AIDS & HIV

Category: AIDS & HIV

Fifteen years ago, MIT professor John Essigmann and colleagues from the University of Washington had a novel idea for an HIV drug. They thought if they could induce the virus to mutate uncontrollably, they could force it to weaken and eventually die out — a strategy that our immune system uses against many viruses.

HIV-1, the virus responsible for most cases of AIDS, is a very selective virus. It does not readily infect species other than its usual hosts – humans and chimpanzees. While this would qualify as good news for most mammals, for humans this fact has made the search for effective treatments and vaccines for AIDS that much more difficult; without an accurate animal model of the disease, researchers have had few options for clinical studies of the virus.

By analyzing the blood of almost 100 treated and untreated HIV-infected volunteers, a team of scientists has identified previously unknown characteristics of B cells in the context of HIV infection. B cells are the immune system cells that make antibodies to HIV and other pathogens. The findings augment the current understanding of how HIV disease develops and have implications for the timing of treatment. Researchers at the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health, led the study

An interdisciplinary team of scientists from KU Leuven in Belgium has developed a new technique to examine how proteins interact with each other at the level of a single HIV viral particle. The technique allows scientists to study the life-threatening virus in detail and makes screening potential anti-HIV drugs quicker and more efficient. The technique can also be used to study other diseases.

A team of researchers has reported a novel method for tracking CD4+ T cells in people infected with HIV. CD4+ T cells are critical for immune defense against an array of pathogens and are a primary target of HIV. In the study, researchers used a unique, replication-incompetent (defective) form of HIV identified in a patient in the early 1990s. The defective virus had integrated into the genome of a single CD4+ T cell. Like a barcode, this "provirus" marked the originally infected CD4+ T cell and its progeny, enabling researchers to track its lineage for 17 years. This new method allows scientists to distinguish dividing cells from dying ones, something that has not been possible with existing labeling techniques, but is essential for studying how immune cells survive HIV infection.

The human intestinal tract, or gut, is best known for its role in digestion. But this collection of organs also plays a prominent role in the immune system. In fact, it is one of the first parts of the body that is attacked in the early stages of an HIV infection. Knowing how the virus infects cells and accumulates in this area is critical to developing new therapies for the over 33 million people worldwide living with HIV. Researchers at the California Institute of Technology (Caltech) are the first to have utilized high-resolution electron microscopy to look at HIV infection within the actual tissue of an infected organism, providing perhaps the most detailed characterization yet of HIV infection in the gut.

A recently discovered HIV strain leads to significantly faster development of AIDS than currently prevalent forms, according to new research from Lund University in Sweden.


The HIV envelope protein has long been considered one of the most difficult targets in structural biology and of great value for medical science
Collaborating scientists at The Scripps Research Institute (TSRI) and Weill Cornell Medical College have determined the first atomic-level structure of the tripartite HIV envelope protein—long considered one of the most difficult targets in structural biology and of great value for medical science.

The key to future HIV treatment could be hidden right in our own genes. Everyone who becomes infected deploys defense strategies, and some even manage to hold the virus at bay without any therapy at all. This immune system struggle leaves its mark within the pathogen itself – genetic mutations that indicate how the virus reacted to its host's attacks. Scientists from EPFL and the Vaud university hospital center (UNIL-CHUV) retraced the entire chain of events in these battles, from the genome of the virus to the genome of the victim. They have created the first map of human HIV resistance. The goal of their research, which has been published in the journal eLife on the 29th of October, is to find new therapeutic targets and to enable individualized treatment strategies.

A 3-year-old Mississippi child born with HIV and treated with a combination of antiviral drugs unusually early continues to do well and remains free of active infection 18 months after all treatment ceased, according to an updated case report published Oct. 23 in the New England Journal of Medicine.

In many ways, the spread of HIV has been fueled by substance abuse. Shared needles and drug users' high-risk sexual behaviors are just some of the ways that narcotics such as cocaine have played a key role in the AIDS epidemic in much of the world.

A mutant of an immune cell protein called ADAP (adhesion and degranulation-promoting adaptor protein) is able to block infection by HIV-1 (human immunodeficiency virus 1), new University of Cambridge research reveals. The researchers, who were funded by the Wellcome Trust, believe that their discovery will lead to new ways of combatting HIV.

It's often said that the HIV/AIDS epidemic has a woman's face. The proportion of women infected with HIV has been on the rise for a decade; in sub-Saharan Africa, women constitute 60 percent of people living with disease. While preventative drugs exist, they have often proven ineffective, especially in light of financial and cultural barriers in developing nations.


This image shows the HIV virus.
A team of researchers led by King's College London has for the first time identified a new gene which may have the ability to prevent HIV, the virus that causes AIDS, from spreading after it enters the body.

August 21, 2013—The HIV/AIDS epidemic is changing in unexpected ways in countries around the world, showing that greater attention and financial investment may be needed in places where the disease has not reached epidemic levels, according to a new study from the Institute for Health Metrics and Evaluation (IHME) at the University of Washington.

Infection by human immunodeficiency virus (HIV) causes acquired immunodeficiency syndrome (AIDS), a debilitating disorder in which progressive weakening of the immune system makes affected individuals more susceptible to potentially life-threatening infections and chronic diseases. Despite advances in the treatment and management of AIDS, there is no cure, and HIV infection remains a major global health problem. According to the WHO, there were an estimated 34 million infected individuals in 2011. Over the last three decades, a number of animal models have been developed to study aspects of HIV infection, pathogenesis and control. However, the currently available models do not recapitulate the physiological environment of the most common route of HIV transmission worldwide, vaginal intercourse. Now, Mary Jane Potash and colleagues from St. Luke's-Roosevelt Hospital Center and Columbia University Medical Center in New York, NY, have developed an approach for modelling heterosexual transmission of HIV in vivo. Their work was published recently in Disease Models & Mechanisms.

Millions more people could get access to life-saving HIV drug therapy, following a landmark study led by Australian researchers based at the Kirby Institute at the University of New South Wales (UNSW).

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.

AIDS & HIVFebruary 27, 2013 05:55 PM


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.

AIDS & HIVDecember 18, 2012 07:17 PM

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.

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