Today, during the 39th Annual Meeting of the American Association for Dental Research, convening at the Walter E. Washington Convention Center in Washington, DC, lead researcher O.A. Gonzalez (University of Kentucky, Lexington) will present a poster of a study titled "TLR2 and TLR9 Activation by Periodontal Pathogens induce HIV-1 Reactivation." Although oral co-infections (e.g. periodontal disease) are highly prevalent in HIV-1 patients and appear to positively correlate with viral load levels, the potential for oral bacteria to induce HIV-1 reactivation in latently infected cells has received little attention. The researchers involved in this study have proved that periodontal pathogens enhanced HIV-1 promoter activation in T-cells, monocytes/macrophages and dendritic cells; however the mechanisms involved in this response remain undetermined.

Elsevier, the world-leading publisher of scientific, technical and medical information products and services, released a special issue of the journal Antiviral Research (www.sciencedirect.com/science/journal/01663542), marking the 25th anniversary of antiretroviral drug development. The guest editors, José Esté from Hospital Germans Trias i Pujol, Barcelona, Spain and Tomas Cihlar, from Gilead sciences Inc., CA, USA were able to attract the key players in the field who all contributed a variety of review articles to this special issue, thereby creating a must-read for anybody interested in AIDS treatment.

UCLA AIDS Institute researchers successfully removed CCR5 — a cell receptor to which HIV-1 binds for infection but which the human body does not need — from human cells. Individuals who naturally lack the CCR5 receptor have been found to be essentially resistant to HIV.

A new international study reported in PLoS Medicine confirms that a single dose of nevirapine (sdNVP) can lead to HIV treatment failure in women who receive the drug to prevent transmission of the AIDS virus to their infants. However, the increased risk of failure could only be detected in women who began full HIV treatment within about a year after receiving sdNVP.

Researchers have made a breakthrough in HIV research that had eluded scientists for over 20 years, potentially leading to better treatments for HIV, in a study published today in the journal Nature.

Research from a five-year international clinical study shows that acyclovir, a commonly prescribed drug used to suppress symptoms of the herpes virus, does not affect HIV transmission by people with both viruses.

Circumcision, which substantially lowers HIV risk in men, also dramatically changes the bacterial communities of the penis, according to a study led by scientists at the Translational Genomics Research Institute (TGen) and Johns Hopkins University and published Jan. 6 in the scientific journal PLoS ONE.

Scientists at the Gladstone Institute of Virology and Immunology (GIVI) have discovered a new agent that might inhibit the infectivity of HIV. The agent, surfen, impairs the action of a factor in semen that greatly enhances the viral infection. Surfen might be used to supplement current HIV microbicides to greatly reduce HIV transmission during sexual contact.

Scientists seeking to understand how to make an AIDS vaccine have found the cause of a major roadblock. It turns out that the immune system can indeed produce cells with the potential to manufacture powerful HIV-blocking antibodies – but at the same time, the immune system works equally hard to make sure these cells are eliminated before they have a chance to mature.

Free infectious HIV-1 is widely thought to be the major form of the virus in the blood of infected persons. U.S. Military HIV Research Program (MHRP) researchers, however, have demonstrated that essentially all of the infectious virus particles can bind to the surface of red blood cells isolated from each of 30 normal (non-infected) human donors. The results were published today in PLoS ONE, and can be accessed here.

Publishing in PLoS Pathogens, researchers at from the Kimmel Cancer Center at Jefferson have found a novel mechanism by which drugs block HIV-1 from entering host cells.

The AIDS virus inserts its genetic material into the genome of the infected cell. Scientists of the German Cancer Research Center have now shown for the first time that the virus almost entirely spares particular sites in the human genetic material in this process. This finding may be useful for developing new, specific AIDS drugs.

Structural biologists at the University of Pittsburgh School of Medicine have described the architecture of the complex of protein units that make up the coat surrounding the HIV genome and identified in it a "seam" of functional importance that previously went unrecognized. Those findings, reported today in Cell, could point the way to new treatments for blocking HIV infection.

A very close and detailed study of how the most robust antibodies work to block the HIV virus as it seeks entry into healthy cells has revealed a new direction for researchers hoping to design an effective vaccine.

Researchers at Yale University have developed synthetic molecules capable of enhancing the body's immune response to HIV and HIV-infected cells, as well as to prostate cancer cells. Their findings, published online in the Journal of the American Chemical Society, could lead to novel therapeutic approaches for these diseases.

Sperm, and not just the fluid it bathes in, can transmit HIV to macrophages, T cells, and dendritic cells (DCs), report a team led by Ana Ceballos at the University of Buenos Aires in Argentina. By infecting DCs, which carry the virus and potently pass it to T cells, sperm may play a leading role in spreading HIV. The article appears in the November 23, 2009 issue of the Journal of Experimental Medicine (online October 26).

Highly active antiretroviral therapy has increased the longevity and quality of life for people living with human immunodeficiency virus. But it requires strict adherence in taking the medicine, something that is extremely difficult for many individuals to do.

An international research team has demonstrated that treating HIV-AIDS with interleukin-2 (IL-2) is ineffective. As a result, the researchers recommend that clinical trials on this compound be stopped. Their finding was published in the New England Journal of Medicine in an article co-authored by 14 researchers, including Dr. Jean-Pierre Routy of the Research Institute of the McGill University Health Centre (RI-MUHC).

Scientists working to develop a vaccine for the human immunodeficiency virus (HIV) report they have created the first antigen that induces protective antibodies capable of blocking infection of human cells by genetically-diverse strains of HIV. The new antigen differs from previously-tested vaccines by virtue of its chemically-activated property that enables close sharing of electrons and produces strong covalent bonding. Researchers used a mouse model to generate the antibodies. The report by researchers at The University of Texas Health Science Center at Houston is online and will appear in a print issue of the Journal of Biological Chemistry in November.

Researchers at and associated with the International AIDS Vaccine Initiative (IAVI), at The Scripps Research Institute, and at the biotechnology companies Theraclone Sciences and Monogram Biosciences have discovered two powerful new antibodies to HIV that reveal what may be an Achilles heel on the virus. They published their work in Science this week.

For the first time, researchers have experimentally induced antibodies that neutralize HIV-1 and simultaneously recognize both HIV-1 envelope protein and lipids. The results were reported by U.S. Military HIV Research Program (MHRP) researchers on Aug. 25 in the online version of AIDS, the official journal of the International AIDS Society.

With the help of the human immunodeficiency virus (HIV) and molecular engineering, researchers have designed synthetic protein-like mimics convincing enough to interrupt unwanted biological conversations between cells.

The structure of an entire HIV genome has been decoded for the first time by researchers at the University of North Carolina at Chapel Hill. The results have widespread implications for understanding the strategies that viruses, like the one that causes AIDS, use to infect humans.

Not satisfied with simply thwarting its host's defensive maneuvers, HIV actually twists one to its advantage, based on new findings from Kyei et al. in the July 27, 2009 issue of the Journal of Cell Biology (www.jcb.org). Vojo Deretic and colleagues suggest that autophagy—a stress response process—helps HIV to proliferate and that conversely, blocking autophagy lessens HIV production.

Researchers in Israel and Kenya have shown that the contribution of variable degrees of immune suppression, either due to existing chronic infections such as parasitemias and/or nutrition, in different populations may influence and prolong the serological-diagnostic window period of HIV. However, the immunosuppression can be overcome, by in-vitro enhancement of antibody production (termed- Stimmunology). The results, which appear in the August 2009 issue of Experimental Biology and Medicine, show that pre-treating the whole blood sample in the SMARTube™ containing immune potentiating agents promoted the synthesis and release of antibodies against HIV-1 prior to their detection in corresponding plasma samples in a group of donors who would otherwise be classified as HIV-1 seronegative blood donors. The identification of techniques that can lead to detection of HIV infection during this window period is of obvious public health importance especially in resource poor settings highlighting the importance of these findings. Overcoming the suppression, in-vitro, led to the production of detectable levels of anti-HIV antibodies in the whole blood sample and to the detection of potentially infectious blood units which were missed by regular HIV serology. Interestingly, the ratio of missed infections among the total HIV infected blood donors was higher among the younger (high-school) donors versus adult donors.

One of the continuing mysteries of the HIV/AIDS epidemic is why women usually develop lower viral levels than men following acute HIV-1 infection but progress faster to AIDS than men with similar viral loads. Now a research team based at the Ragon Institute of Massachusetts General Hospital (MGH), MIT and Harvard has found that a receptor molecule involved in the first-line recognition of HIV-1 responds to the virus differently in women, leading to subsequent differences in chronic T cell activation, a known predictor of disease progression. Their paper, which will be published in an upcoming issue of Nature Medicine, is receiving early online release.

Scientists at Albert Einstein College of Medicine of Yeshiva University have devised a laboratory test for predicting whether microbicides against HIV are safe for human use. The researchers have also discovered why several supposedly "safe" microbicides made women more susceptible to HIV infection. The study appears today in the online version of the Journal of Infectious Disease.

A discovery by a team of Canadian and American researchers could provide new ways to fight HIV-AIDS. According to a new study published in Nature Medicine, HIV-AIDS could be treated through a combination of targeted chemotherapy and current Highly Active Retroviral (HAART) treatments. This radical new therapy would make it possible to destroy both the viruses circulating in the body as well as those playing hide-and-seek in immune system cells.

New research by scientists at The Scripps Research Institute and other institutions provides a close-up look at the cone-shaped shell that is the hallmark of human immunodeficiency virus (HIV), revealing how it is held together—and possible ways to break it apart.

Researchers at McGill University and the affiliated Lady Davis Institute for Medical Research at Montreal's Jewish General Hospital – along with colleagues at the University of Manitoba and the University of British Columbia – may have found a chink in the armour of the human immunodeficiency virus type 1 (HIV-1), the microorganism which causes AIDS. They have pinpointed the key cellular machinery co-opted by HIV-1 to hijack the human cell for its own benefit. Their study was published in May in the Journal of Biological Chemistry.