2016-06-07T07:55:00+00:00An effective treatment that can prevent HIV infection and reduce the human and financial costs of the preventable condition is taking too long to be commissioned and made available on the NHS, warns Deborah Gold, chief executive of the National Aids Trust, in an article published by The BMJ today. Compelling evidence of the effectiveness of pre-exposure prophylaxis (PrEP) for HIV prevention has been known for over five years, but “we are still waiting for the NHS to embrace this potentially revolutionary intervention,” explains Gold. NHS England undertook a lengthy process to decide whether to commission the treatment, but after 18 months it announced that the specialised commissioning process was inappropriate for PrEP because it is a preventative intervention.
2016-05-12T07:31:03+00:00Detecting HIV earlier, through screening programs that can identify the virus shortly after infection, may lead to lower rates of HIV transmission in local epidemics, suggest findings from a new study published in Clinical Infectious Diseases and available online. After an acute infection screening program was implemented in San Diego, there were fewer new HIV diagnoses than would have been expected without such testing. To screen for HIV, the program used nucleic acid and serology testing, which can detect the virus during the acute or primary stage of infection, as soon as 7 to 10 days after exposure, compared to several weeks or months for other tests. An estimated 30 to 50 percent of new infections originate from recently infected individuals, who carry higher viral loads. High-risk sexual behavior is also common during this stage, as individuals are often unaware of their status. The researchers believed that screening for primary infections would reduce HIV transmission during early infection and lead to lower overall incidence of the virus. Their cohort study analyzed HIV testing data collected by the San Diego County Department of Public Health and the San Diego Primary Infection Cohort between 1996 and 2012, and used genetic analysis to identify local chains of transmission.
2016-05-08T00:42:37+00:00The development of antiretroviral therapy, a combination of drugs that slows the replication of HIV in the body, has transformed the treatment of this infection. What was once a certain death sentence is now a chronic condition that people can live with for decades. But this therapy has drawbacks. There are side effects, including kidney problems, decreased bone density, and gastrointestinal problems. And if a person discontinues his or her treatment, even missing a few doses, the level of the virus in the body is able to rebound quickly. Researchers from The Rockefeller University, along with collaborators from the University of Cologne, are developing a new kind of treatment, an antibody-based drug that may provide a better strategy for long-term control of HIV. Recent findings from a Phase 1 clinical trial, published on May 5 in Science, offer new insights about how the antibody functions.
2016-04-14T09:26:47+00:00Scientists at the University of North Carolina (UNC) School of Medicine and Sanford Burnham Prebys Medical Discovery Institute (SBP) have identified a human (host) protein that weakens the immune response to HIV and other viruses. The findings, published today in Cell Host & Microbe, have important implications for improving HIV antiviral therapies, creating effective viral vaccines, and advance a new approach to treat cancer. “Our study provides critical insight on a paramount issue in HIV research: Why is the body unable to mount an efficient immune response to HIV to prevent transmission?” said Sumit Chanda, Ph.D., professor and director of SBP’s Immunity and Pathogenesis Program and co-senior author of the study. “This research shows that the host protein NLRX1 is responsible - it’s required for HIV infection and works by repressing the innate immune response.” The innate immune response works by producing a cascade of signaling chemicals (interferons and cytokines) that trigger cytotoxic T cells to kill pathogens. Increasing evidence suggests that mounting an early, potent innate immune response is essential for the control of HIV infection, and may improve the effectiveness of vaccines.
2016-01-28T11:05:12+00:00In HIV-infected patients undergoing antiretroviral therapy (ART), ongoing HIV replication in lymphoid tissues such as the lymph nodes helps maintain stores, or reservoirs, of the virus, a new study funded by the National Institutes of Health suggests. A better understanding of how HIV persists in the body is essential for developing strategies to eliminate viral reservoirs - a prerequisite to achieving a cure for HIV infection. Current ART regimens quickly suppress HIV to levels undetectable in the blood in most patients, but cannot eliminate persistent viral reservoirs in the tissues. Scientists have debated whether these reservoirs are maintained because latently infected cells are long-lived, because low-level HIV replication persists or for both reasons. To help address this question, Northwestern University’s Steven Wolinsky, M.D., and colleagues sequenced viral DNA from lymph-node and blood cells collected from three HIV-infected patients before and during the first six months of ART. In these patients, the virus evolved over time, indicating ongoing replication, but did not accumulate mutations conferring drug resistance. Previous work had suggested that antiretroviral drug concentrations are lower in lymphoid tissue than in blood, and that HIV can hide in sanctuaries that drugs do not penetrate well. In this study, researchers demonstrated that continued HIV replication in lymphoid tissue sanctuaries refills viral reservoirs in patients on ART who have achieved undetectable blood levels of HIV.
2015-12-11T21:20:34+00:00In rural Malawi, roughly 10 percent of the adult population has HIV. At the peak of the epidemic, in the 1990s and early 2000s, nearly everyone knew someone infected with or affected by the virus, what demographer Hans-Peter Kohler of the University of Pennsylvania describes as a generalized epidemic. The problem snowballed to the extent that life expectancy dropped dramatically. In just a short period, the epidemic undid nearly two decades of life-expectancy improvements. “The probability of surviving from 15 to 50 declined substantially,” Kohler said.
2015-10-27T00:51:43+00:00A computer model developed by Johns Hopkins health care delivery specialists predicts that strengthening a handful of efforts to keep people with HIV in lifetime care, along with more rigorous testing, would potentially avert a projected 752,000 new HIV infections and 276,000 AIDS deaths in the United States alone over the next 20 years. In a report on their HIV epidemic-economic model, published online in October by the journal Clinical Infectious Diseases, the researchers say that efforts to encourage people with HIV to follow up regularly with their provider and maintain long-term drug therapy may be more fruitful in preventing HIV transmission than efforts to increase HIV testing alone. Encouraging patient engagement with care is known as retention in care. Combining increased retention among those diagnosed with increased HIV screening and rapid enrollment into care among high-risk groups would have even greater impact. Such comprehensive improvements would cost an estimated $96 billion, according to the model, but could reduce HIV incidence in the U.S. by 54 percent and the mortality rate by 64 percent, at a cost-effectiveness ratio of $45,300 per quality-adjusted life year, or QALY, a standard economic measure of the value of a medical intervention. Spending $50,000 or less per QALY is widely considered a good value, the Johns Hopkins team reports.
2015-10-09T18:12:55+00:00Scientists are now better able to predict how quickly the HIV virus will return after individuals stop treatment following a discovery by researchers at UNSW Australia and the University of Oxford. The significant development, resulting from a decade-long partnership between the two institutions and other international partners, opens up new avenues for understanding why the HIV virus persists in some patients and remains dormant and undetectable in others. The study is published today in the prestigious journal Nature Communications. While existing antiretroviral therapy (ART) stops the HIV virus from replicating, it does not completely remove the virus. Destroying the ‘hidden’ reservoirs of the virus remains one of the ‘holy grails’ of HIV research.
2015-09-25T02:52:31+00:00The next five years of HIV research should shift gears from the classic single-therapy development model to moving directly from in vitro studies to combination therapy trials, authors argue in a new paper published online today. The opinion piece - co-authored Dr. Francoise Barré-Sinoussi of the Institut Pasteur who, together with Dr. Luc Montagnier, was awarded the Nobel Prize for discovering HIV and by Dr. Jintanat Ananworanich with the US Military HIV Research Program (MHRP) - was published online in The Lancet HIV. “Our proposed data-driven approach to combination cure research is designed to accelerate efforts to transform HIV from an incurable disease to one where we can achieve durable remissions,” said Dr. Barré-Sinoussi.
2015-08-18T15:40:36+00:00There may be two new ways to fight AIDS - using a heat shock protein or a small molecule - to attack fibrils in semen associated with the human immunodeficiency virus (HIV) during the initial phases of infection, according to new research from the Perelman School of Medicine at the University of Pennsylvania. HIV is most commonly transmitted between individuals in semen, the male reproductive fluid, which contains deposits of protein fragments called amyloid fibrils. These fibrils can increase the transmission of HIV by helping the virus attach to the membrane surrounding human cells. The scientists surmise that therapies that reduce the levels of amyloid fibrils in semen might be able to reduce the transmission of HIV. Senior author James Shorter, PhD, an associate professor of Biochemistry and Biophysics, notes the first paper, published in Chemistry & Biology earlier this month, describes how the investigators repurposed a yeast heat shock protein called Hsp104 to attack amyloid fibrils. First, Hsp104 and an enhanced engineered variant directly remodeled fibrils into non-amyloid forms. They also made inactive Hsp104 scaffolds that reorganized fibrils into larger, innocuous assemblies. And finally, they modified Hsp104 to interact with a chambered enzyme to irreversibly degrade fibrils from semen. “Each strategy diminished the ability of amyloid to promote HIV infection, so this approach has potential as a therapeutic,” Shorter said. The work was a team effort driven by lead author Laura Castellano, PhD, who obtained her doctoral degree in the Shorter lab, and coauthor Drew Weissman, MD, PhD, a professor of Medicine in the division of Infectious Diseases.