AIDS & HIV

Category: AIDS & HIV

In cells with latent HIV infection, the virus is dormant, and such cells are therefore not attacked by the immune system or by standard antiretroviral therapy. To eradicate the virus from the human body and truly cure a patient, reservoirs of latently infected cells need to be activated and eliminated "the so-called "kick-and-kill" approach. Two studies published on July 30th in PLOS Pathogens report encouraging results on the use of a combination of several drugs to efficiently reactivate HIV in cells with latent infection.

A Canadian research team at the IRCM in Montreal, led by molecular virologist Eric A. Cohen, PhD, made a significant discovery on how HIV escapes the body's antiviral responses. The team uncovered how an HIV viral protein known as Vpu tricks the immune system by using its own regulatory process to evade the host's first line of defence. This breakthrough was published yesterday in the scientific journal PLOS Pathogens and will be presented at the upcoming IAS 2015 conference in Vancouver. The findings pave the way for future HIV prevention or cure strategies.


Susana Valente is an associate professor at the Florida campus of The Scripps Research Institute.
HIV-infected patients remain on antiretroviral therapy for life because the virus survives over the long-term in infected dormant cells. Interruption of current types of antiretroviral therapy results in a rebound of the virus and clinical progression to AIDS.


The HIV capsid protein plays a critical role in the virus' life cycle. Mizzou researchers recently developed the most complete model yet of this vital protein.
HIV, or human immunodeficiency virus, is the retrovirus that leads to acquired immunodeficiency syndrome or AIDS. Globally, about 35 million people are living with HIV, which constantly adapts and mutates creating challenges for researchers. Now, scientists at the University of Missouri are gaining a clearer idea of what a key protein in HIV looks like, which will help explain its vital role in the virus' life cycle. Armed with this clearer image of the protein, researchers hope to gain a better understanding of how the body can combat the virus with the ultimate aim of producing new and more effective antiviral drugs.


This image shows cell intrinsic responses against HIV-1 in conventional dendritic cells from Elite Controllers.
Elite controllers (EC) are a small group of HIV-infected individuals who are able to suppress the virus in the absence of antiretroviral therapy. EC demonstrate that the human immune system, in principle, is capable of rendering HIV harmless. A study published on June 11th in PLOS Pathogens shows that dendritic cells (DC) of EC are supersensitive to early signs of HIV infection, and contribute to a stronger immune response than that seen in individuals who fail to control the virus in the long term.


Probing HIV Env's incorporation into viral particles could inform design of virus-like particle vaccines.
Virologists at Emory University School of Medicine, Yerkes National Primate Research Center, and Children's Healthcare of Atlanta have uncovered a critical detail explaining how HIV assembles its infectious yet stealthy clothing.

Antiretroviral therapy (ART) has proven lifesaving for people infected with HIV; however, the medications are a lifelong necessity for most HIV-infected individuals and present practical, logistical, economic and health-related challenges. A primary research goal is to find an HIV cure that either clears the virus from an infected person's body or enables HIV-infected individuals to suppress virus levels and replication to extremely low levels without the need for daily ART.

HIV-1 replication requires the coordinated movement of the virus's components toward the plasma membrane of an immune cell, where the virions are assembled and ultimately released. A study in The Journal of Cell Biology reveals how a Rab protein that controls intracellular trafficking supports HIV-1 assembly by promoting high levels of an important membrane lipid.


This photo shows HIV, the AIDS virus (yellow), infecting a human immune cell.
The AIDS virus can genetically evolve and independently replicate in patients' brains early in the illness process, researchers funded by the National Institutes of Health have discovered. An analysis of cerebral spinal fluid (CSF), a window into brain chemical activity, revealed that for a subset of patients HIV had started replicating within the brain within the first four months of infection. CSF in 30 percent of HIV-infected patients tracked showed at least transient signs of inflammation - suggesting an active infectious process - or viral replication within the first two years of infection. There was also evidence that the mutating virus can evolve a genome in the central nervous system that is distinct from that in the periphery.

Two of the four known groups of human AIDS viruses (HIV-1 groups O and P) have originated in western lowland gorillas, according to an international team of scientists from the Perelman School of Medicine at the University of Pennsylvania, the University of Montpellier, the University of Edinburgh, and others. The scientists, led by Martine Peeters from Montpellier, conducted a comprehensive survey of simian immunodeficiency virus (SIV) infection in African gorillas. Beatrice Hahn, MD, a professor of Medicine and Microbiology, and others from Penn were part of the team, whose findings appear online this week in the Proceedings of the National Academy of Sciences.

Engaging in unprotected sex with multiple partners increases the risk of contracting multiple strains of HIV, the virus that causes AIDS. Once inside a host, these strains can recombine into a new variant of the virus. One such recombinant variant observed in patients in Cuba appears to be much more aggressive than other known forms of HIV. Patients progress to AIDS within three years of infection - so rapidly that they may not even realise they were infected.

Researchers who conducted VOICE, a major HIV prevention trial involving more than 5,000 women in Africa, describe the study's primary results in this week's issue of the New England Journal of Medicine (NEJM), outlining in detail how the three products tested were safe but overall not effective in preventing HIV.

While antiretroviral therapies have significantly improved and extended the lives of many HIV patients, another insidious and little discussed threat looms for aging sufferers - HIV-associated neurocognitive disorders (HAND). The disorders, which strike more often in HIV patients over age 50, can result in cognitive impairment, mild to severe, making everyday tasks a challenge.

Although it is known that HIV can enter the brain early during infection, causing inflammation and memory/cognitive problems, exactly how this occurs has been largely unknown. A new research report appearing in the February 2015 issue of the Journal of Leukocyte Biology solves this mystery by showing that HIV relies on proteins expressed by a type of immune cell, called "mature monocytes," to enter the brain. These proteins are a likely drug target for preventing HIV from reaching brain cells. Although not a direct focus of this research, these proteins might also shed light on novel mechanisms for helping drugs penetrate the blood-brain barrier.


Fewer newly diagnosed adults seek HIV care, possibly because they do not yet feel sick.
Between December 2009 and February 2011, health workers with the AMPATH Consortium sought to test and counsel every adult resident in the Bunyala subcounty of Kenya for HIV. A study in the journal Lancet HIV reports that the campaign yielded more than 1,300 new positive diagnoses, but few of those new patients sought health care.

AIDS & HIVOctober 25, 2014 05:50 AM


This image shows, from the left: Katherine Jones, Salk professor, and first authors Yupeng Chen and Lirong Zhang.
Like a slumbering dragon, HIV can lay dormant in a person's cells for years, evading medical treatments only to wake up and strike at a later time, quickly replicating itself and destroying the immune system.

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.

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