The weak point of HIV

Modern antiretroviral therapy has significantly increased the survival rate of patients infected with HIV. Despite impressive progress, it is still impossible to achieve complete destruction of the virus. Patients are forced to take antiviral drugs for life. It is believed that this is due to the ability of HIV to create reservoirs inside infected cells that can survive almost indefinitely.

If we find out how the virus creates such a reservoir, and what are the survival programs that are activated in infected cells, it will be possible to identify a potential target for effective antiviral therapy.

Researchers from Brigham and Women's Hospital and the Massachusetts Institute of Technology have found out how HIV reservoir cells activate factors that prevent programmed death (apoptosis) and ensure its long life. These results demonstrate clinical strategies that will help destroy viral reservoirs.

Using the methods of proteomics, the authors studied in detail the proteins, the number of which was increased in HIV-infected cells. They found that two of them (BIRC5 and OX40) are involved in the long-term survival of these cells.

Drawing from an article in Immunity

Protein BIRC5, also known as survivin (from the English survive – to survive), belongs to a family of proteins that regulate the natural death of cells. Normally, it is synthesized in stem cells during embryonic development and is absent in adult cells. One exception is cancer: cancer cells often restore the expression of BIRC5, and its presence is associated with resistance to chemotherapy. This study shows that BIRC5 also helps HIV-infected cells to avoid apoptosis and causes the preservation of viral reservoirs for decades, despite effective antiretroviral therapy.

In recent years, clinicians have reported HIV-infected patients who have received aggressive chemotherapy. Against this background, the viral load decreased to an undetectable level, but after a while HIV returned.

The current study points to a promising new approach to HIV therapy: inhibiting the BIRC5-OX40 pathway can reduce the number of reservoir cells or completely destroy them.

Article by J. H. Kuoetal. Anti-apoptoticProtein BIRC5 MaintainsSurvivalof HIV-1-Infected CD4+ T Cells is published in the journal Immunity.

Aminatadzhieva, portal "Eternal youth" http://vechnayamolodost.ru based on the materials of EurekAlert: unlockingthesecretsofhiv'spersistance.