A team of NIH scientists has developed a new tool to identify broadly neutralizing antibodies (bNAbs) capable of preventing infection by the majority of HIV strains found around the globe, an advance that could help speed HIV vaccine research. Scientists have long studied HIV-infected individuals whose blood shows powerful neutralization activity because understanding how HIV bNAbs develop and attack the virus can yield clues for HIV vaccine design. But until now, available methods for analyzing blood samples did not easily yield specific information about the HIV bNAbs present or the parts of the virus they targeted. In addition, determining where and how HIV bNAbs bind to the virus has been a laborious process involving several complicated techniques and relatively large quantities of blood from individual donors.

Observing the evolution of a particular type of antibody in an infected HIV-1 patient, a study spearheaded by Duke University, including analysis from Los Alamos National Laboratory, has provided insights that will enable vaccination strategies that mimic the actual antibody development within the body.

Human cells have an intrinsic capacity to destroy HIV. However, the virus has evolved to contain a gene that blocks this ability. When this gene is removed from the virus, the innate human immune system destroys HIV by mutating it to the point where it can no longer survive.

A two-year-old child born with HIV infection and treated with antiretroviral drugs beginning in the first days of life no longer has detectable levels of virus using conventional testing despite not taking HIV medication for 10 months, according to findings presented today at the Conference on Retroviruses and Opportunistic Infections (CROI) in Atlanta.

This image shows new HIV particles exiting an infected T-cell. Studying HIV-1, the most common and infectious HIV subtype, Johns Hopkins scientists have identified 25 human proteins "stolen" by the virus that may be critical to its ability to infect new cells. HIV-1 viruses capture many human proteins from the cells they infect but the researchers believe these 25 proteins may be particularly important because they are found in HIV-1 viruses coming from two very different types of infected cells. A report on the discovery, published online in the Journal of Proteome Research on Feb. 22, could help in building diagnostic tools and novel treatment strategies to fight HIV infection.

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.

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.

At least 2 million people worldwide will be infected with HIV this year, driving the need for better HIV prevention strategies to slow the global pandemic. A better understanding of how to prevent HIV transmission using antiviral drugs led to approval of the first oral pill for HIV prevention, and microbicides delivered as topical gels or via intravaginal rings are in clinical testing and have yielded both positive and negative results. The complex factors involved in the sexual transmission of HIV, the urgent need for new preventive approaches, and the most promising methods currently in development are examined in a special issue of AIDS Research and Human Retroviruses, a peer-reviewed journal published by Mary Ann Liebert, Inc, publishers. The entire issue is available free on the AIDS Research and Human Retroviruses website at http://www.liebertpub.com/aid.

Wits researchers have played a pivotal role in an AIDS study published today in the journal, Nature Medicine, which describes how a unique change in the outer covering of the virus found in two HIV infected South African women enabled them to make potent antibodies which are able to kill up to 88% of HIV types from around the world.

A team of scientists led by virologists Prof. Oliver T. Fackler and Prof. Oliver T. Keppler from Heidelberg University Hospital have decoded a mechanism used by the human immune system to protect itself from HIV viruses. A protein stops the replication of the virus in resting immune cells, referred to as T helper cells, by preventing the transcription of the viral genome into one that can be read by the cell. The ground-breaking results provide new insights into the molecular background of the immunodeficiency syndrome AIDS and could open up starting points for new treatments. The study has now been published – ahead of print online – in the international journal Nature Medicine.

One of the big mysteries of AIDS is why some HIV-positive people take more than a decade to progress to full-blown AIDS, if they progress at all.

A new study has discovered one more way the human immunodeficiency virus (HIV) exploits the immune system. Not only does HIV infect and destroy CD4-positive helper T cells – which normally direct and support the infection-fighting activities of other immune cells – the virus also appears to use those cells to travel through the body and infect other CD4 T cells. The study from Massachusetts General Hospital (MGH) investigators, which will appear in the journal Nature and has received advance online release, is the first to visualize the behavior of HIV-infected human T cells within a lymph node of a live animal, using a recently developed "humanized" mouse model of HIV infection.

The rare ability of some individuals to control HIV infection with their immune system alone appears to depend – at least partially – on specific qualities of the immune system's killer T cells and not on how many of those cells are produced. In a Nature Immunology paper that has received advance online publication, researchers at the Ragon Institute of Massachusetts General Hospital, MIT and Harvard report that – even among individuals sharing a protective version of an important immune system molecule – the ability of HIV-specific killer T cells to control viral replication appears to depend on the particular sequence of the protein that recognizes HIV infected cells.

Scientists have identified a new HIV-suppressing protein in the blood of people infected with the virus. In laboratory studies, the protein, called CXCL4 or PF-4, binds to HIV such that it cannot attach to or enter a human cell. The research was led by Paolo Lusso, M.D., Ph.D., chief of the Section of Viral Pathogenesis in the Laboratory of Immunoregulation at the National Institute of Allergy and Infectious Diseases (NIAID), part of NIH.

Tenofovir, one of the most effective and commonly prescribed antiretroviral medications for HIV/AIDS, is associated with a significant risk of kidney damage and chronic kidney disease that increases over time, according to a study of more than 10,000 patients led by researchers at the San Francisco VA Medical Center and the University of California, San Francisco (UCSF).

A saliva test used to diagnose the human immunodeficiency virus (HIV), is comparable in accuracy to the traditional blood test, according to a new study led by the Research Institute of the McGill University Health Centre (RI-MUHC) and McGill University. The meta-analysis, which compared studies worldwide, showed that the saliva HIV test, OraQuick HIV1/2, had the same accuracy as the blood test for high-risk populations. The test sensitivity was slightly reduced for low risk populations. The study, published in this week's issue of The Lancet Infectious Diseases, has major implications for countries that wish to adopt self-testing strategies for HIV.

__IMAGE_2 Scientists at the Gladstone Institutes have discovered new protein fragments in semen that enhance the ability of HIV, the virus that causes AIDS, to infect new cells -- a discovery that one day could help curb the global spread of this deadly pathogen.

A cheaper laboratory test that helps guide anti-retroviral drug treatment for people with HIV/AIDS may be just as effective as a more sophisticated test, a group of international researchers has found – a discovery that could be particularly important in rural Africa.

WHAT: HIV is coated in sugars that usually hide the virus from the immune system. Newly published research reveals how one broadly neutralizing HIV antibody actually uses part of the sugary cloak to help bind to the virus. The antibody binding site, called the V1/V2 region, represents a suitable HIV vaccine target, according to the scientists who conducted the study. In addition, their research reveals the detailed structure of the V1/V2 region, the last part of the virus surface to be visualized at the atomic level.

The Centre de recherche du Centre hospitalier de l'Université de Montréal (CRCHUM) announced today that one of its researchers will receive funding of 100,000 US $ through Grand Challenges Explorations, an initiative created by the Bill & Melinda Gates Foundation that enables researchers worldwide to test unorthodox ideas that address persistent health and development challenges. Dr. Andrés Finzi will pursue an innovative global health research project, titled "Reverse Fusion: a new approach to eradicate HIV/AIDS" to deliver toxic genes to HIV-infected cells and eliminate them.

Timing is everything when treating patients with both HIV and tuberculosis. Starting HIV therapy in such patients within two weeks of TB treatment, rather than two months as is the current practice, increases survival by 33 percent, according to a large-scale clinical trial in Cambodia led by researchers at Children's Hospital Boston and the Immune Disease Institute (IDI).

Researchers at Duke University Medical Center, Beth Israel Deaconess Medical Center and Harvard Medical School have demonstrated an approach to HIV vaccine design that uses an altered form of HIV's outer coating or envelope protein.

Aeras and the Oxford-Emergent Tuberculosis Consortium (OETC) announce today the start of a Phase IIb proof-of-concept efficacy trial of a new investigational tuberculosis (TB) vaccine that involves people living with the human immunodeficiency virus (HIV). The trial will be conducted at research sites in Senegal and South Africa with primary funding support from the European and Developing Countries Clinical Trials Partnership (EDCTP).

A new study shows for the first time that natural killer (NK) cells, which are part of the body's first-line defence against infection, can contribute to the immune response against HIV. In an article in the August 4 issue of Nature, a research team based at the Ragon Institute of MGH, MIT and Harvard reports that the HIV strains infecting individuals with particular receptor molecules on their NK cells had variant forms of key viral proteins, implying that the virus had mutated to avoid NK cell activity.

HIV epidemics are emerging among men who have sex with men (a term that encompasses gay, non-gay identified homosexual men, transgendered, and bisexual men) in several countries in the Middle East and North Africa. Importantly, the high level of risky sexual behavior practiced by many men who have sex with men in these countries indicates that they could become the pivotal risk group for HIV sexual transmission in this region.

A landmark study by the BC Centre for Excellence in HIV/AIDS (BC-CfE) and the University of British Columbia (UBC) shows that patients in Africa receiving combination antiretroviral therapy (cART) for HIV can expect to live a near normal lifespan.

Astrocytes (pictured in green) help to support blood vessels (red) that act as the blood‑brain barrier ‑ a network that keeps potentially harmful chemicals and toxins out of the brain.... HIV weakens the blood-brain barrier — a network of blood vessels that keeps potentially harmful chemicals and toxins out of the brain — by overtaking a small group of supporting brain cells, according to a new study in the June 29 issue of The Journal of Neuroscience. The findings may help explain why some people living with HIV experience neurological complications, despite the benefits of modern drug regimens that keep them living longer.

Scientists at the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, have demonstrated why certain immune cells chronically exposed to HIV shut down, and how they can be reactivated.

A key step in the processing of HIV within cells appears to affect how effectively the immune system's killer T cells can recognize and destroy infected cells. Researchers at the Ragon Institute of MGH, MIT and Harvard have found that – as HIV proteins are broken down within cells, a process that should lead to labeling infected cell for destruction by CD8 T cells – there is a great variability in the stability of resulting protein segments, variations that could significantly change how well cells are recognized by the immune system. Their report appears in the June Journal of Clinical Investigation.

Thanks to a certain protein, rhesus monkeys are resistant to HIV. Known as TRIM5, the protein prevents the HI virus from multiplying once it has entered the cell. Researchers from the universities of Geneva and Zurich have now discovered the protein's mechanism, as they report in Nature. This also opens up new prospects for fighting HIV in humans.