The Gladstone Institutes, a leading biomedical-research organization, today announced its participation in a bold new consortium intended to help the global community better identify, prevent and treat outbreaks of new or re-emerging viruses.
For the AIDS community, Thanksgiving came a bit early this year, and after many difficult years, three announcements give hope and reason for celebration during this year's World AIDS Day. First, the UNAIDS reported that the pandemic might have crested, and second, two studies from the Gladstone Institutes showed the first evidence that HIV infection can be prevented by drugs and solved a long-standing mystery about how HIV destroys the immune system.
Scientists at Gladstone Institute of Virology and Immunology have solved a long-standing mystery about HIV infection—namely how HIV promotes the death of CD4 T cells. It is the loss of this critical subset of immune cells that leads to the development of AIDS. Most immune cells that die during HIV infection are seemingly not infected, a phenomenon formerly described as “bystander cell killing.” Now the Gladstone scientists report that these “bystander” cells are actually the victims of a failed or abortive form of viral infection. Their findings are published in today's issue of the journal Cell.
In a finding with the potential to fundamentally change strategies to slow the global HIV epidemic, a new study called iPrEx shows that individuals at high risk for HIV infection who took a single daily tablet containing two widely used HIV medications, emtricitabine and tenofovir (FTC/TDF), experienced an average of 43.8% fewer HIV infections than those who received a placebo pill (95% CI 15.4 to 62.6%; P=0.005). The study, reported in the New England Journal of Medicine, is the first evidence that this new HIV prevention method, called pre-exposure prophylaxis or PrEP, reduces HIV infection risk in people.
Scientists at the Gladstone Institute of Virology and Immunology (GIVI) have found that an enzyme associated with the storage of fat in the liver is required for the infectious activity of the hepatitis C virus (HCV). This discovery may offer a new strategy for treating the infection.
With obesity and obesity-related diseases epidemic in the developed world, a clear understanding of how metabolism is regulated is crucial. One of the key metabolic pathways involves the oxidation of fat. In the current edition of the journal Nature, scientists at the Gladstone Institute of Virology and Immunology report on a new mechanism that governs this pathway and in the process identified a novel potential therapeutic target for controlling fat metabolism. The target is a protein from the mitochondria, or the “power plants” of every cell that are responsible for processing oxygen and converting substances from the foods we eat into energy for essential cell functions.
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 at the Gladstone Institute of Virology and Immunology (GIVI) have found another clue that may lead to eradication of HIV from infected patients who have been on antiretroviral therapy. A real cure for HIV has been elusive because the virus can “hide” in a latent form in resting CD4-T cells. By understanding this “latency” effect, researchers can identify ways to reactivate the virus and enable complete clearance by current or future therapies.