Currently, HIV-infected individuals can live a near normal life span if, every day, they take a complex combination of drugs called antiretroviral therapy (ART). The bad news is if they stop ART, the small amounts of HIV that still lurk in their bodies can bounce back and infect key immune cells, called CD4 T cells, resulting in life-threatening suppression of their immune systems.
Now, a study of rhesus macaques infected with a close relative of HIV, the simian immunodeficiency virus (SIV), suggests there might be a new therapeutic option that works by a mechanism that has researchers both excited and baffled . By teaming ART with a designer antibody used to treat people with severe bowel disease, NIH-funded researchers report that they have been able to keep SIV in check in macaques for at least two years after ART is stopped. More research is needed to figure out exactly how the new strategy works, and whether it would also work for humans infected with HIV. However, the findings suggest there may be a way to achieve lasting remission from HIV without the risks, costs, and inconvenience associated with a daily regimen of drugs.
Left untreated, both SIV and HIV attack and destroy CD4 T cells. Previous studies have shown that these viruses preferentially target CD4 T cells expressing high levels of a particular integrin receptor, called α4β7, on their surfaces. The receptor has also been thought to act as a kind of “zipcode” that routes CD4 T cells to the gastrointestinal tract, where they serve as a reservoir for HIV replication.
In a study published in the journal Science, researchers at Emory University School of Medicine, Atlanta, and NIH’s National Institute for Allergy and Infectious Diseases set out to explore whether response to ART might be improved by interfering with CD4 T cells that express the key integrin receptor.