Mammalian fatty acid synthase is one of the most complex molecular synthetic machines in human cells. It is also a promising target for the development of anti-cancer and anti-obesity drugs and the treatment of metabolic disorders. Now researchers at ETH Zurich have determined the atomic structure of a mammalian fatty acid synthase. Their results have just been published in Science magazine.

Researchers have discovered a new 'trick' that allows HIV to overtake resting T cells that are normally highly resistant to HIV infection, according to a report in the September 5th issue of the journal Cell, a Cell Press publication. The binding of the virus to the surface of those cells sends a signal that breaks down the cells' internal skeleton, a structure that otherwise may present a significant barrier to infection.

As antiviral treatment for HIV infection allows patients to live longer, many will be confronted with additional health challenges. A new study shows for the first time that one of these may be significantly increased risk of bone fractures. The report in the September Journal of Clinical Endocrinology and Metabolism finds that fracture prevalence was increased more than 60 percent in those infected with HIV compared to patients without HIV infection.

India is home to the third-largest number of human immunodeficiency virus (HIV) cases in the world and, as in the U.S. and many African nations, the rate of infection among women continues to rise faster than that among men. In a new study, researchers at the Harvard School of Public Health (HSPH) have found that married Indian women who experienced physical and sexual abuse at the hands of their husbands were approximately four times more likely to become infected with HIV than married women who were not abused. This first large-scale, national study to examine the relationship between intimate partner violence (IPV) against wives and clinically verified HIV infection appears in the August 13, 2008 issue of JAMA.

Patients receiving rifampicin-based anti-tuberculosis therapy are more likely to experience virological failure when starting nevirapine-based antiretroviral therapy, an HIV treatment that is widely used in developing countries because of lower cost, than when starting efavirenz-based antiretroviral therapy, according to a study in the August 6 issue of JAMA, a theme issue on HIV/AIDS.

The life expectancy for patients with human immunodeficiency virus (HIV) has increased by more than 13 years since the late 1990s thanks to advancements in antiretroviral therapy, according to researchers at the University of Alabama at Birmingham (UAB) and Simon Fraser University in Vancouver, British Columbia.

Researchers at Wake Forest University Baptist Medical Center have disproved a long-standing clinical belief that the hepatitis C virus slows or stunts the immune system's ability to restore itself after HIV patients are treated with a combination of drugs known as the "cocktail."

Persons infected with schistosomes, and possibly other parasitic worm infections, may be more likely to become infected with HIV than persons without worm infections, according to a study published July 23rd in the open-access journal PLoS Neglected Tropical Diseases. Researchers at the U.S. Centers for Disease Control and Prevention (Atlanta, United States) and the Dana-Farber Cancer Institute and Harvard Medical School (Boston, United States) found that the infectious dose of an HIV-like virus necessary to infect rhesus macaques was 17-fold lower in animals with acute schistosomiasis than in controls.

The National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health (NIH), is reshaping its research enterprise to broaden HIV vaccine discovery activities. Many of the initiatives have evolved from ideas and opinions recently expressed by scientists either at NIAID's HIV Vaccine Summit on March 25 or in response to two Requests for Information that NIAID issued in April.

CD4+ T lymphocytes, or simply CD4 T cells, are the "brains" of the immune system, coordinating its activity when the body comes under attack. They are also the cells that are attacked by HIV, the devastating virus that causes AIDS and has infected roughly 40 million people worldwide. The virus slowly eats away at CD4 T cells, weakening the immune system.

When individuals infected with HIV become infected with a second strain of the virus, the two viral strains can exchange genetic information, creating a third, recombinant strain of the virus. It is known that the presence of multiple viral strains, called superinfection, frequently leads to a loss of immune control of viral levels. Now a study from the Partners AIDS Research Center at Massachusetts General Hospital (PARC/MGH) shows that how and where viral strains swap DNA may be determined by the immune response against the original infecting strain. Their report will appear in the Journal of Experimental Medicine and has been released online.

New research into the earliest events occurring immediately upon infection with HIV-I shows that the virus deals a stunning blow to the immune system earlier than was previously understood. According to scientists at Duke University Medical Center, this suggests the window of opportunity for successful intervention may be only a matter of days – not weeks – after transmission, as researchers had previously believed.

After soliciting and considering broad input from the scientific and HIV advocacy communities, the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health (NIH), has determined that it will not conduct the HIV vaccine study known as PAVE 100. However, NIAID believes the vaccine developed by its Vaccine Research Center (VRC) is scientifically intriguing and sufficiently different from previously tested HIV vaccines to consider testing it in a smaller, more focused clinical study. Therefore, NIAID will entertain a proposal for an alternative study with one specific goal: to determine if the vaccine regimen significantly lowers viral load—the amount of HIV in the blood of vaccinated individuals who may later become infected with HIV.

Recent studies have shown that HIV causes a vigorous and prolonged immune response that eventually leads to the exhaustion of key immune system cells--CD4+ and CD8+ T-cells--that target HIV. These tired cells become less and less able to fight the virus, and the cells' fatigue contributes to the inability of an HIV-infected person's immune system to clear the virus from the body.

In battle with an epidemic that has outpaced nearly all efforts to contain it, researchers are turning to strategies centered on the same antiretroviral (ARV) drugs that have been used successfully to treat HIV in hopes they will be as effective a stronghold for preventing the virus. For women, who make up nearly half of the 33 million people living with HIV/AIDS worldwide, the ARV tenofovir has particular promise because it can be formulated as either an oral tablet or a vaginal gel to be used daily. But ARV-based prevention approaches are not without scientific and practical challenges. The Microbicide Trials Network (MTN) is taking aim at among the most pressing of these challenges in the first clinical trial to directly compare the tablet and vaginal gel formulations of tenofovir.

Weak HIV viruses piggyback onto stronger ones, raising the possibility that the human body may harbor many more HIV viruses capable of replicating and contributing to the development of AIDS than previously thought, a New York University College of Dentistry AIDS research team has found.

Acquired Immune Deficiency Syndrome (AIDS) is a global epidemic threatening the lives of millions of people. Because there is no known cure, prevention of the transmission of the virus that causes AIDS, the Human Immunodeficiency Virus (HIV), is critical for controlling the disease. The transmitting routes of HIV include breastfeeding, which passes the virus from mothers to infants. This is a major problem in many areas of Africa, where HIV-positive mothers have no alternative to breastfeeding. So far, no practical and effective methods are available to prevent HIV transmission by this route.

The widespread use of highly active antiretroviral therapy may reduce the incidence of HIV in individuals and populations but has been overlooked by public health as a prevention strategy, write Dr. Julio Montaner and colleagues in CMAJ.

Clinical trials hoping to identify a vaginal microbicide that is both safe and effective against HIV have all but skirted questions befitting the evaluation of an approach intended primarily for sexually active women of childbearing age: What if a woman becomes pregnant while using a product? Can exposure to a product, especially early in pregnancy, pose a risk to the developing fetus? Does pregnancy affect how a particular microbicide is supposed to work?

By identifying a protein that restricts the release of HIV-1 virus from human cells, scientists believe they may be closer to identifying new approaches to treatment. The research is published in the advance online edition of Nature Medicine.

A mapmaker and a mathematician may seem like an unlikely duo, but together they worked out a way to measure longitude – and kept millions of sailors from getting lost at sea. Now, another unlikely duo, a virologist and a biophysicist at Rockefeller University, is making history of their own. By using a specialized microscope that only illuminates the cell’s surface, they have become the first to see, in real time and in plain view, hundreds of thousands of molecules coming together in a living cell to form a single particle of the virus that has, in less than 25 years, claimed more than 25 million lives: HIV.

Researchers at North Carolina State University have discovered that adding tiny bits of gold to a failed HIV drug rekindle the drug’s ability to stop the virus from invading the body’s immune system.

Today, Advanced BioScience Laboratories, Inc. (ABL) and the University of Massachusetts Medical School (UMMS) report that their unique HIV vaccine formulation was effective in eliciting strong and balanced immune responses in healthy human volunteers. The findings are published in the journal Vaccine (“Cross-subtype antibody and cellular immune responses induced by a polyvalent DNA prime–protein boost HIV-1 vaccine in healthy human volunteers,” Vaccine online, May 22, 2008) In light of these initial findings, additional assays on volunteers’ samples were done by researchers at the University of Alabama at Birmingham, independently confirming the presence of long lasting and high quality T cell responses against HIV antigens. Results from this confirmatory study are currently available online in the Journal of Virology (April 30, 2008).

A new study reveals the genetic identity of human immunodeficiency virus (HIV), the version responsible for sexual transmission, in unprecedented detail.

On the 25th anniversary of the first scientific article linking a retrovirus to AIDS, Anthony S. Fauci, M.D., director of the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health, reflects in an essay in Nature on his experience treating and studying HIV/AIDS for the past quarter century. Outlining the peaks and valleys of the scientific community’s journey so far, Dr. Fauci writes, “…we must learn from our mis-steps, build on our successes in treatment and prevention, and renew our commitment to developing the truly transforming tools that will one day put this scourge behind us.”

Researchers have developed what they believe is the first new mechanism in nearly 20 years for inhibiting a common target used to treat all HIV patients, which could eventually lead to a new class of AIDS drugs.

Using ingenious molecular espionage, scientists have found how a single key enzyme, seemingly the Swiss army knife in HIV's toolbox, differentiates and dynamically binds both DNA and RNA as part of the virus' fierce attack on host cells. The work is described this week in the journal Nature.

As HIV disease progresses in a person infected with the HIV virus, a group of cells in the immune system, the CD8+ T lymphocytes, become “exhausted,” losing many of their abilities to kill other cells infected by the virus. For many years scientists have debated whether this exhaustion of CD8+ T cells is the cause, or the consequence, of persistence of the HIV virus. In a study published this week in PLoS Medicine, Marcus Altfeld and colleagues studied the immune response over time amongst 18 individuals who had very recently become infected with HIV.

Social factors, including economic pressures caused by climate change, could lead to an increase in HIV infection rates world-wide, warns a leading researcher from the University of New South Wales (UNSW).

A research group supported by the National Institutes of Health (NIH) has uncovered a new route for attacking the human immunodeficiency virus (HIV) that may offer a way to circumvent problems with drug resistance. In findings published today in the online edition of the Proceedings of the National Academy of Sciences, the researchers report that they have blocked HIV infection in the test tube by inactivating a human protein expressed in key immune cells.