelona, Spain
Centro de Investigação em Saúde de Manhiça (CISM), Manhiça, Mozambique
Instituto Nacional de Saúde, Ministerio de Saúde, Maputo, Mozambique
Novartis Vaccines Institute for Global Health S.r.l. (NVGH), Via Fiorentina 1, 53100 Siena, Italy
MRC Centre for Immune Regulation, School of Immunity and Infection, College of Medicine and Dental Sciences, University of Birmingham, Birmingham, B15 2TT, UK.
Center for Vaccine Development, University of Maryland, Baltimore, HSFI 480, 685 West Baltimore St., Baltimore, MD 21201, USA
Department of Medicine, University of Maryland, Baltimore, HSFI 480, 685 West Baltimore St., Baltimore, MD 21201, USA
The Wellcome Trust Sanger Institute is one of the world’s leading genome centres. Through its ability to conduct research at scale, it is able to engage in bold and long-term exploratory projects that are designed to influence and empower medical science globally. Institute research findings, generated through its own research programmes and through its leading role in international consortia, are being used to develop new diagnostics and treatments for human disease.
The Wellcome Trust is a global charitable foundation dedicated to achieving extraordinary improvements in human and animal health. We support the brightest minds in biomedical research and the medical humanities. Our breadth of support includes public engagement, education and the application of research to improve health. We are independent of both political and commercial interests.
Don Powell Media Manager Wellcome Trust Sanger Institute Hinxton, Cambridge, CB10 1SA, UK Tel +44 (0)1223 496 928 Mobile +44 (0)7753 7753 97 Email email@example.com
End of Notes to Editors
Popular HIV drug may cause memory declines
Johns Hopkins study suggests the commonly prescribed anti-retroviral drug efavirenz attacks brain cells
The way the body metabolizes a commonly prescribed anti-retroviral drug that is used long term by patients infected with HIV may contribute to cognitive impairment by damaging nerve cells, a new Johns Hopkins research suggests.
Nearly 50 percent of people infected with HIV will eventually develop some form of brain damage that, while mild, can affect the ability to drive, work or participate in many daily activities. It has long been assumed that the disease was causing the damage, but Hopkins researchers say the drug efavirenz may play a key role.
People infected with HIV typically take a cocktail of medications to suppress the virus, and many will take the drugs for decades. Efavirenz is known to be very good at controlling the virus and is one of the few that crosses the blood-brain barrier and can target potential reservoirs of virus in the brain. Doctors have long believed that it might be possible to alleviate cognitive impairment associated with HIV by getting more drugs into the brain, but researchers say more caution is needed because there may be long-term effects of these drugs on the brain.
“People with HIV infections can’t stop taking anti-retroviral drugs. We know what happens then and it’s not good,” says Norman J. Haughey, Ph.D., an associate professor of neurology at the Johns Hopkins University School of Medicine. “But we need to be very careful about the types of anti-retrovirals we prescribe, and take a closer look at their long-term effects. Drug toxicities could be a major contributing factor to cognitive impairment in patients with HIV.”
For the study led by Haughey and described online in the Journal of Pharmacology and Experimental Therapeutics, researchers obtained samples of blood and cerebrospinal fluid from HIV-infected subjects enrolled in the NorthEastern AIDS Dementia study who were taking efavirenz. Researchers looked for levels of the drug and its various metabolites, which are substances created when efavirenz is broken down by the liver. Performing experiments on neurons cultured in the lab, the investigators examined the effects of 8-hydroxyefavirenz and other metabolites and found major structural changes when using low levels of 8-hydroxyefavirenz, including the loss of the important spines of the cells.
Haughey and his colleagues found that 8-hydroxyefavirenz is 10 times more toxic to brain cells than the drug itself and, even in low concentrations, causes damage to the dendritic spines of neurons. The dendritic spine is the information processing point of a neuron, where synapses — the structures that allow communication among brain cells — are located.
In the case of efavirenz, a minor modification in the drug’s structure may be able block its toxic effects but not alter its ability to suppress the virus. Namandje N. Bumpus, Ph.D., one of the study’s other authors, has found a way to modify the drug to prevent it from metabolizing into 8-hydroxyefavirenz while maintaining its effectiveness as a tool to suppress the HIV virus.
“Finding and stating a problem is one thing, but it’s another to be able to say we have found this problem and here is an easy fix,” Haughey says.
Haughey says studies like his serve as a reminder that while people infected with HIV are living longer than they were 20 years ago, there are significant problems associated with the drugs used to treat the infection.
“Some people do seem to have this attitude that HIV is no longer a death sentence,” he says. “But even with anti-retroviral treatments, people infected with HIV have shortened lifespans and the chance of cognitive decline is high. It’s nothing you should treat lightly.”
The study was supported by grants from the National Institute on Alcohol Abuse and Alcoholism (AA0017408), the National Institute of Mental Health (MH077543, MH075673 and MH71150), the National Institute on Aging (AG034849) and the National Institute of Neurological Disorders and Stroke (NS049465).
Other Hopkins researchers involved in the study include Luis B. Tovar y Romo, Ph.D.; Lindsay B. Avery, Ph.D.; Ned Sacktor, M.D.; and Justin McArthur, M.B.B.S., M.P.H.
For more information:http://www.hopkinsmedicine.org/neurology_neurosurgery/research/jhu_nimh/researchers
FRIDAY, SEPTEMBER 21, 2012
09/12/2012 2:02 pm
A Florida State University researcher is on a mission to explore the gene-controlling effects of addictive drugs in pursuit of new HIV treatments.
Working under the support of a $1.8 million grant from the National Institutes of Health (NIH), Florida State biologist Jonathan Dennis is studying a unique ability shared between a promising class of HIV treatments known as histone deacetylase inhibitors (HDIs) and psychostimulant drugs such as cocaine.
“Current HIV treatments do just that — they treat the disease by preventing the spread of HIV in the body, rather than eliminating the disease entirely,” Dennis said. “I want to find out how to root out those dormant HIV cells that are evading the treatment, and I believe the gene-controlling functions shared by HDIs and psychostimulant drugs hold the key to helping us do that.”
HDIs and addictive drugs such as cocaine share the ability to control gene expression through changes in the chromatin structure within DNA. In the case of HDI treatment, the chromatin changes are used to wake up dormant HIV virus cells that are hiding in the body.
Dennis believes that addictive drugs do the same thing. Dennis’ work will focus on identifying and understanding the overlapping gene changes that occur between these two types of substances, ultimately providing other researchers with the foundational information they need to turn HDI treatments into HIV cures.
Florida State professor Jonathan Dennis is researching the similarities between addictive drugs and HIV treatments in hopes of finding a cure for the disease.Using the resources available through Florida State University’s unique Integrating Genotype and Phenotype research cluster, Dennis was able to lure the attention of the NIH and obtain the grant. Genotype is the genetic constitution of an organism while the phenotype is its appearance and functional properties.
This research cluster combines cross-disciplinary expertise in the areas of evolutionary biology, molecular biology, genomics and epigenetics to solve one of the most important problems facing biology in the 21st century — the relationship between genotype and phenotype.
“The Integrating Genotype and Phenotype cluster has been critical in my work to unravel the mysteries behind chromatin and gene expression through direct access to other researchers and their areas of expertise,” Dennis said. “Without it I would not have been able to obtain this grant and be able to focus my work on helping the scientific community find a cure for HIV.”
To learn more about the scope and purpose of Dennis’ NIH grant, visit the grant website. To learn more about Dennis, visit his Department of Biological Science Web page. To find out more about the work of the research cluster, visit Integrating Genotype and Phenotype.
Florida State University, rated RU/VH (“Research University/Very High” research activity) by the Carnegie Foundation for the Advancement of Teaching, is one of the nation’s leading research and creative-activity institutions. With nearly $204 million in external research funding in 2011 and a large collection of unique, cutting-edge scientific and performing arts facilities, Florida State offers faculty and students unparalleled opportunities to expand the frontiers of knowledge and discovery in their areas of expertise. To learn more about Florida State research, locate a subject matter expert or arrange an interview on a specific research or creative topic, contact Tom Butler at firstname.lastname@example.org, or Florida State’s News and Research Communications Office at (850) 644-4030.
Editors Top Five:
1. Statins have unexpected effect on pool of powerful brain cells 2. Cholesterol drugs recommended for some 8-year-olds 3. Newborn vitamin A reduces infant mortality 4. Fish oil and red yeast rice studied for lowering blood cholesterol 5. New report: The truth about drug innovation
In this issue:
1. A blue curing light used to harden dental fillings also may stunt tumor growth, Medical College of Georgia researchers say. 2. New report: The truth about drug innovation 3. Salutary pizza spice 4. Morbid thoughts whet the appetite 5. Seniors with type 2 diabetes may experience memory declines immediately after eating unhealthy meal 6. Higher Coffee Consumption Associated with Lower Liver Cancer Risk 7. Prebiotic potential of almonds 8. The tummy’s taste for red wine with red meat 9. A good cup of coffee might be just the wake-up call scientists need to stop multiple sclerosis. 10. United States has highest level of illegal cocaine and cannabis use, and more 11. Watermelon May Have Viagra-Effect 12. Post-exercise caffeine helps muscles refuel 13. Designer diet for prostate cancer 14. Weight Watchers Versus Fitness Centers, MU Study Finds Both Work Best in Combination 15. Red wine ingredient wards off effects of age on heart, bones, eyes and muscle 16. Statins have unexpected effect on pool of powerful brain cells 17. Cholesterol drugs recommended for some 8-year-olds 18. The benefits of green tea in reducing an important risk factor for heart disease 19. Infant formula blocks HIV transmission via breastfeeding 20. Mother’s vitamin D status during pregnancy will affect her baby’s dental health 21. Herbal remedy reduces obesity and heart disease? 22. Newborn vitamin A reduces infant mortality 23. Some antidepressants associated with gastrointestinal bleeding 24. Argyrin: natural substance raises hope for new cancer therapies 25. Leading worldwide cause of cardiovascular disease may be modified by diet 26. Fish oil and red yeast rice studied for lowering blood cholesterol
Health Technology Research Synopsis
34th Issue Date 08 JUL 2008
Compiled By Ralph Turchiano
Re-Post Filing 2008
New findings show a link between micronutrient supplementation and reduced risk of recurrence during tuberculosis chemotherapy, according to a study published in the June 1 issue of The Journal of Infectious Diseases, now available online.
Nutritional assessment and support in tuberculosis therapy, once common before the advent of anti-TB drugs, is no longer an integral part of clinical therapy in most low-income countries even though poor nutrition impairs the immune system and leads to risk of further infection and relapse.
In Tanzania, Eduardo Villamor, MD, DrPH, of the Harvard School of Public Health, and a team of researchers conducted a randomized trial of micronutrients using doses of vitamins A, B-complex, C, E, and selenium or placebo in 887 patients receiving tuberculosis therapy, who were then followed for a medium of 43 months; 471 were HIV-coinfected and not receiving antiretroviral therapy and 416 were HIV-uninfected.
The study showed that micronutrient supplementation was associated with reduced rates of TB recurrence. In the study, both HIV-infected and uninfected patients with pulmonary TB who were receiving the supplements had a decreased risk of TB recurrence during the next few months after the TB culture had become negative: 45 percent overall and 63 percent in HIV-infected patients. Supplementation also reduced the incidence of peripheral neuropathy by 57 percent, irrespective of HIV status, and increased the levels of certain cells (CD3 and CD4) important in immune response in HIV-uninfected patients.
As Villamor noted, “We found that providing micronutrients to patients with tuberculosis who were undergoing anti-TB treatment appeared to decrease the risk of recurrences. This effect was stronger in patients infected with HIV than in those who were HIV-negative. This could be relevant because TB reactivation is common among HIV-infected persons.” Villamor further noted, “that it will be important to find out whether micronutrients improve the outcome of TB treatment in TB-HIV co-infected patients who are undergoing antiretroviral therapy.”
Christine Stabell Benn, MD, and colleagues in Copenhagen noted in their accompanying editorial that results to date relating to TB recurrence and mortality are inconsistent, with previous studies using different dosages and combinations of micronutrients. Dr. Stabell pointed out that the promising results of the Villamor study show that further investigations are needed to develop optimal combinations of micronutrients that can be provided inexpensively in TB therapy to reduce relapses and increase survival.
1) Supplements of common vitamins and other micronutrients may reduce the risk of recurrence in patients receiving tuberculosis treatment.
2) Further studies of micronutrient supplementation offer the potential for an inexpensive treatment strategy for vitamin-deficient tuberculosis patients in low-income countries.
3) The effects of micronutrient supplementation in TB-HIV co-infected patients undergoing antiretroviral therapy have yet to be studied.
Founded in 1904, The Journal of Infectious Diseases is the premier publication in the Western Hemisphere for original research on the pathogenesis, diagnosis, and treatment of infectious diseases; on the microbes that cause them; and on disorders of host immune mechanisms. Articles in JID include research results from microbiology, immunology, epidemiology, and related disciplines. JID is published under the auspices of the Infectious Diseases Society of America (IDSA). Based in Arlington, Va., IDSA is a professional society representing more than 8,000 physicians and scientists who specialize in infectious diseases. Nested within the IDSA, the HIV Medicine Association (HIVMA) is the professional home for more than 3,600 physicians, scientists and other health care professionals dedicated to the field of HIV/AIDS. HIVMA promotes quality in HIV care and advocates policies that ensure a comprehensive and humane response to the AIDS pandemic informed by science and social justice. For more information, visit www.idsociety.org and www.hivma.org.
Bethesda, MD (Jan. 28, 2008) – Patients with chronic hepatitis C (HCV) infection should not use marijuana (cannabis) daily, according to a study published in Clinical Gastroenterology and Hepatology, the official journal of the American Gastroenterological Association (AGA) Institute. Researchers found that HCV patients who used cannabis daily were at significantly higher risk of moderate to severe liver fibrosis, or tissue scarring. Additionally, patients with moderate to heavy alcohol use combined with regular cannabis use experienced an even greater risk of liver fibrosis. The recommendation to avoid cannabis is especially important in patients who are coinfected with HCV/HIV since the progression of fibrosis is already greater in these patients.
“Hepatitis C is a major public health concern and the number of patients developing complications of chronic disease is on the rise,” according to Norah Terrault, MD, MPH, from the University of California, San Francisco and lead investigator of the study. “It is essential that we identify risk factors that can be modified to prevent and/or lessen the progression of HCV to fibrosis, cirrhosis and even liver cancer. These complications of chronic HCV infection will significantly contribute to the overall burden of liver disease in the U.S. and will continue to increase in the next decade.”
This is the first study that evaluates the relationship between alcohol and cannabis use in patients with HCV and those coinfected with HCV/HIV. It is of great importance to disease management that physicians understand the factors influencing HCV disease severity, especially those that are potentially modifiable. The use and abuse of both alcohol and marijuana together is not an uncommon behavior. Also, individuals who are moderate and heavy users of alcohol may use cannabis as a substitute to reduce their alcohol intake, especially after receiving a diagnosis like HCV, which affects their liver.
Researchers found a significant association between daily versus non-daily cannabis use and moderate to severe fibrosis when reviewing this factor alone. Other factors contributing to increased fibrosis included age at enrollment, lifetime duration of alcohol use, lifetime duration of moderate to heavy alcohol use and necroinflammatory score (stage of fibrosis). In reviewing combined factors, there was a strong (nearly 7-fold higher risk) and independent relationship between daily cannabis use and moderate to severe fibrosis. Gender, race, body mass index, HCV viral load and genotype, HIV coinfection, source of HCV infection, and biopsy length were not significantly associated with moderate to severe fibrosis.
Of the 328 patients screened for the study, 204 patients were included in the analysis. The baseline characteristics of those included in the study were similar to those excluded with the exception of daily cannabis use (13.7 percent of those studied used cannabis daily versus 6.45 percent of those not included). Patients who used cannabis daily had a significantly lower body mass index than non-daily users (25.2 versus 26.4), were more likely to be using medically prescribed cannabis (57.1 percent versus 8.79 percent), and more likely to have HIV coinfection (39.3 percent versus 18.2 percent).
The prevalence of cannabis use amongst adults in the U.S. is estimated to be almost 4 percent. Regular use has increased in certain population subgroups, including those aged 18 to 29.
Hepatitis is an inflammation of the liver. Hepatitis C is the most common form of hepatitis and infects nearly 4 million people in the U.S., with an estimated 150,000 new cases diagnosed each year. While it can be spread through blood transfusions and contaminated needles, for a substantial number of patients, the cause is unknown. This form of viral hepatitis may lead to cirrhosis, or scarring, of the liver. Coinfection of hepatitis C in patients who are HIV positive is common; about one quarter of patients infected with HIV are infected with hepatitis C. The majority of these patients, 50 to 90 percent, were infected through injection drug use. Hepatitis C ranks with alcohol abuse as the most common cause of chronic liver disease and leads to about 1,000 liver transplants yearly in the U.S.
About the AGA Institute
The American Gastroenterological Association (AGA) is dedicated to the mission of advancing the science and practice of gastroenterology. Founded in 1897, the AGA is one of the oldest medical-specialty societies in the United States. Comprised of two non-profit organizations—the AGA and the AGA Institute—our more than 16,000 members include physicians and scientists who research, diagnose and treat disorders of the gastrointestinal tract and liver. The AGA, a 501(c6) organization, administers all membership and public policy activities, while the AGA Institute, a 501(c3) organization, runs the organization’s practice, research and educational programs. On a monthly basis, the AGA Institute publishes two highly respected journals, Gastroenterology and Clinical Gastroenterology and Hepatology. The organization’s annual meeting is Digestive Disease Week®, which is held each May and is the largest international gathering of physicians, researchers and academics in the fields of gastroenterology, hepatology, endoscopy and gastrointestinal surgery. For more information, please visit www.gastro.org.
About Clinical Gastroenterology and Hepatology
The mission of Clinical Gastroenterology and Hepatology is to provide readers with a broad spectrum of themes in clinical gastroenterology and hepatology. This monthly peer-reviewed journal includes original articles as well as scholarly reviews, with the goal that all articles published will be immediately relevant to the practice of gastroenterology and hepatology. For more information, visit
Novel vaccine additive to enhance the body’s immune response shows promise in mice
Oxford University scientists have discovered a compound that greatly boosts the effect of vaccines against viruses like flu, HIV and herpes in mice.
An ‘adjuvant’ is a substance added to a vaccine to enhance the immune response and offer better protection against infection.
The Oxford University team, along with Swedish and US colleagues, have shown that a type of polymer called polyethyleneimine (PEI) is a potent adjuvant for test vaccines against HIV, flu and herpes when given in mice.
The researchers were part-funded by the UK Medical Research Council and report their findings in the journal Nature Biotechnology.
Mice given a single dose of a flu vaccine including PEI via a nasal droplet were completely protected against a lethal dose of flu. This was a marked improvement over mice given the flu vaccine without an adjuvant or in formulations with other adjuvants.
The Oxford researchers now intend to test the PEI adjuvant in ferrets, a better animal model for studying flu. They also want to understand how long the protection lasts for. It is likely to be a couple of years before a flu vaccine using the adjuvant could be tested in clinical trials in humans, the researchers say.
‘Gaining complete protection against flu from just one immunisation is pretty unheard of, even in a study in mice,’ says Professor Quentin Sattentau of the Dunn School of Pathology at Oxford University, who led the work. ‘This gives us confidence that PEI has the potential to be a potent adjuvant for vaccines against viruses like flu or HIV, though there are many steps ahead if it is ever to be used in humans.’
HIV, flu and herpes are some of the most difficult targets to develop vaccines against. HIV and flu viruses are able to change and evolve to escape immune responses stimulated by vaccines. There aren’t any effective vaccines against HIV and herpes as yet, and the flu vaccine needs reformulating each year and doesn’t offer complete protection to everyone who receives it. Finding better adjuvants could help in developing more effective vaccines against these diseases.
Most vaccines include an adjuvant. The main ingredient of the vaccine – whether it is a dead or disabled pathogen, or just a part of the virus or bacteria causing the disease – primes the body’s immune system so it knows what to attack in case of infection. But the adjuvant is needed as well to stimulate this process.
While the need for adjuvants in vaccines has been recognised for nearly 100 years, the way adjuvants work has only recently been understood. The result has been that only a small set of adjuvants is used in current vaccines, often for historical reasons.
The most common adjuvant by far is alum, an aluminium-containing compound that has been given in many different vaccines worldwide for decades. However, alum is not the most potent adjuvant for many vaccine designs.
‘There is a need to develop new adjuvants to get the most appropriate immune response from vaccines,’ says Professor Sattentau, who is also a James Martin Senior Fellow at the Oxford Martin School, University of Oxford.
The Oxford University team found that PEI, a standard polymer often used in genetic and cell biology, has strong adjuvant activity.
When included in a vaccine with a protein from HIV, flu or herpes virus, mice subsequently mounted a strong immune response against that virus. The immune response was stronger than with other adjuvants that are currently being investigated.
The team also showed that PEI is a potent adjuvant in rabbits, showing the effect is not just specific to mice and could be general.
Another potential advantage of PEI is that it works well as an adjuvant for ‘mucosal vaccines’. These vaccines are taken up the nose or in the mouth and absorbed through the mucus-lined tissues there, getting rid of any pain and anxiety from a needle. Mucosal vaccines may also be better in some ways as mucosal tissues are the sites of infection for these diseases (airways for respiratory diseases, genital mucosa for HIV and herpes).
Professor Sattentau suggests that: ‘In the best of all possible worlds, you could imagine people would have one dose of flu vaccine that they’d just sniff up their nose or put under their tongue. And that would be it: no injections and they’d be protected from flu for a number of years.
‘It’s just a vision for the future at the moment, but this promising adjuvant suggests it is a vision that is at least possible.’
Notes to Editors
* The body’s immune system is made up of two arms: the innate immune system and the adaptive immune system. The adaptive immune system consists of the antibodies and immune cells (T and B cells) the body develops specifically to combat a particular foreign agent.
The innate immune system had been thought of as playing a more primitive, non-specific role in protecting against invaders like viruses and parasites. However, it is now realised that the innate immune system is essential in kicking off any immune response. It needs to be activated first to generate an adaptive immune response.
But the innate immune system doesn’t just press the start button. It tailors the body’s adaptive immune response, deciding on what particular mix of antibodies and T cells is needed and teaching them what to attack.
It is the adjuvants in vaccines that stimulate the innate immune system. So having the right adjuvant can help the body produce the most appropriate immune response to protect against future infection.
* The paper ‘Polyethyleneimine is a potent mucosal adjuvant for glycoproteins with innate and adaptive immune activating properties’ is to be published in the journal Nature Biotechnology with an embargo of 18:00 UK time / 13:00 US Eastern time on Sunday 26 August 2012.
* The study was funded by the UK Medical Research Council, European Commission, the International AIDS Vaccine Initiative (IAVI), the Bill and Melinda Gates Foundation and Dormeur Investment Service Ltd.
* Professor Sattentau is an investigator in the Jenner Institute at Oxford University and a James Martin Senior Fellow at the Oxford Martin School, Oxford University.
* For almost 100 years the Medical Research Council has improved the health of people in the UK and around the world by supporting the highest quality science. The MRC invests in world-class scientists. It has produced 29 Nobel Prize winners and sustains a flourishing environment for internationally recognised research. The MRC focuses on making an impact and provides the financial muscle and scientific expertise behind medical breakthroughs, including one of the first antibiotics penicillin, the structure of DNA and the lethal link between smoking and cancer. Today MRC funded scientists tackle research into the major health challenges of the 21st century. www.mrc.ac.uk
* The Oxford Martin School
is a unique interdisciplinary community within the University of Oxford. The School fosters innovative thinking, deep scholarship and collaborative activity to address the most pressing risks and realise new opportunities of the 21st century. It was founded in 2005 through the vision and generosity of James Martin, and currently comprises over 35 interdisciplinary research programmes on global future challenges. The Oxford Martin School’s Director is Ian Goldin, Professor at the University of Oxford. http://www.oxfordmartin.ox.ac.uk
* Oxford University’s Medical Sciences Division is one of the largest biomedical research centres in Europe, with over 2,500 people involved in research and more than 2,800 students. The University is rated the best in the world for medicine, and it is home to the UK’s top-ranked medical school.
From the genetic and molecular basis of disease to the latest advances in neuroscience, Oxford is at the forefront of medical research. It has one of the largest clinical trial portfolios in the UK and great expertise in taking discoveries from the lab into the clinic. Partnerships with the local NHS Trusts enable patients to benefit from close links between medical research and healthcare delivery.
A great strength of Oxford medicine is its long-standing network of clinical research units in Asia and Africa, enabling world-leading research on the most pressing global health challenges such as malaria, TB, HIV/AIDS and flu. Oxford is also renowned for its large-scale studies which examine the role of factors such as smoking, alcohol and diet on cancer, heart disease and other
Of the 25 million people infected with HIV-1 in Africa, as many as half are thought to be co-infected with worms (helminths), and there is evidence that these worms may result in a more rapid progression of HIV infection to AIDS. Does treating these worms (“de-worming”) slow down this progression.
In a new study published in the open access journal PLoS Neglected Tropical Diseases, Judd Walson and Grace John-Stewart at the University of Washington, Seattle, USA set out to answer this question. Their study found that there were simply not enough data to make any firm conclusions, and they call for larger, well-designed studies to help come to a definitive answer.
There were five studies in the final analysis. All five were limited by short follow up times. Only one of these was a randomized controlled trial (RCT)—it compared the effects of treating worms in people with HIV against no treatment. The trial did find some benefit from the de-worming treatment. In patients with HIV who did not receive the de-worming treatment, their viral load (a measure of the amount of HIV in their bloodstream) went up. In contrast, the viral load of patients who were de-wormed remained stable. However, de-worming was not associated with improvements in the patients’ immune status (as measured by the CD4 count) or in their clinical condition.
*Reposted at Request
* This is Just a Report I do every 2 weeks…Only a few of these articles do I post on this Conduit. Link is at the Bottom:
Editors Top Five:1. Chemical widely used in antibacterial hand soaps may impair muscle function 2. Butter flavoring in microwave popcorn, thought safe for food industry workers, is respiratory hazard 3. Turmeric Spices Up Virus Study 4. Scientists find protein that promotes cancers, heart disease; create substance to block its effects 5. Green tea compound shows promise for tackling cancer
In This issue:1. Yale team discovers how stress and depression can shrink the brain 2. Common antibiotics pose a rare risk of severe liver injury in older patients 3. Chemical widely used in antibacterial hand soaps may impair muscle function 4. Consuming flavanol-rich cocoa may enhance brain function 5. Diabetes drugs taken by over 15 million Americans raises risk of bladder cancer 6. Butter flavoring in microwave popcorn, thought safe for food industry workers, is respiratory hazard 7. Why are people overconfident so often? 8. UC Davis researchers identify cellular basis for how anti-aging cosmetics work 9. Blood type may influence heart disease risk 10. Cocoa compounds may reduce blood pressure 11. Potent human toxins prevalent in Canada’s freshwaters 12. Study finds that yo-yo dieting does not thwart weight loss efforts or alter metabolism long term 13. A pack of walnuts a day keeps the fertility specialist away? 14. BPA link to narrowing of the arteries 15. Spiteful behavior is ‘extreme’, according to study 16. Breastfeeding may protect infants from HIV transmission 17. Yoga: a cost-effective treatment for back pain sufferers? 18. Turmeric Spices Up Virus Study 19. Why are elderly duped? 20. Common parasite may trigger suicide attempts 21. Pan-fried Meat Increases Risk of Prostate Cancer, New Study Finds 22. Photographic cholesterol test 23. Good mood foods: Some flavors in some foods resemble a prescription mood stabilizer 24. Red wine compound could help seniors walk away from mobility problems 25. Coconut water is an excellent sports drink — for light exercise 26. Drink made from berry wine may provide tasty drug for diabetes 27. Vitamin D supplementation can decrease risk of respiratory infections in children 28. Scientists find protein that promotes cancers, heart disease; create substance to block its effects 29. In your future: More healthful foods to nourish the non-human you 30. New form of long-used food ingredient for ‘anti-hunger’ yogurts, smoothies 31. Antibiotic use in infants before 6 months associated with being overweight in childhood 32. Study shows long term effects of radiation in pediatric cancer patients 33. First identification of a strong oral carcinogen in smokeless tobacco 34. First evidence from humans on how alcohol may boost risk of cancer 35. With a little training, signs of schizophrenia are averted 36. Many medications for elderly are prescribed inappropriately 37. Potency of statins linked to muscle side effects 38. Menopause evolved to prevent competition between in-laws 39. Green tea compound shows promise for tackling cancer 40. Menopause evolved to prevent competition between in-laws 41. How does body temperature reset the biological clock? http://healthresearchreport.me/
Washington, D.C. — A purified extract prepared from a common microbe and delivered to the lungs of laboratory mice in a spray set off a healthy immune response and provided powerful protection against all four major classes of pathogens including those responsible for anthrax and bubonic plague, according to a presentation at the American Society for Cell Biology’s 47th Annual Meeting.
In addition, when the researchers exposed another group of mice to an aerosol of live Streptococcus pneumoniae, the only animals that survived were the ones that had been pre-treated with the spray. A total of 83 percent of these mice survived. None of the untreated animals lived.
The researchers at the M.D. Anderson Cancer Center in Houston developed the spray from a purified extract of the common coccobacillus named Haemophilus influenzae, the cause of ear and sinus infections in human children.
Their “aerosolized lung innate immune stimulant,” as the scientists have named the spray treatment, could benefit immune-compromised patients with cancer, HIV or other diseases as well as emergency workers and the general public facing uncommon threats like an aerosolized bioterror attack or a spreading respiratory epidemic.
According to Brenton Scott who with his postdoctoral advisor, Burton Dickey, developed the spray, the treatment works best if administered four to 24 hours before exposure. Nearly all mice survived when treated before exposure to lethal doses of anthrax, influenza, and the dangerous mold, Aspergillus. But, the treatment also has some benefit when given after exposure. Effectiveness declines over time but seems to last up to five days after a single dose.
The researchers report that protection by stimulant is associated with rapid pathogen killing in the airways, does not depend on recruitment of other immune defense cells such as neutrophils, and correlates with increased levels of antimicrobial polypeptides in the lung lining fluid. The host response is localized to the airways, and safety studies indicate that the treatment causes minimal side effects, even with repeated doses.
Preclinical testing is being completed, and clinical trials are being designed.
* reposted on request
People who lack a cell surface protein called CCR5 are highly resistant to infection by HIV but may be at increased risk of developing West Nile virus (WNV) illness when exposed to the mosquito-borne virus, report researchers from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health (NIH). The study, by Philip M. Murphy, M.D., and colleagues, appears online today in The Journal of Experimental Medicine. The findings may have cautionary implications for physicians who are treating HIV-positive individuals with experimental CCR5-blocking drugs, say the scientists.
“This is the first genetic risk factor to be identified for West Nile virus infection,” says NIH Director Elias A. Zerhouni, M.D. “While infection does not always lead to illness, the virus can sometimes cause serious problems and, according to the Centers for Disease Control and Prevention, there were 102 deaths in the United States from West Nile virus infection in 2005.”
“A decade ago, a number of research groups, including Dr. Murphy’s, determined that CCR5 is the primary co-receptor used by HIV to infect cells,” says NIAID Director Anthony S. Fauci, M.D. “Their work laid the foundation for the development of CCR5-blocking drugs, which are designed to slow the spread of HIV from cell to cell.”
Most people inherit two normal copies (one from each parent) of the gene that codes for CCR5 protein. About 1 percent of North American whites, however, have a mutation in both copies (are homozygous) and thus do not produce any CCR5. These individuals have the good fortune of being highly resistant to HIV infection and otherwise seemed to suffer no ill effects from the absence of this receptor protein, scientists noted. But the new research by Dr. Murphy’s team suggests that lacking CCR5 may not be an unalloyed good after all.
In 2005 Dr. Murphy and his coworkers developed a mouse model to clarify the roles of various immune system cells in responding to WNV infection. They discovered that while most mice survived WNV infection, mice genetically engineered to lack CCR5 receptors suffered rapid and uniformly fatal infection by the virus. Further investigation showed that CCR5 promoted the movement of several classes of immune system cells into the brain and central nervous system, which appeared to protect normal mice from the encephalitis (brain inflammation) characteristic of serious WNV infection.
“We wanted to know if humans lacking CCR5 might be at greater risk of the more serious complications of WNV infection,” says Dr. Murphy. The researchers examined human blood and cerebrospinal fluid samples from 417 laboratory-confirmed cases of WNV infection that occurred in Arizona and Colorado in 2003 and 2004. Of these, 395 were suitable for genetic testing for the presence or absence of the HIV-protective mutation.
Dr. Murphy and his colleagues determined that 4.5 percent of 247 WNV-positive samples from Arizona were from patients who had two copies of the CCR5 mutation. In contrast, a control group of 145 WNV-negative blood samples showed 0.7 percent were from people who had two copies of the CCR5 mutation–a number in line with the expected 0.8 to 1 percent range believed to be present in all North American whites. Next, the researchers analyzed the WNV-positive samples from Colorado and determined that 4.1 percent of the entire set of 148 samples came from individuals homozygous for the CCR5 mutation. Among those Coloradans who provided WNV-positive samples and who self-reported their race as white, the percentage of homozygous individuals was 8.3.
The absence of normal CCR5 genes is a strong genetic risk factor for developing symptomatic cases of WNV infection, the researchers conclude. “The findings may have important clinical implications for physicians who treat people with HIV,” notes Dr. Murphy. For example, he says, it may be prudent for HIV-positive individuals who are taking experimental CCR5-blockers to strictly limit mosquito exposure.
NIAID is a component of the National Institutes of Health, an agency of the U.S. Department of Health and Human Services. NIAID supports basic and applied research to prevent, diagnose and treat infectious diseases such as HIV/AIDS and other sexually transmitted infections, influenza, tuberculosis, malaria and illness from potential agents of bioterrorism. NIAID also supports research on transplantation and immune-related illnesses, including autoimmune disorders, asthma and allergies.
References: WG Glass et al. Chemokine receptor CCR5 promotes leukocyte trafficking to the brain and survival in West Nile virus infection. The Journal of Experimental Medicine 202:1087-98 (2005). DOI: 10.1084/jem.20042530.
WG Glass et al. CCR5 deficiency increases risk of symptomatic West Nile virus infection. The Journal of Experimental Medicine. (Published online Jan. 17, 2006) DOI: 10.1084/jem.20051970.
News releases, fact sheets and other NIAID-related materials are available on the NIAID Web site at http://www.niaid.nih.gov.
* Reposted for Filing
Posted: August 15, 2012 at 10:47 am, Last Updated: August 15, 2012 at 1:33 pm
Aarthi Narayanan. Photo by Evan Cantwell
The popular spice turmeric packs more than just flavor — , Mason researchers recently discovered.
Curcumin, found in turmeric, stopped the potentially deadly Rift Valley Fever virus from multiplying in infected cells, says Aarthi Narayanan, lead investigator on a new study and a research assistant professor in Mason’s National Center for Biodefense and Infectious Diseases.
Mosquito-borne Rift Valley Fever virus (RVF) is an acute, fever-causing virus that affects domestic animals such as cattle, sheep and goats, as well as humans. Results of the study were publishedthis month in the Journal of Biological Chemistry.
“Growing up in India, I was given turmeric all the time,” says Narayanan, who has spent the past 18 months working on the project. “Every time my son has a throat infection, I give (turmeric) to him.”
There’s more work to do before curcumin-based pharmaceuticals become commonplace, Narayanan emphasizes. She plans to test 10 different versions of curcumin to determine which one works the best. She also intends to apply the research to other viruses, including HIV.
Narayanan has long wanted to explore the infection-fighting properties of turmeric, in particular its key component, curcumin. “It is often not taken seriously because it’s a spice,” she says.
But science is transforming the spice from folk medicine to one that could help a patient’s body fight off a virus because it can prevent the virus from taking over healthy cells. These “broad-spectrum inhibitors” work by defeating a wide array of viruses.
Turmeric is often used as a spice in curry dishes. Photo by Sanjay Acharya from Wikipedia Commons
“Curcumin is, by its very nature, broad spectrum,” Narayanan says. “However, in the published article, we provide evidence that curcumin may interfere with how the virus manipulates the human cell to stop the cell from responding to the infection.”
Kylene Kehn-Hall, a co-investigator on the study, adds, “We are very excited about this work, as curcumin not only dramatically inhibits RVFV replication in cell culture but also demonstrates efficacy against RVFV in a mouse model.”
Narayanan and her colleagues study the connection between a virus and how it impacts the host — human or animal. Symptoms clue in the researcher about the body’s inner workings. Rift Valley Fever and Venezuelan Equine Encephalitis kick off with flu-like symptoms.
Symptoms can make it challenging for someone to recover. The body usually starts with an exaggerated inflammatory response because it doesn’t know where to start to rid itself of the virus, she says.
“Many times, the body goes above and beyond what is necessary,” Narayanan says. “And that’s not good because it’s going to influence a bunch of cells around the infection, which haven’t seen the bug. That’s one way by which disease spreads through your body. And so it is very important to control the host because a lot of times the way the host responds contributes to the disease.”
Controlling the symptoms means more than simply making the patients feels better. “You’re giving the antiviral a chance to work. Now an antiviral can go in and stop the bug. You’re no longer trying to keep the host alive and battling the bug at the same time.”
Narayanan works with a graduate student in Mason’s National Center for Biodefense and Infectious Diseases. Photo by Evan Cantwell
Once Narayanan knows how the body responds to a virus, it’s time to go after the bug itself.
She’s applying this know-how to a family of viruses called Bunyaviruses, which feature Rift Valley fever, and such alphaviruses as Venezuelan equine encephalitis and retroviruses, which notably include HIV.
She delves into uncovering why and how each virus affects the patient. “Why are some cell types more susceptible to one type of infection than another?”
HIV goes after the immune system. Bunyaviruses will infect a wide range of cells but do maximum damage to the liver. “What is it about the liver that makes it a sitting duck compared to something like the brain?” Narayanan asks.
Ultimately, curcumin could be part of drug therapies that help defeat these viruses, Narayanan says.
“I know this works. I know it works because I have seen it happen in real life,” Narayanan says. “I eat it every day. I make it a point of adding it to vegetables I cook. Every single day.”
Other Mason researchers involved in the study are Charles Bailey, Ravi Das, Irene Guendel, Lindsay Hall, Fatah Kashanchi, Svetlana Senina and Rachel Van Duyne. Several researchers from other institutions also collaborated.
Write to Michele McDonald at email@example.com
Breastfeeding may protect infants from HIV transmission
An international team of researchers has found that certain bioactive components found in human milk are associated with a reduced risk of HIV transmission from an HIV infected mother to her breast-fed infant. Their study will be published in the August 15 online edition of American Journal of Clinical Nutrition.
“In developing countries, HIV-infected mothers are faced with the decision of whether or not to breastfeed their babies,” said Lars Bode, PhD, assistant professor in the Department of Pediatrics at the University of California, San Diego School of Medicine. “Breastfeeding exposes the baby to the virus and increases the risk of the baby dying from HIV infection; but not breastfeeding increases the risk for the baby to die from other intestinal or respiratory infections.”
Bode and colleagues set out to find why the vast majority of breast-fed infants do not acquire HIV-1, despite continuous exposure to the virus in their mother’s milk over many months. Even in the absences of antiretroviral drugs, only 10 to15 percent of infants will acquire HIV infection from their HIV-infected mothers.
They discovered that immunologically active components called human milk oligosaccharides (HMO) – a type of carbohydrate made up of several simple sugars linked together – may protect from HIV transmission. These complex oligosaccharides are the third-most abundant component of breast milk, yet are not digestible and therefore become highly concentrated in the mucosal surfaces of the infant’s gastrointestinal tract.
“HMO act as prebiotics that promote the growth of desirable bacterial communities in the infant’s intestine,” said Bode. Additionally, HMO structurally resembles sugar chains called glycans that are normally found on epithelial cell surfaces, and can serve as “decoy” receptors to inhibit pathogens from binding. Last, HMO exhibit anti-inflammatory activity and have been shown to modulate immune cell responses in cell and animal models.
The researchers analyzed HMO amount and composition in breast milk samples collected from more than 200 women as part of a larger study of HIV-infected women and their infants in Lusaka, Zambia, following them from birth to 24 months. (Most were recruited to the study and followed before antiretroviral therapy became available to them, thus offering a unique look at associations between HMO and HIV transmission.)
Higher concentrations of HMO in milk were associated with protection against postnatal HIV transmission, independent of other known risk factors. In the future, a better understanding of how individual HMO facilitate or obstruct HIV transmission may guide the development of interventions to complement antiretroviral strategies and more effectively prevent transmission, according to the researchers.
Additional contributors to the study included Lauren Hsiao and Caroline Nissan, UC San Diego; Louise Kuhn and Hae-Young Kim, Columbia University; Moses Sinkala, Lusaka District Health Management Team, Zambia; Chipepo Kankasa and Mwiya Mwiya, University Teaching Hospital, University of Zambia; Donald M. Thea, Boston University; and Grace M. Aldrovandi, Children’s Hospital Los Angeles, USC.
Funding was provided by the National Institute of Dental and Craniofacial Research (NIDCR) (DE021238) and the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH) (HD39611, HD40777, HD57617) and a University of California, San Diego, Center for AIDS Research Pilot Development Grant
For every £1 spent on basic research a whopping £19 is spent on marketing, claim experts
Current reward system discourages innovation, they add
PUBLISHED:10:13 EST, 8 August 2012| UPDATED:11:08 EST, 8 August 2012
The pharmaceutical industry is in crisis because companies are rewarded for developing new drugs that have few clinical advantages over existing ones, experts say.
Writing in the British Medical Journal, Professor Donald Light from the University of Medicine and Dentistry of New Jersey and Joel Lexchin from York University in Toronto, say this has discouraged innovation for the past five decades.
They pointed to independent reviews that found between 85 and 90 per cent of all new drugs developed over the past 50 years have provided few benefits and considerable harms.
They said most research funds don’t go towards finding breakthrough drugs but towards developing scores of minor variations that produce a steady stream of profits. Heavy promotion of these drugs can account for up to 80% of a nation’s drug spending, they add.
The duo warn that companies exaggerate research and development costs to lobby for more protection from free market competition. Yet, according to an independent analysis, the 1.3 per cent of revenues devoted to discovering new molecules compares with an estimated 25 per cent spent on promotion.
This means for every £1 spent on basic research a whopping £19 is spent on marketing.
Professor Light and Mr Lexchin said urgent changes needed to be made to make the industry focus on more cost effective and safer medicines.
They said the first step should be to stop approving so many new drugs of little therapeutic value.
‘EU countries are paying billions more than necessary for drugs that provide little health gain because prices are not being set to reward new drugs in proportion to their clinical value,’ they say.
‘This approach would save countries billions in healthcare costs and produce real gains for people’s health’, they conclude.
In a second paper, researchers from the London School of Economics said drug manufacturers should be made to demonstrate that their products are superior to existing treatments.
However, Stephen Whitehead, chief executive of the Association of the British Pharmaceutical Industry, said: ‘We strongly disagree with the claims made in these papers.
‘Medical research has always rested on iterative and gradual innovation rather than breakthrough advances which are very rare. If it were not for the incremental improvements made in the treatment of HIV, the disease would still be terminal rather than a manageable long term condition.
‘The pharmaceutical industry’s medicines pipeline is promising with many new treatments in development. But the discovery of medicines is an increasingly difficult process as the cost of research and development continues to rise and regulation becomes more onerous. In 2012, it costs on average over £1 billion to develop a new medicine and takes between 12 and 15 years to develop
Olive oil has become part of the fight against the Human Immunodeficiency Virus (HIV) – the cause of AIDS – thanks to the research carried out by the Bionat team, from the University of Granada, headed by Prof. Andrés García-Granados, senior lecturer in Organic Chemistry. Their work shows that maslinic acid – a natural product extracted from dry olive-pomace oil in oil mills – inhibits serin-protease, an enzyme used by HIV to release itself from the infected cell into the extracellular environment and, consequently, to spread the infection into the whole body. These scientists from Granada determined that the use of olive-pomace oil can produce an 80% slowing down in AIDS spreading in the body.
Maslinic or crataegolic acid is a pentacyclic terpene with antioxidant and anticancer effects found in wax from olive skin, alongside oleanolic acid. The effects of this compound in the fight against AIDS are simultaneously being studied in the UGR and in Hospital Carlos III in Madrid by a team headed by Prof. Vallejo Nájera.
Maslinic acid innovative properties stem from its powerful protease-inhibition activity, allowing researchers from Granada to register two patents on behalf of the UGR to produce drugs for treatment of diseases caused by protozoa Cryptosporidium – a parasite causing small intestine infection and diarrhoea – and by HIV. The University of Granada has already registered almost ten other patents related to this compound’s properties.
Maslinic acid is also a very active compound in opportunistic parasitic infections seriously affecting HIV patients.
In trials carried out by these researchers with the MT2 cell line, for concentrations of 25 and 30 µg/ml maslinic acid inhibited replication of a primary HIV-1 isolate. For 25 µg/ml a decrease in the cytopathic effect and in p24 antigen levels in the supernatant culture medium was detected. For 30 µg/ml, there was total absence of the cytopathic effect and also a decrease of p24 antigen levels.
The UGR Faculty of Sciences hosts a unique maslinic acid production pilot plant where the company MANINVEST S.L. – staffing scientists from the UGR departments of Organic Chemistry, Biochemistry and Parasitology, as well as a coordinating economist – is carrying out research on technology implementation and business programmes tuning aimed at making manitol and maslinic and oleanolic acids programmes more profitable.
Whilst manitol is obtained from olive oil waste water (alpechín) and olive-tree leaves, both acids are extracted from dry olive-pomace oil (orujo) produced at the olive-milling stage during olive oil elaboration process.
To this day, only oleanolic acid – produced in China – has been marketed. However, maslinic acid has gained importance as it is not still on the market and has a greater biological activity.
Prof. Andrés García-Granados’s team intends to continue working in the design and implementation of new maslinic acid by-products to fight against HIV, as well as in other innovative research projects financed by the Spanish Ministry of Science and Technology and the Andalusian Regional Government.
* Reposted before being submitted to Category
Contact: Tim Parsons or Ming Tai firstname.lastname@example.org 410-955-6878 Johns Hopkins University Bloomberg School of Public Health
Study finds acute measles supresses HIV replication
Replication of human immunodeficiency virus (HIV) is briefly suppressed during acute measles, according to researchers at the Johns Hopkins Bloomberg School of Public Health. A study of HIV-infected children living in Zambia found that HIV levels in the blood were significantly lower while having measles compared to HIV-infected children who did not have measles. The researchers say the only other illness previously reported to suppress HIV is O. tsutsugamushi, which causes scrub typhus. The study appears in the April 15, 2002 issue of The Journal of Infectious Diseases.
“We were surprised by these findings, because we expected to see HIV replication increase, not decrease with measles,” says the study’s lead author William Moss, MD, MPH, assistant research professor of international health and molecular microbiology and immunology at the Johns Hopkins Bloomberg School of Public Health. “Measles is a very immunosuppressive virus. It results in many secondary infections and is a major cause of death among children. Our findings show that measles also triggers intense immune system activation that temporarily suppresses HIV,” explains Dr. Moss.
For the study, Dr. Moss and his colleagues followed 93 children diagnosed with measles and HIV at the University Teaching Hospital in Lusaka, Zambia. The children’s HIV levels were measured from blood samples taken when they were admitted to the hospital for measles treatment. More samples were taken when the children were discharged from the hospital, and again one month later. They were compared with samples taken from HIV-infected children who did not have measles or other illnesses and with samples from children with measles, but not HIV.
The study found that 33 of the children diagnosed with measles and HIV had a median HIV level of 5,339 copies per milliliter when they first entered the hospital for treatment. The HIV levels increased to 60,121 copies per milliliter when measured at the time of discharge and to 387,148 copies per milliliter one month later. HIV-infected children who did not have acute measles had a median HIV level of 228,454 copies per milliliter.
The researchers also noticed that the CD8 T-cell level, which is an indicator of immune system response, was elevated in the children with both measles and HIV compared to children in the control groups. The increase in the CD8 level occurred during the same time as the suppression of HIV levels.
“More research will be needed with a larger study group to fully understand how measles suppresses HIV and activates the immune system, but our findings may provide clues to understanding both HIV pathogenesis and immunity,” says Diane Griffin, MD, PhD, professor and chair of the W. Harry Feinstone Department of Molecular Microbiology and Immunology at the Johns Hopkins Bloomberg School of Public Health.
“Suppression of Human Immunodeficiency Virus Replication during Acute Measles,” is published in the April 15, 2002 edition of The Journal of Infectious Diseases and was written by William J. Moss, Judith J. Ryon, Mwaka Monze, Felicity Cutts, Thomas C. Quinn, and Diane E. Griffin.
Funding was provided by the National Institutes of Health, World Health Organization, and from the Wyeth-Lederle Vaccines and Pediatrics Young Investigators Award in Vaccine Development of the Infectious Diseases Society of America.
For more information, visit the Johns Hopkins Bloomberg School of Public Health online at www.jhsph.edu
* Requested Repost
After this Global Aids Day Conference, I noticed large sums of money going into the “U.S. President’s Emergency Plan for AIDS Relief” http://www.pepfar.gov . There are two Red Flags that need cleaning up.
- In order to determine which companies are profiting from this U.S. Government charitable organization. We would need to go to see who the Donor list is….
- So we follow the link Contributions to the Global Fund: http://www.pepfar.gov/coop/globalfund/contributions/index.htm
- Then we click on the list: http://www.theglobalfund.org/en/resources/?lang=en
- At this point in time we have a broken link. Which I find surprising with all these public commitments to donate.
Next Let us see who is actually getting the Grant Money:
For this we go to:
Download Grant Data
Then from there we go to:
While there are some worthy organizations receiving grant money.
I would like you to take notice of the 100’s of millions of USD going to Russian and China…. Countries in far better financial shape than the U.S.
I am not here to speculate, nor form a hypothesis. All I see is an Inconsistency that requires clarification
* Keep in mind the U.S. is the largest Contributor to the Global Fund..Even though we can’t find the documentation, it is through their verbal statements..