HIV infection
Certain strains of bacteria that occur naturally in the human mouth can snare the HIV virus and even cells it has infected, according to researchers at the University of Illinois at Chicago College of Dentistry. In laboratory tests, the researchers found that the bacteria latched onto the sugar coating on the envelope that encases the virus particle and blocked infection. The bacteria also bound the sugar coating on immune cells, causing them to clump ? a feature that could render those harboring HIV incapable of infecting other cells.
Heterosexual intercourse during periods of acute HIV infection may account for a substantial amount of transmission of the virus, according to a new study. The study found that HIV levels in semen rise and fall with HIV levels in blood, indicating an increased risk of transmission during acute infection, when HIV levels in the blood are known to be higher than those in chronic infection. These finding suggest one important mechanism by which the HIV pandemic is sustained.
Scientists have identified a protein that blocks HIV replication in monkey cells. Humans have a similar protein, although it is not as effective at stopping HIV, say the researchers whose work is published in this week's issue of Nature. "Identification of this HIV-blocking factor opens new avenues for intervening in the early stage of HIV infection, before the virus can gain a toehold," says NIAID Director Anthony S. Fauci, M.D. "The discovery also gives us critical insights about viral uncoating, a little understood step in the viral lifecycle. Basic discoveries like this provide the scientific springboard to future improvements in therapies for HIV disease."
Like most persistent viruses, HIV uses a variety of strategies to counteract its host's response to infection. HIV infects the very cells that coordinate the immune response, which compromises the immune system and leaves the body susceptible to normally harmless microorganisms. It is these opportunistic infections, rather than the virus itself, that make HIV so deadly. Victor Appay and colleagues now show that an important effect of persistent HIV infection is generally elevated immune activation. Rather than being beneficial to the host, this causes non-specific premature maturation of many of the remaining functional T-cells. The resulting premature aging and exhaustion of the immune system increase the likelihood of opportunistic infection.
In the Jan. 16 issue of the journal Science, several national AIDS experts criticize a U.S. government-sponsored clinical research trial of an AIDS vaccine in Thailand. The 22 researchers, including Michael Lederman, M.D., professor of medicine at the Case Western Reserve University School of Medicine and director of the AIDS Clinical Trials Unit at University Hospitals of Cleveland, say that there is no "persuasive data" to suggest that the experimental vaccine, a combination of ALVAC +gp120, would help to protect against HIV infection. The research trial involves16,000 volunteers in Thailand.
The major component of green tea prevents the binding of HIV to human T cells, the first step in HIV infection, according to a new study. Green tea is the nonoxidized, unfermented product of the leaves from the evergreen plant, Camellia sinensis. It is made up of catechins, the most abundant of which is Epigallocatechin Gallate (EGCG). It is believed that EGCG is responsible for the vast array of presumed health benefits green tea possesses, such as the prevention of cancer and cardiovascular disease. Several studies have reported that EGCG may also have a protective effect against HIV infection.
Researchers have proposed for the first time that HIV and other retroviruses can use a Trojan horse style of infection, taking advantage of a cloak of human proteins to sneak into cells. The hypothesis explains 20 years of perplexing observations and suggests new ways to reduce HIV transmission and treat HIV infection, but it also implies that existing approaches to developing vaccines against HIV won't work. A description of the hypothesis and its supporting evidence appear in the Proceedings of the National Academy of Sciences, scheduled for publication online this week.
HIV-positive adults ages 18 to 34 may be more likely to suffer coronary heart disease than HIV-negative persons their age, a new study suggests. The findings emphasize the need for physicians to monitor HIV patients' cardiac health. "Our study suggests that coronary heart disease may be accelerated in younger HIV-infected people," said Dr. Judith Currier, a researcher at the UCLA AIDS Institute and associate professor of infectious diseases at the David Geffen School of Medicine at UCLA. "It's important for physicians to incorporate heart-disease risk prevention into HIV primary care."
A controversial vaccine against HIV, the virus that causes AIDS, has been shown to stimulate a critical part of the HIV-specific immune response in chronically infected patients. The small study conducted by researchers at Massachusetts General Hospital (MGH) finds that a vaccine made from an inactivated form of the AIDS virus (Remune) induces the proliferation of CD4 cells ? also called T helper cells ? that specifically target HIV. Appearing in the June issue of the journal AIDS, the study is the first clear demonstration of the potential reconstitution of the immune response in chronic HIV infection. However, this pilot study was not designed to tell whether or not the vaccine would have any effect on the eventual course of the disease.
Mayo Clinic researchers have identified a naturally occurring "good guy" for patients infected with HIV. It is a helpful gene mutation that impairs the HIV virus' cell-killing machinery, thus preserving immune system function. Moreover, Mayo's experiments in mice suggest that the presence or absence of this mutation in the gene known as Vpr may play a central role in determining which HIV-infected patients develop full-blown, fatal AIDS.
In a new study in mice, a modified form of an innocuous chimpanzee virus has shown marked potency as a protective vaccine against HIV, itself believed to have crossed into the human population from chimpanzees sometime in the 1930s. The study, led by researchers at The Wistar Institute, appears in the February issue of the Journal of Immunology. "Our results show this new vaccine is capable of inducing the kind of powerful immune response that we and others believe will be critical for controlling HIV infection," says Hildegund C.J. Ertl, M.D., professor and immunology program leader at The Wistar Institute, and senior author on the new study.
In a new study in mice, a modified form of an innocuous chimpanzee virus has shown marked potency as a protective vaccine against HIV, itself believed to have crossed into the human population from chimpanzees sometime in the 1930s. The study, led by researchers at The Wistar Institute, appears in the February issue of the Journal of Immunology. "Our results show this new vaccine is capable of inducing the kind of powerful immune response that we and others believe will be critical for controlling HIV infection," says Hildegund C.J. Ertl, M.D., professor and immunology program leader at The Wistar Institute, and senior author on the new study.
No cases of HIV transmission through unprotected receptive oral sex were found by researchers at UCSF's Center for AIDS Prevention Studies in a new study. The study looked at men who have sex with men and who exclusively practice oral sex as the receptive partner. "HIV infection through receptive oral sex is a very rare event?statistically our study showed a probability of zero?and is rarer than HIV infection through receptive anal intercourse using a condom," said the study's lead author Kimberly Page Shafer, PhD, MPH, assistant professor of medicine at UCSF's CAPS. The findings are being published in the November 22, 2002 issue of AIDS.
