CTLs play a major role fighting HIV in the body by recognizing and killing CD4 cells that are infected with the virus. When HIV infects CD4 cells, small pieces of viral proteins are displayed on the surface of the cell, allowing CTLs to identify and destroy them. Unfortunately, most people living with HIV do not develop a CTL response that is sufficiently potent to control HIV replication. There are, however, a small group of people living with HIV, known as “elite controllers,” who are able to maintain undetectable viral loads without the help of antiretroviral drugs—sometimes indefinitely.

Harris Goldstein, MD, and his colleagues at Yeshiva University theorized that the CTLs of elite controllers may have special properties that make them particularly good at killing infected CD4 cells. They found that these “super CTLs,” as Dr. Goldstein describes them, had receptors that were able to bind very tightly to infected cells and to recognize the viral proteins on the cell surface.

Dr. Goldstein’s team next isolated some of the genes responsible for these hyper-efficient receptors found on the CTLs from elite HIV controllers. The group then bound the genes to a lentivirus, so that they could be effectively delivered into the nuclei of CTLs that do not naturally carry the genes. Once the CTLs began expressing the more efficient receptors, Dr. Goldstein’s team infused them into mice, along with HIV-infected human cells.

After one week, the researchers report, the infected cells had been almost completely destroyed.

Dr. Goldstein intends to locate other genes responsible for boosting the HIV-fighting effectiveness of super CTLs. This may involve reprogramming CTLs using multiple genes, just as HIV-positive people are currently treated with multiple antiretrovirals at one time.