'Taste for sugar' could be HIV's major weakness

It turns out that having a sweet tooth is not just the downfall of many of us humans. According to a new study, a taste for sugar could also be HIV's major weakness and a target for future treatment.

The study, published in PLOS Pathogens, suggests that if the virus is unable to access sugar and other nutrients after invading a cell, it is unable to replicate itself and, therefore, unable to grow and spread.

Researchers from Northwestern Medicine, IL, and Vanderbilt University, TN, were able to utilize an experimental new compound to shut down the sugar and nutrient pipeline in immune cells and starve HIV to death.

"This compound can be the precursor for something that can be used in the future as part of a cocktail to treat HIV that improves on the effective medicines we have today," says Harry Taylor, research assistant professor in medicine at Northwestern University Feinberg School of Medicine.

HIV grows in specific types of immune cells called CD4+ T cells. When these cells are active, responding to pathogens in the blood, their supplies of sugar and other nutrients necessary for growth are increased. The virus purposefully seeks out activated T cells and hijacks their glucose supplies.

The researchers discovered that turning on a cell component called phospholipase D1 (PLD1) signaled for activated T cells to increase their supplies of sugar and the vital nutrients. By blocking this component, the researchers were able to in turn block the sugar pipeline, depriving the invading HIV of the building blocks required for it to grow.

A previous attempt to prevent the virus from stealing immune cells' sugar and nutrients using drugs was carried out in the 1990s, but the drugs led to serious side effects in patients with HIV and sometimes ended up killing healthy cells.

Blocking sugar supplies could also prevent premature organ damage

The new approach appears to not only be safer but has the additional effect of slowing the spread of abnormally activated immune cells. HIV triggers the excess activation and growth of T cells which can lead to inflammation in the body, causing premature organ damage in patients with HIV even when the virus is suppressed by medicine.

"Perhaps this new approach, which slows the growth of the immune cells, could reduce the dangerous inflammation and thwart the life-long persistence of HIV," Prof. Taylor speculates.

Before joining Northwestern University, Prof. Taylor was on the faculty at Vanderbilt, where we knew that researchers had managed to identify a compound that could stop breast cancer cells from spreading by blocking PLD1.

The researchers speculated whether blocking this same cell component in CD4+ T cells would have the same effect in slowing the spread of HIV by blocking the supply of glucose and nutrients. They tested their theory in vitro and, sure enough, HIV was unable to access enough resources to reproduce.

Dr. Richard D'Aquila, director of Northwestern's HIV Translational Research Center, believes that the study's findings could hopefully lead on to future breakthroughs.

"This discovery opens new avenues for further research to solve today's persisting problems in treating HIV infection: avoiding virus resistance to medicines, decreasing the inflammation that leads to premature aging, and maybe even one day being able to cure HIV infection," he states.

Prof. Taylor hopes to identify additional compounds with the potential for development into medicines that could starve HIV in this way without harming cells. This discovery could also have application in the treatment of other diseases such as cancer that similarly rely on access to sugar and other nutrients found in cells to grow and spread.

Last month, Medical News Today reported on a study that identified a "can opener" molecule that renders HIV vulnerable to antibodies that could kill off infected cells.

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GSK team up with US researchers to advance search for HIV cure

With more than 35 million people worldwide living with HIV/AIDS, the need for a cure is more vital than ever. Now, global pharmaceutical giant GlaxoSmithKline and the University of North Carolina at Chapel Hill announce they have teamed up to create an HIV Cure center dedicated to finding a way to eradicate the disease once and for all.

One major focus of the new collaboration will be the "shock and kill" approach for curing HIV, which involves unmasking dormant HIV present in patients' immune cells, before boosting the immune system to destroy all traces of the virus.

Due to be located at the University of North Carolina at Chapel Hill (UNC-Chapel Hill) campus, the new center will consist of a small team of researchers from GlaxoSmithKline (GSK), who will work with UNC-Chapel Hill researchers to discover a cure for HIV/AIDS.

The new collaboration aims to advance recent scientific approaches to curing HIV, including a "shock and kill" approach. This involves unmasking dormant HIV present in patients' immune cells, before boosting the patients' immune system to destroy all traces of the virus.

Such an approach has become a major focus in the treatment of HIV. Only last week, Medical News Todayreported on a study in which researchers identified a molecule that they believe could be used as part of a "shock and kill" treatment strategy for the virus.

The researchers, from the Centre Hospitalier de l'Université de Montréal (CHUM) Research Centre in Canada, revealed how a molecule called JP-III-48 acts as a "can opener," forcing the HIV virus to open up and expose its weaknesses, allowing it to be attacked by the immune system.

A team of researchers from UNC-Chapel Hill were one of the first to identify the "shock and kill" approach, and it is hoped the collaboration with GSK can move it forward.

"The 'shock and kill' approach has shown significant promise in early translational research on humans and has been the focus of research for the last several years," says Dr. David Margolis, professor of medicine at UNC-Chapel Hill and leader of the Collaboratory of AIDS Researchers for Eradication (CARE).

"After 30 years of developing treatments that successfully manage HIV/AIDS without finding a cure," he adds, "we need both new research approaches to this difficult medical problem and durable alliances of many partners to sustain the effort that will be needed to reach this goal."

'We must dedicate the next 30 years to finding a cure for HIV'

Since the HIV epidemic first hit in the early 1980s, almost 78 million people worldwide have been infected with the virus and around 39 million people have died from it.

The primary treatment for people with HIV is antiretroviral therapy (ART), which involves taking a combination of at least three antiretroviral medications. While these medications do not destroy the HIV virus, they can stop it from progressing.

Though such medications are life-saving, the virus is still widespread, particularly in sub-Saharan Africa where the population accounts for 71% of all HIV cases worldwide.

"Although today's treatments for HIV mean that millions of lives have been saved, people still have to take a lifetime of treatments, which takes an emotional toll and places an economic burden on society that is particularly challenging in countries with limited resources," says Zhi Hong, senior vice president and head of the Infectious Diseases Therapy Area Unit at GSK.

"This is why we must dedicate the next 30 years to finding a cure and scaling it up so that one day we will end the HIV/AIDS epidemic."

GSK will invest $20 million into the new research center - $4 million per year for 5 years - funding they say is separate from their investment into new antiretroviral therapies through their HIV Discovery Performance Unit based in North Carolina.

GSK CEO Sir Andrew Witty says the pharmaceutical company has a "long legacy of HIV research success" that he believes will be valuable to the new collaboration with UNC-Chapel Hill. He adds:

"This partnership is a testament to our past and present leadership, innovation and commitment to this field. We are inspired by the confidence that with the right resources and research teams, we will be able to make a meaningful impact toward a cure for HIV."

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HIV cure may lie in radioimmunotherapy

A new study suggests targeting HIV with radioimmunotherapy could eradicate HIV from infected cells. If given in conjunction with highly active antiretroviral therapy, it may form the basis of a cure.
Although highly active antiretroviral therapy (HAART) kills human immunodeficiency virus (HIV) in the bloodstream, it does not completely eliminate it from the body because the virus can linger in infected cells and replicate.
Researchers from the Albert Einstein College of Medicine of Yeshiva University in New York presented their findings at the 99th Scientific Assembly and Annual Meeting of the Radiological Society of North America (RSNA) in Chicago, IL, this week.
Study leader Ekaterina Dadachova, professor of radiology and of microbiology & immunology, says although there has been enormous progress in HIV treatments that slow progression to AIDS, the search for a permanent cure continues. She explains:

"To combat HIV, we need a method that will completely eliminate all HIV-infected cells without damaging non-infected cells."

In radioimmunotherapy (RIT), which has been used for a while to treat cancer, antibodies charged with radioactive isotopes target and destroy cancer cells.
The antibody selects the particular type of cancer cell and the attached radioisotope delivers a lethal dose of radiation that kills the target cell, while leaving untargeted (healthy) cells unharmed.

HIV infection reduced to undetectable levels

In previous work, Prof. Dadachova had already managed to use the approach in the lab to target and destroy human immune cells infected with HIV.
At the meeting, she and her colleagues presented the results of a study in which they used the approach to treat blood samples from people infected with HIV.
The blood samples came from 15 HIV patients receiving HAART treatment at the AIDS Center at Montefiore, the University Hospital for Einstein College and academic medical center.
The results showed that RIT targeted and killed HAART-treated lymphocytes - types of white blood cells - and in most samples, reduced HIV infection to undetectable levels.
The team then went on to see if RIT could reach HIV-infected cells in the brain and central nervous system.
This would be a big step because current antiretrovirals do not cross the blood-brain barrier very well, which is why so many HIV patients treated with HAART often have severe mental impairment.
For this test, they used a lab model of the blood-brain barrier made with human cells and discovered that the same radioisotope-charged antibodies used in earlier experiments could destroy HIV-infected cells in the brain without damaging the barrier.
Prof. Dadachova says:

"We found that radioimmunotherapy could kill HIV-infected cells both in blood samples that received antiretroviral treatment and within the central nervous system, demonstrating RIT offers real potential for being developed into an HIV cure."

In another study published recently in the Journal of Infectious Diseases, researchers from Lund University in Sweden describe how they found that an aggressive new HIV strain leads to AIDS more quickly than other current strains.

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HIV spread may be prevented with discovery of new gene

Scientists have discovered a new gene that may have the ability to prevent human immunodeficiency virus (HIV) from spreading once it enters the body, according to a study published in the journal Nature.
Researchers from King's College London in the UK say the gene, called MX2, could lead to new effective and less toxic treatment against HIV - the virus that causes acquired immunodeficiency syndrome (AIDS).
For the study, the researchers conducted experiments on human cells, in which they introduced the HIV virus to two different cell lines. One cell line had the MX2 gene "switched on," while the other cell line had no MX2 expression.
On observing the effects, the researchers found that in the cells in which the MX2 gene was expressed, the HIV virus was unable to replicate, therefore stopping new viruses from being produced.
In the cell line in which the MX2 gene was switched off, the HIV virus replicated and spread.
Professor Mike Malim of the Department of Infectious Disease at King's College London, says:

"This is an extremely exciting finding which advances our understanding of how HIV virus interacts with the immune system and opens up opportunities to develop new therapies to treat the disease.
Until now, we knew very little about the MX2 gene, but now we recognize both its potent anti-viral function and a key point of vulnerability in the life cycle of HIV."

Researchers say a gene called MX2 may prevent the HIV virus (pictured) from spreading once in the body.
Photo credit: King's College London

According to the Mayo Clinic, HIV patients are currently recommended to take a minimum of three different anti-HIV drugs in order to avoid creating a form of drug resistance.
However, many of these drugs can cause serious side effects, including abnormal heartbeats, shortness of breath, skin rash, weakened bones and even bone death.
"Although people with HIV are living longer, healthier lives with the virus thanks to current effective treatments, they can often be toxic for the body, and drug resistance can become an issue with long-term use," says Prof. Malim.
He notes that it is important to continue finding new ways of mobilizing the body's natural defense system, and the MX2 gene appears to play an important role in initiating viral control in HIV sufferers.
"Developing drugs to stimulate the body's natural inhibitors is a very important approach because you are triggering a natural process and therefore won't have the problem of drug resistance," he adds.

"There are two possible routes - it may be possible to develop either a molecule that mimics the role of MX2 or a drug which activates the gene's natural capabilities."

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Two Men HIV-Free After Bone Marrow Transplants

Two HIV-positive men no longer have detectable virus in their blood after receiving bone-marrow transplants to treat Hodgkin's lymphoma. Timothy Henrich and Daniel Kuritzkes , from Brigham and Women's Hospital, Boston, USA, explained at the International AIDS Society Conference, Kuala Lumpur, Malaysia, that one patient has been off HIV medications for over fifteen weeks and the other seven weeks, and there are still no signs of the virus rebounding.

Completely ridding a patient of HIV is extremely difficult. The virus hides within human DNA in such a way as to become "untouchable". ART (anti-retroviral therapy) helps control the virus in the bloodstream. However, as soon as ART stops, HIV usually replicates rapidly.

The two patients had been HIV-positive for over thirty years. They had both developed Hodgkin's lymphoma, a blood cancer that requires a bone marrow transplant if chemotherapy and other treatments failed. Blood cells are made in the bone marrow - experts believe the bone marrow is a major HIV reservoir.

After undergoing the bone marrow transplants, one man has had no detectable HIV in his blood for four years, and the other for two years.

Lead researcher, Dr. Timothy Henrich warned against using the C-word (cure), saying it is still early days.

In an interview with the BBC, Henrich said:

"We have not demonstrated cure, we're going to need longer follow-up. What we can say is if the virus does stay away for a year or even two years after we stopped the treatment, that the chances of the virus rebounding are going to be extremely low."

Last year, Kuritzkes and Henrich announced that HIV was easily detected in the blood lymphocytes of the two patients before their transplants, but within eight months post- transplant the virus had become undetectable. At the time the patients were still on ART.

The two patients came off ART earlier this year. They are regularly monitored and have no detectable HIV virus. Henrich said "We demonstrated at least a 1,000 to 10,000 fold reduction in the size of the HIV reservoir in the peripheral blood of these two patients. But the virus could still be present in other tissues such as the brain or gastrointestinal track."

If the virus were to rebound, it would mean that the brain, GI tract, lymph nodes or some other sites are important reservoirs of infectious virus "(and) new approaches to measuring the reservoir at relevant sites will be needed".

Bone marrow transplant not the answer to HIV infection

Bone-marrow transplant as a way of curing people infected with HIV is unlikely to ever become standard clinical practice.

In this case, the two patients had blood cancer; the transplants were performed to treat the cancer, not the HIV infection.

Most HIV-positive people do not have blood cancer. Bone marrow transplants are costly and risky - patients face a 20% risk of death. Before undergoing a transplant, the patient's immune system needs to be weakened to minimize the risk of rejection.

A third patient, who also had lymphoma and was HIV-positive and had received the same transplant as the two Boston subjects, died from cancer.

With ART, a person with HIV can enjoy the same life expectancy as other people.

Doctors "cured" baby born with HIV infection

In March this year, doctors from Johns Hopkins Children's Center, the University of Mississippi Medical Center and the University of Massachusetts Medical School announced that an HIV-positive baby who was administered ART within 30 hours of being born had been "cured".

Deborah Persaud, M.D., explained that it is very uncommon to treat a baby for HIV-infection so soon after birth. She added that this was the first case of a functional cure in an HIV-positive infant. The medical team believes that the prompt administration of antiretroviral therapy led to the newborn's cure.

Dr. Persaud said "Prompt antiviral therapy in newborns that begins within days of exposure may help infants clear the virus and achieve long-term remission without lifelong treatment by preventing such viral hideouts from forming in the first place."

First apparent HIV-infection cure probably occurred in Germany, 2010

In December 2010, researchers from Charite - University Medicine Berlin, Germany, wrote in the journal Blood than an acute myeloid leukemia patient, Timothy Brown, who was also HIV-positive had been cured of HIV infection after receiving a bone marrow transplant.

The scientists wrote "Our results strongly suggest that cure of HIV has been achieved in this patient."

In 2007 Timothy Brown stopped receiving ART, had his own immune system effectively wiped out with high-dose chemotherapy and radiation therapy, and received a bone marrow transplant.

In this case, the donor had a very rare gene mutation - CCR5-delta32 - which protected him from HIV infection, meaning that Brown acquired that protection. In July 2012, scientists in California found traces of HIV in his tissue. However, Brown says that any virus that remains in his body is completely inactive ("dead") and cannot replicate.

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Antibody Treatment For HIV

Data on SEEK's Novel Immunotherapy for HIV Published in Virology Journal

SEEK, a privately-owned UK drug discovery group, announces that pre-clinical results on its HIV immunotherapy have been published in the peer-reviewed journal Virology Journal.

SEEK's HIV immunotherapy triggers the immune system's cellular and antibody responses to selectively identify and kill HIV infected cells. The most exciting aspect of this therapy is that it directs the immune system towards short highly conserved regions of proteins produced by most circulating HIV strains. The triggered immune responses are highly effective both independently and in combination.

This opens up developing the antibody response into a monoclonal based therapy for treating HIV.

Monoclonal antibodies have revolutionised the treatment of cancer by improving outcomes and survival. In HIV/AIDS there is new interest in these products, as shown by the recent work of Duke University (USA) in developing a monoclonal antibody that prevents the virus from infecting cells. A monoclonal antibody capable of killing HIV-infected cells (potentially curative effect) would represent a radical new development in HIV therapy, which to this day relies on slowing down the virus rate of growth rather than in killing the cells that harbour it.

By targeting a HIV component that is found only in infected cells and never in healthy cells, such monoclonal antibody therapy offers the potential of high specificity, reduced frequency of administration and minimal side-effects. This would represent a significant improvement over current anti-HIV drugs which require daily treatment and are associated with significant side effects.

Commenting on today's announcement, Gregory Stoloff, CEO of SEEK Group, said: "It is very exciting to be at the forefront of this new approach which opens up HIV therapy to established and available antibody technology."

In July 2011, SEEK announced the results of a Phase Ib/II study in humans which demonstrated that HIV immunotherapy showed a one log(approx 90 percent) difference in viral count in HIV-infected people compared with the placebo group, after just a single administration.

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Scientists Get Inside Look At How AIDS Virus Grooms Its Assault Team

A new study by Los Alamos National Laboratory and University of Pennsylvania scientists defines previously unknown properties of transmitted HIV-1, the virus that causes AIDS. The viruses that successfully pass from a chronically infected person to a new individual are both remarkably resistant to a powerful initial human immune-response mechanism, and they are blanketed in a greater amount of envelope protein that helps them access and enter host cells.

These findings will help inform vaccine design and interpretation of vaccine trials, and provide new insights into the basic biology of viral/host dynamics of infection.

During the course of each AIDS infection, the HIV-1 virus evolves within the infected person to escape the host's natural immune response and adapt to the local environment within the infected individual. Because HIV evolves so rapidly and so extensively, each person acquires and harbors a complex, very diverse set of viruses that develops over the years of their infection. Yet when HIV is transmitted to a new person from their partner, typically only a single virus from the diverse set in the partner is transmitted to establish the new infection.

The key discoveries here are the specific features that distinguish those specific viruses which successfully move to the new host, compared with the myriad forms in the viral population present in a chronically infected individual.

"The viruses that make it through transmission barriers to infect a new person are particularly infectious and resilient," said Los Alamos National Laboratory scientist Bette Korber. "Through this study we now better understand the biology that defines that resilience."

The team set out to determine whether the viruses that were successfully transmitted to a new patient might share distinct biological properties relative to those typically isolated from people with long-term, chronic infection. To do this, the group at U Penn cloned a set of intact viruses from acute infection, and a set of viruses from chronically infected people, and characterized them by measuring quantities that might be related to the virus's ability to successfully establish a new infection. They discovered several clear correlations. For example, transmitted viruses were both more infectious and contained more protective "envelope" per virus; envelope is the protein the virus uses to enter host cells.

The team identified an additional interesting property that could be a general characteristic of new viral infections: the transmitted HIV was capable of replicating and growing well in the presence of alpha interferon. Alpha interferon production is part of our innate human immune response to a new infection. As soon as a new viral infection is initiated in our bodies, local immune cells at the site of infection start secreting molecules called cytokines that have general antiviral activity and can inhibit the production of the newly infected virus. Alpha interferon is one of these potent cytokines.

In the early days of an HIV infection, this innate immune response increases to an intense level, called a "cytokine storm," which gradually recedes during infection. For a newly transmitted HIV to successfully establish infection, it must grow and expand in the new host while facing this cytokine storm. Although typical chronic viruses are sensitive to and inhibited by alpha interferon, transmitted HIV-1 viruses grew well in the presence of interferon.

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Bee Venom Destroys HIV And Spares Surrounding Cells

Scientists have discovered a powerful toxin in bee venom that could end up playing a crucial role in preventing the spread of HIV.

Nanoparticles containing bee venom toxin melittin can destroy human immunodeficiency virus (HIV) while at the same time leaving surrounding cells unharmed, scientists from Washington University School of Medicine reported in the March 2013 issue of Antiviral Therapy.

The researchers said that their finding is a major step toward creating a vaginal gel that can prevent HIV spread. HIV is the virus that causes AIDS.

Joshua L. Hood, MD, PhD, a research instructor in medicine, said:

"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."

Melittin destroys some viruses and malignant tumor cells

Melittin is a powerful toxin found in bee venom. It can poke holes in the protective viral envelope that surrounds the human immunodeficiency virus, as well as other viruses. Free melittin in large-enough quantities can cause considerable damage.

Senior author, Samuel A. Wickline, MD, the J. Russell Hornsby Professor of Biomedical Sciences, has demonstrated that nanoparticles loaded with melittin have anti-cancer properties and have the capacity to kill tumor cells. Linking bee venom with anticancer therapies is not new, in 2004 Croatian scientists reported in the Journal of the Science of Food and Agriculture that honey-bee products, including venom, could well have applications in cancer treatment and prevention.

Normal cells remain intact - the scientists showed that nanoparticles loaded with melittin do not harm normal, healthy cells. Protective bumpers were added to the nanoparticles surface, so that when they come into contact with normal cells (which tend to be much larger), the nanoparticles bounce off rather than attach themselves.

HIV is much smaller than the nanoparticles and fits in between the bumpers. When HIV comes across a nanoparticle it goes in between the bumpers and comes into direct contact with its surface, which is coated with the bee toxin, which destroys it.

Hood explained "Melittin on the nanoparticles fuses with the viral envelope. The melittin forms little pore-like attack complexes and ruptures the envelope, stripping it off the virus."

While most anti-HIV medications work on inhibiting the virus' ability to replicate, this one attacks a vital part of its structure. The problem with attacking a pathogen's ability to replicate is that it does not stop it from starting an infection. Some HIV strains have found ways to circumvent replication-inhibiting drugs, and reproduce regardless.

Hood said:

"We are attacking an inherent physical property of HIV. 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."

Melittin nanoparticles may prevent and treat existing HIV infections

Hood believes that the melittin-loaded nanoparticles have the potential for two types of therapies:

• A vaginal gel to prevent the spread of HIV infection
• Therapy for existing HIV infections, particularly drug-resistant ones

In theory, if the nanoparticles were injected into the patient's bloodstream, they should be able to clear the blood of HIV.

Hood said "The basic particle that we are using in these experiments was developed many years ago as an artificial blood product. 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."

Melittin attacks double-layered membranes indiscriminately, making it a potential for drug therapies beyond HIV infections. The hepatitis B and C viruses, among several others, rely on the same type of protective envelope and could be targeted and destroyed by administering melittin-loaded nanoparticles.

The gel also has the potential to target sperm, the researchers explained, making it a possible contraceptive medication. The study, however, did not look at contraception.

Hood said "We also are looking at this for couples where only one of the partners has HIV, and they want to have a baby. These particles by themselves are actually very safe for sperm, for the same reason they are safe for vaginal cells."

This study was carried out in cells in a laboratory environment. However, the nanoparticles are easy to produce - enough of them could easily be supplied for future human studies.

Recent research on HIV

Over the last few years, scientists have made strides in improving HIV/AIDS treatments and prevention strategies.

Baby "functionally cured" of HIV infection - researchers from Johns Hopkins Children's Center, the University of Mississippi Medical Center and the University of Massachusetts Medical School reported that a baby who was administered antiretroviral therapy thirty hours after being born was "functionally cured". A functional cure means that there is no detectable viral replication after retroviral therapy has stopped.

Ramping up HIV antiretroviral treatments worth the extra cost - investigators from Harvard University, USA, reported that scaling up HIV antiretroviral treatment in a remote province of South Africa (KwaZulu-Natal) reduced the risk of transmitting HIV to sexual partners by 96%.

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HIV Patients May Benefit From Probiotics

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

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

View this article at: http://www.jci.org/articles/view/66736?key=64b158b04e2a168811a3

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CDC Reports HIV Infection Rates Steady

The number of new human immunodeficiency virus (HIV) infections nationwide has continued to remain stable, according to a new report by the Centers for Disease Control and Prevention.

HIV is still a serious issue, with an estimated 47,500 new infections in the United States in 2010. Certain groups, including latinos, gay and bisexual men of all ethnicities, and African Americans, remain disproportionately affected.

Two other significant trends were also noted: early signs of a reduction in new HIV infections among black women as well as a worrisome and consistent rise in new infections among bisexual and gay men.

Homosexual men continue to be the group that is most affected. New infections for this group rose from 26,700 in 2008 to 29,800 in 2010. These men account for four percent of the U.S. population, however, they make up 63 percent of the total of new infections.

Previous research suggests that individual risk behavior does not represent the disproportionate presence of HIV among men who have sex with men.

Other factors that contribute include: a high incidence of HIV among men having sex with other men (MSM), causing a higher risk of HIV exposure with each sexual experience; the high proportion of MSM who do not know about their infection; stigma and homophobia; lack of insurance and worries about confidentiality; and high rates of some STDs. Also MSM typically underestimate their own personal risk.

Women account for 66 percent of new HIV cases among heterosexuals, however, that portion has declined since 2007.

Blacks account for 14 percent of the population and represent about 44 percent of new HIV infections, while hispanics account for 16 percent of the population and make up 21 percent of new infections. New infections continued to be steady among Hispanics and blacks between 2008 and 2010, according to the CDC. These numbers show that minorities are still disproportionately affected.

Whites make up a third (31 percent) of all new HIV infections but had a much lower infection rate than Hispanics or African Americans. There was no significant change in total HIV incidence among whites from 2008 to 2010.

The research indicates that the annual number of new infections has continued to be steady even though there has been a rise in the number of people living with HIV. This suggests that treatment, prevention programs, and testing are all having a significant impact. However, rates of new infections remain too high.

The CDC has planned a new approach in an attempt to achieve an AIDS-free generation. They will focus on the following five areas:

• Supporting Prevention Programs
• Tracking the Epidemic
• Supporting HIV Prevention
• Raising Awareness
• Supporting Structural Interventions

More involvement will also be put into action among community leaders from the African American, Latino and gay populations. The CDC hopes all people will be able to get the facts regarding HIV, get tested and take proper actions to protect their partners and themselves.

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Tracking The Origins Of HIV

Human immunodeficiency virus (HIV) may have affected humans for much longer than is currently believed. Alfred Roca, an assistant professor in the College of Agricultural, Consumer and Environmental Sciences at the University of Illinois, thinks that the genomes of an isolated West African human population provide important clues about how the disease has evolved.

HIV is thought to have originated from chimpanzees in central Africa that were infected with simian immunodeficiency virus (SIV), a retrovirus. "If you look at the diversity present across SIV in chimpanzees, it suggests that they have had it for tens of thousands of years," Roca said.

HIV-1 Type M, which accounts for 90 percent of human infections, is believed to have crossed the species barrier into human populations between 1884 and 1924. Roca said that it may have crossed much earlier and many times, selecting for genetic resistance in isolated rural populations while remaining undetected.

"Some of the scientific literature suggests that the persistence of HIV in humans required population densities typical of the larger cities that appeared in West Central Africa during the colonial era," he said.

Perhaps an even more important factor is that, before modern medicine and vaccinations, infectious diseases such as smallpox killed large numbers of people. People with compromised immune systems may have succumbed first, preventing the immunodeficiency virus from spreading.

If HIV crossed the species barrier many times, it is possible that selection favored protective genetic variants in the affected populations. Roca and his co-investigators looked for evidence of this selection in the Biaka genomes.

The Biaka are a human community that inhabits forests in the range of the chimpanzee subspecies believed to be the source of the current HIV pandemic. The researchers compared Biaka genomes with the genomes of four other African populations who live outside the chimpanzee's range.

Biaka genotypes were available through the Human Genome Diversity Project, which collected biological samples from 52 different population groups across the world. The project genotyped these diverse human communities for single nucleotide polymorphisms (SNPs, pronounced "snips"), or genomic variation, at around 650,000 locations across the genome.

Previous research that used cell lines made in the 1980s from individuals who had AIDS or were believed to be at risk for it had identified 26 genomic locations as being involved in resistance to HIV. Kai Zhao, a graduate student working in Roca's laboratory, examined these locations.

Zhao ran all 10 possible pairwise comparisons for the five human populations and looked for selection signatures. Specifically, selection for a genetic trait tends to reduce diversity in the surrounding genomic region within the affected population, increasing the differences between populations.

The researchers looked at the genomic regions that contain genes known to have a protective effect against HIV to see if there was any overlap with the selection signatures. Eight of the comparisons found overlap. Seven involved the Biaka.

They identified four genes in these overlaps that code for proteins affecting either the ability of HIV to infect the host cell or the disease progression. The researchers also found that for several genes, SNPs associated with protection against HIV-1 were common among the Biaka.

Roca cautions that these results should not be considered definitive. It is not possible to rule out false positives.

"You may detect a signature of selection, but it doesn't necessarily mean that selection has caused it. It's just a good sign that selection may have occurred," he said. Also, the signature of selection may span several genes, of which only one is actually protective against HIV-1.

However, he said that the results are intriguing and indicate that this line of research is worth pursuing.

"If additional studies confirm that these genes have undergone selection and that human populations in the region have some genetic resistance to HIV-1, one could try to find additional genes in the population that may also be protective against HIV but have not yet been identified," he said.

"The mechanism by which these genes work could be determined," he continued. "It could open up a new line of research for fighting retroviruses."

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Ribosome Regulates Viral Protein Synthesis, Revealing Potential Therapeutic Target

Viruses can be elusive quarry. RNA viruses are particularly adept at defeating antiviral drugs because they are so inaccurate in making copies of themselves. With at least one error in every genome they copy, viral genomes are moving targets for antiviral drugs, creating resistant mutants as they multiply. In the best-known example of success against retroviruses, it takes multiple-drug cocktails to corner HIV and narrow its escape route.

Rather than target RNA viruses themselves, aiming at the host cells they invade could hold promise, but any such strategy would have to be harmless to the host. Now, a surprising discovery made in ribosomes may point the way to fighting fatal viral infections such as rabies.

Results were published online in Proceedings of the National Academy of Sciences.

The ribosome has traditionally been viewed as the cell's molecular machine, automatically chugging along, synthesizing proteins the cell needs to carry out the functions of life. But Amy Lee, a former graduate student in the program of virology, and Sean Whelan, HMS professor of microbiology and immunobiology, now say the ribosome appears to take a more active role, regulating the translation of specific proteins and ultimately how some viruses replicate.

The researchers were studying differences between how viruses and the host cells they infect carry out the process of translating messenger RNAs (mRNAs) into proteins. Focusing on protein components found on the surface of the ribosome, they discovered a protein that some viruses depend on to make other proteins, but that the vast majority of cellular mRNAs do not need.

Called rpL40, this ribosomal protein could represent a target for potential treatments; blocking it would disable certain viruses while leaving normal cells largely unaffected.

"Because certain viruses are very sensitive to the presence and absence of these ribosomal proteins, it might be a useful way for us to think about targeting ribosomes for therapeutic purposes from an antiviral standpoint," said Whelan. "This is a way to think about interfering with rabies virus infection. There are no therapeutics for rabies infection."

The team screened protein constituents of the ribosome to see which ones might be involved in specialized protein synthesis. Studying the vesicular stomatitis virus, a rhabdovirus in the same family as the rabies virus, they found that its mRNAs depended on rpL40 but only 7 percent of host-cellular mRNAs did. Some of the cellular mRNAs that depend upon rpL40 were stress response genes.

Experiments in yeast and human cells revealed that a class of viruses, which includes rabies and measles, depended on rpL40 for replication.

"This work reveals that the ribosome is not just an automatic molecular machine but instead also acts as a translational regulator," said first author Amy Lee, who is now a post-doctoral researcher at the University of California, Berkeley.

The concept of targeting cellular functions such as protein synthesis for antiviral therapies is being explored by a number of research groups, but there are no drugs based on this.

"We think the principle is bigger than just this single protein," Whelan said. "Viruses have an uncanny way of teaching us new biology all the time."

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HIV/AIDS Pandemic Started 100 Years Ago

An international team of scientists investigating African human tissue samples preserved for nearly 50 years have suggested that the HIV/AIDS pandemic started around 100 years ago, between 1884 and 1924, at the same time as urbanization started growing in west central Africa.

The finding is published in the 2nd October issue of the journal Nature and was the work of Dr Michael Worobey, an assistant professor of ecology and evolutionary biology at The University of Arizona in Tucson, and colleagues at research centres in Australia, Belgium, France, Democratic Republic of Congo, Denmark and the USA.

Worobey and colleagues suggested that the growing urbanization of colonial Africa around the dawn of the 20th century, characterized by the growth of cities and a rise in high risk behaviours, set the stage for the HIV/AIDS pandemic and created the conditions that allowed the most pervasive strain of HIV, the HIV-1 group M, to spread among humans.

This is some 30 years before previous estimates, which suggested HIV started spreading around 1930.

For the study, Worobey and colleagues spent 8 years screening endless quantities of tissue samples until they discovered a genetic sequence of HIV-1 group M. Dating from 1960, this is the second oldest ever found. It came from a lymph-node tissue biopsy from a woman who lived in present day Kinshasa in the Democratic Republic of the Congo.

The oldest genetic fragment of HIV-1 group M came from a 1959 blood sample from another Kinshasa resident, this time a man.

First the researchers created a range of plausible family trees for the HIV-1 group M, using the 1960 sample and other known HIV-1 genetic sequences. From this it was possible to make time estimates of when the strains diverged from their ancestors, and the rates at which the branches of the trees grew. By projecting backwards the researchers then estimated when the trees took root, that is when the HIV-1 M strain began, which they put at around the beginning of the 20th century.

They then compared the same genetic region in the 1959 virus to the 1960 virus and found more evidence that their common ancestor existed around 1900; it took more than 40 years for the genetic divergence between them to evolve, said the researchers.

Worobey said:

"Previous work on HIV sequencing had been done on frozen samples and there are only so many of those samples available. The 1959 and 1960 samples are presently the oldest links to the HIV epidemic."

"From that point on," explained Worobey, "the next oldest sequences that anyone has recovered are from the late 1970s and 1980s, the era when we knew about AIDS. Now for the first time we have been able to compare two relatively ancient HIV strains."

That helped us to calibrate how quickly the virus evolved and make some really robust inferences about when it crossed into humans, how quickly the epidemic grew from that time and what factors allowed the virus to enter and become a successful human pathogen," he added.

Previous research has shown that HIV started in chimps and spread to humans in southeastern Cameroon.

The present day city of Kinshasa, in the Democratic Republic of the Congo, was once Léopoldville, the centre of a Belgian colony that went through rapid urban growth at the turn of the 19th century, as did the neighbouring regions of Central African Republic, Congo, Gabon and Equatorial Guinea. This coincides with the spread of HIV among humans, said Worobey.

The genetic diversity of the virus suggests that a lot of people in the area were already infected with HIV by 1960, and from there it spread to the rest of the world, until 1981 when it came to public awareness.

The technical preparation that went into researching the ancestry of the HIV strains was "extraordinarily painstaking" said Worobey, who described the condition of the RNA and the DNA in the near 50 year old samples as a "really sorry state". In those days, tissue samples were preserved rather indelicately. First they were treated with chemicals, then embedded in paraffin wax, and there was no refrigeration, so these samples will have been at room temperature for decades.

Instead of a "nice, pearl-strand of DNA or RNA, you have a jumbled mass that's all jammed together," said Worobey.

The research team's next step will be to recover more samples, get more DNA and RNA fragments, and try to piece together more of the jigsaw of the history of HIV. This study has done a lot to "snap everything into sharp focus and allows us to understand the timing of these events and the growth of the epidemic," said Worobey.

Drawing a broader conclusion from the research, Worobey said it would seem HIV was encouraged to spread because of changes in human population, and therein lies the clue to its demise, by making changes in human population to reverse the epidemic.

"If HIV has one weak spot, it is that it is a relatively poorly transmitted virus. From better testing and prevention, to wider use of antiretroviral drug therapy, there are a number of ways to reduce transmission and force this virus back into extinction. Our results suggest that there are reasons for such optimism," said Worobey.

"Direct evidence of extensive diversity of HIV-1 in Kinshasa by 1960."

Click here for Abstract.

Source: Nature, The University of Arizona .

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Circumcision, Fidelity More Effective HIV Prevention Methods Than Condoms, Abstinence, Researchers Say

Promoting male circumcision and fidelity to one partner seems to be more effective at curbing the spread of HIV than promoting abstinence and condom use, USAID researcher and technical adviser Daniel Halperin said last week, the Chicago Tribune reports. As Halperin and other researchers analyze 20 years of studies on HIV/AIDS throughout Africa, they have tried to "put aside intuitions, emotions, ideologies and look at the evidence in as coldhearted a way as we can," Halperin said. During a speech at a meeting of the Southern African HIV Clinicians Society in Johannesburg, South Africa, Halperin said he and his colleagues discovered that regular sex partners rarely use condoms, and abstinence merely delays HIV infection among young people by one or two years. For example, condom use in Ghana and Senegal seems to have helped in the reduction of the spread of the HIV, which in those countries is particularly prevalent among commercial sex workers and their partners. However, condom use in South Africa and Botswana has had little effect in reducing those countries' HIV epidemics -- which have reached the general population -- because regular sex partners rarely use condoms consistently. In comparison, faithfulness to one partner has worked at reducing HIV prevalence in Uganda and Kenya, according to Halperin. Because a person is more likely to transmit HIV during the first three weeks of contracting the virus, an HIV-positive person who has just one partner during that time is likely to pass the disease to that one person. But if an HIV-positive person in the highly infectious stage has many sexual partners at a time, "the virus spreads like wildfire" as those people in turn have sex with other people, Halperin said. In addition, circumcision has been shown to reduce male-to-female HIV transmission by 60% to 75% (Goering, Chicago Tribune, 4/23). A study published in the November 2005 issue of PLoS Medicine of men living in South Africa finds that male circumcision might reduce the risk of men contracting HIV through sexual intercourse with women by about 60%. Male circumcision might also reduce the risk of HIV transmission from HIV-positive men to their female partners, according to a study of couples in Rakai, Uganda (Kaiser Daily HIV/AIDS Report, 2/9). Poverty Reduction, Status Awareness
In addition, poverty does not appear necessarily to make a person more susceptible to HIV. "[C]ontrary to popular wisdom, as income levels go up in both men and women, we see higher rates of HIV," Halperin said, adding that people who make more money tend to have more sexual partners. Other HIV prevention methods such as encouraging people to know their status and treating secondary sexually transmitted infections also have not proven effective, Halperin said (Chicago Tribune, 4/23).

"Reprinted with permission from http://www.kaisernetwork.org. You can view the entire Kaiser Daily Health Policy Report, search the archives, or sign up for email delivery at http://www.kaisernetwork.org/dailyreports/healthpolicy. The Kaiser Daily Health Policy Report is published for kaisernetwork.org, a free service of The Henry J. Kaiser Family Foundation . © 2005 Advisory Board Company and Kaiser Family Foundation. All rights reserved.

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South Africa Recalls Millions Of Condoms

Health authorities in South Africa have recalled more than a million condoms that were handed out in the lead up to the African National Congress centenary celebrations.

The action was taken after South Africa's HIV group Treatment Action Campaign (TAC) issued a warning, having received complaints from the public, that large numbers of faulty condoms appeared to be in circulation in the Bloemfontein area.

8,700 boxes of condoms, with the South African Bureau of Standards stamp, were delivered to guesthouses, hotels, restaurants and bars before the ANC celebrations. Authorities are still investigating complaints that the condoms are porous. The Free State Health Department said the recall, which they estimate at 1.35 million condoms is just a "precautionary measure" and asked the public not to be alarmed.

TAC's Sello Mokhalipi told the BBC that condoms :

"Are still out there in large numbers and that is of great concern to us ... The complaints are that the condoms broke during intercourse."

He continued that the TAC conducted its own investigations using some of the condoms handed out during the centenary celebrations and discovered them to be porous :



Free State Health Department spokesperson Jabu Mbalula said the health authority would not be able to make a clear statement on the issue until it had conducted its own tests on the condoms recovered from the handouts.

This is the first time that Free State province, which has a population of 5.5 million people, needed to recall condoms, although it's not the first time that South Africa has had problems of this kind. In August 2007 when 20 million contraceptives were recalled after "hundreds of thousands" were found to be faulty.

South Africa, having one of the highest rates of HIV infection in the world, has in recent years made a push to promote awareness and condom use.

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World AIDS Day, December 1, "The End Is In Sight"

Michel Sidibé, Executive Director of UNAIDS, says that this coming AIDS day, December 1st, will be unique in that health care professionals, health authorities and scientists may be able to say with confidence that the end of AIDS really is in sight. Collective international actions have resulted in solid achievements in the fight against AIDS. Despite the global economic crisis which started three years ago, and scarce resources in comparison to what would be realistically needed in the AIDS campaign, millions of of lives have still been saved - results for HIV treatment, prevention and accessibility to medical care have been impressive, Sidibé explained.

Sidibé has thanked world leaders for their pledges; promises he describes as "bold, tangible and realistic." It is crucial that these pledges are delivered in every single nation, every community, and to every individual who needs help.

At last, Sidibé added, world leaders have joined virtually unanimously to strive for a world where no mother dies of AIDS and no child is born with HIV.

In a letter, Sidibé wrote:

"The gulf between treatment and prevention has ended.
Treatment is prevention."

AIDS has come out of isolation and is now part of integrated and holistic health services, Sidibé explained - the gulf between health and AIDS is now much smaller. We are now well on the way for "people-centered health delivery systems"; systems that value, restore and respect human dignity.

With smart investments, making the most of scientific breakthroughs, and respecting human rights, the fight against AIDS is a clear and feasible one, Sidibé said.

Sidibé explained:

"It is why world leaders must fully fund the AIDS response. The global investment target of US$ 22-24 billion is a shared responsibility of all countries, donors and others. Only together can we secure the future and provide greater and long-term dividends.

. . . . on this World AIDS Day, I call upon leaders, communities, parents, people living with HIV and young people to look forward and work towards a world with Zero new HIV infections, Zero discrimination and Zero AIDS-related deaths."

New HIV infections and AIDS deaths drop

According to UNAIDS, the numbers of new HIV infections and deaths caused by AIDS have dropped to their lowest levels since 1997 (the peak). Since 2005, the total number of people dying annually from AIDS related illnesses has fallen 21%.

Sidibé said:

"Even in a very difficult financial crisis, countries are delivering results in the AIDS response. We have seen a massive scale up in access to HIV treatment which has had a dramatic effect on the lives of people everywhere."

WHO (World Health Organization) informs that 6.6 million of the 14.2 million (estimated) individuals from developing countries who are eligible for treatment in 2010 had access to lifesaving antiretroviral therapy - 1.35 million more people than in 2009.

By the end of 2010:

• Between 31.6 and 35.2 million individuals were living with HIV globally
• Between 2.4 and 2.9 million new HIV infections were reported in that year
• There were between 1.6 and 1.9 million died of an AIDS-related illness by the end of that year

Number of people living with HIV by country (estimate). Source: UNAIDS

What is AIDS? What is HIV?

AIDS

The acronym AIDS stands for Acquired Immuno Deficiency Syndrome.

• Acquired - simply means it is not a hereditary disease, it develops after birth. In this case, from contact with HIV (human immunodeficiency virus).
• Immunodeficiency - this means the disease weakens the patient's immune system.
• Syndrome - a collection of signs and symptoms that characterize or indicate a disease or condition.

AIDS needs to be diagnosed by a doctor, using specific laboratory or clinical standards.



HIV

HIV stands for (Human Immunodeficiency Virus) - the virus that causes AIDS. HIV can be passed from human-to-human via:

• Infected blood
• Infected semen
• Vaginal secretions
• Coming into contact with an infected person's broken skin or mucous membrane
• From an infected pregnant mother to her baby during pregnancy, childbirth or breastmilk.

Some people with HIV infection will eventually develop AIDS.

Put simply: HIV is the virus that causes AIDS.

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Magic Mushrooms Can Bring About Lasting Personality Changes

Taking magic mushrooms (psilocybin) can have a lasting change on the individual's personality, making them more open about their feelings and the way they perceive things, researchers from Johns Hopkins University School of Medicine, Baltimore, MD, USA, wrote in the Journal of Psychopharmacology. The authors explained that those who had mystic experiences while on psilocybin were more likely to subsequently exhibit certain personality changes, making them more forthcoming about their feelings, becoming more focused on being creative, curious, and appreciative about artistic things.

Psilocybin is a psychedelic drug - a substance whose main action is to alter perception and cognition. Its molecular formula is C₁₂H₁₇N₂O₄P. Its mind-altering effects are similar to those of mescaline and LSD. It effects may include, an altered sense of time, spiritual experiences, perceptual distortions, and thinking processes. Psilocybin can also cause nausea and panic attacks. This psychedelic drug can be found in over 200 types of mushrooms, the most powerful coming from the genus Psilocybe, including P. cubensis, P. semilanceata, and P. cyanescens.



Psilocybe Cubensis - a powerful source of psilocybin


Magic mushrooms are usually eaten. However, they can also be made into a tea beverage, or smoked.

In this latest study, headed by Roland Griffiths, personality changes that occurred in those who took magic mushrooms were still there twelve months later. The authors believe that the psilocybin may well have a long-term effect.

Professor Griffiths said:

"The remarkable piece is that psilocybin can facilitate experiences that change how people perceive themselves and their environment. That's unprecedented."

Magic mushrooms used to be used by Timothy Leary, a former Harvard professor of psychology. Leary founded the Harvard Psilocybin Project.

Openness is one of five main personality traits that span all cultures worldwide, the other four are extroversion, neuroticism, agreeableness and conscientiousness. Degrees of openness are fairly constant throughout an individual's lifetime. The researchers found that the other four personality factors were largely unchanged after people consumed magic mushrooms.

The authors say their study is the first finding of a short-term intervention with long-lasting personality changes.

The study involved 51 individuals who underwent two to five eight-hour psilocybin sessions, with a three-week interval between each session. During a session they lay down on a couch, wore an eye mask and listened to music through headphones while concentrating on an inner experience. Their personalities were screened at the beginning of the studies, and then during a two-month and 12-month follow-up.

Thirty of the volunteers had a mystical experience, according to the researchers' criteria gathered from a set of psychological scales. Their openness scores increased, indicating more focus on aesthetics, inner feeling, values, imagination and ideas. The rest of the participants, those with no mystical experiences, underwent no apparent personality change.

The authors concluded:

"The findings suggest a specific role for psilocybin and mystical-type experiences in adult personality change."

Psychoactive mushrooms used by humans for thousands of years

Archeologists have gathered evidence of the presence of psychoactive mushrooms used in religious rituals for thousands of years.

Ancient paintings in Villar del Humo, Spain, show evidence of Psilocybe hispanica usage in religious ceremonies about 4,000 BC.

Murals in southeast Algeria, in the Sahara desert, dated 7000 to 9000 BC suggest psilocybin mushroom use.

In the Aztec language Nahatl, psychoactive mushrooms were called "teonanacatl" (God flesh). Mayan archives have data pointing to common usage of psilocybin mushrooms in ceremonies and rituals.

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HIV Prevention Scientific Breakthrough Of 2011

The journal Science has named research led by Myron S. Cohen, MD., of the University of North Carolina at Chapel Hill, as the 2011 Scientific Breakthrough of the Year.

The program, known as the HIV Prevention Trials Network 052 study looked into whether antiretroviral drugs can prevent the transmission of HIV amongst couples where only one partner has HIV. They discovered that early treatment with antiretrovirals dropped the contagion rate by 96%.

Science announced their top ten list of scientific breakthrough for 2011 today, and the editors said that :

"In combination with other promising clinical trials, the results have galvanized efforts to end the world's AIDS epidemic in a way that would have been inconceivable even a year ago."

It has been a long term project, spanning twenty years since the first anti HIV drugs came onto the market. It took until 2000 to consider the concept was strong enough to being tested, and another ten to obtain the results.

Cohen, who is Distinguished Professor of Medicine, Microbiology and Epidemiology at UNC, said :

"From the time the first AIDS drugs were developed in the mid-1990s, our UNC team of virologists, pharmacologists, and physicians has been working on the idea that antiretrovirals might make people less contagious ... This idea eventually became HPTN 052."

U.S. Secretary of State Hillary Clinton summed up everyone's feelings :

"The goal of an AIDS-free generation is ambitious,
but it is possible."

The release of the results in May 2011 has been reverberating through the scientific and medical communities ever since, and as a result of Cohen's work, U.S. and international organizations, such as the World Health Organization, the President's Emergency Plan for AIDS Relief, and the Joint United Nations Programme on HIV/AIDS, have begun to incorporate prevention treatments into their policies and planning. The HIV Prevention Trials Network 052 has created somewhat of a revolution in the approach to HIV as it was previously thought that only physical barrier methods could prevent the spread of the virus.

Cohen's work was funded by the HIV Prevention Trials Network, which is funded by the National Institute of Allergy and Infectious Diseases with additional funding from the National Institute on Drug Abuse and the National Institute of Mental Health, both part of the National Institutes of Health. Additional support was provided by the NIAID-funded Adult AIDS Clinical Trials Group. Cohen was grateful for the recognition, but pointed out that science is more important that accolades :

"While I am obviously thrilled to have this research recognized as the Science breakthrough of the year ... witnessing the translation of this scientific discovery on a global scale truly is the best reward."

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Dear HIV

HIV affects thousands of teens and young adults. Between 2006 and 2009, 29,740 teens and young adults between the ages of 13-24 were diagnosed with HIV. In 2009, the young adults between the ages of 20-24 accounted for the highest rate of new HIV diagnoses. Even though HIV has been around in the United States for approximately 30 years and HIV/AIDS education is included in school based health curricula, there are still misconceptions and stigma associated with the disease.
We feel that it is imperative for kids, teens, and adults to have a better understanding of HIV and those who live with it.
Beginning with this entry, the “Living with HIV” blog series will communicate multiple facets of what real life is like for teens and young adults who are currently living with HIV. All of the material was written by teens and young adults living with HIV, and reflects their struggles, worries, and resilience. These entries will cover various aspects of daily life, including school, friendships, and worries about the future.
-The Young Men’s Health Initiative staff
Dear HIV:

• “You’re the annoying eyelash that I can’t get out of my eye. You’re there, bothering me every second and I can’t see you, can’t get you out. You just keep bothering me.”
• “I am MAD because you took my parents away from me.”
• “The medication to treat you sucks, why does it have to be so difficult?”
• “Go away.”
• “I don’t like you; no one likes you, go away!”
• “You know those gnats that you can never get out of your house in the summer, the fruit flies? They’re all up in your business and you keep swatting them away and they go away for a while but then they come right back annoying you? That’s HIV. It’s always there, even if I can forget about it for a little while, I always get sick or something happens and it comes back.”

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