The prescription drug, an enzyme named adenosine deaminase or ADA helps the immune system remember the human immunodeficiency virus (HIV) to prevent or eliminate infection, enabling the immune system to handle HIV on its own without medical interventions. The study was published in the Journal of Leukocyte Biology for its February 2016 issue.

“We hope this study puts ADA in the spotlight as a powerful immune modulator in vaccine strategies enhancing anti-HIV immune responses and limiting the need for life-lasting treatments,”said Núria Climent, one of the study’s researchers from the Retrovirology and Viral Immunopathology Laboratory at AIDS Research Group from Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) in Barcelona, Spain. Eytan Eytan

The new study entailed analysing the effects ADA has on cells in patients with HIV infection and those without. The researchers measured the rate of the lymphocyte propagation, cytokine secretion and the regulatory T cell generation of the dendritic cells, which were taken from blood cells and exposed to HIV-1 proteins as well as inactivated HIV-1 virus, with or without ADA.

The research team discovered that ADA improves anti-HIV-1 specific immune responses by decreasing the action of cells that prevent HIV-specific defences. An increase in CD4+ responder T cells, in CD8+ T cell proliferation and in T cell memory generation were observed. Aside from this increase, the secretion of Th1 cytokines were also boosted.

The number of CD4+ cells decreases as HIV infection progresses. The normal range is about 600-1,500, but this drops below 200 if the patient has acquired immune deficiency syndrome (AIDS).  CD8+ T cells controls HIV replication but majority of the cells generated die within a few weeks during HIV infection.

“We need to find new strategies that will empower the immune system towards long-term control of HIV infection,” Journal of Leukocyte Biology’s editor-in chief, Luis Montaner, said. “The availability of an approved drug that already targets the mechanisms described here ensures the quick translation of this work from the bench to the clinical.”