PLoS Pathogens paper postulates that antiHERV T cells may work better than antiHIV ones in controlling the virus.
Researchers identified a potential new way of fighting HIV infection that relies on the remnants of ancient viruses, human endogenous retroviruses (HERV).
Mounting evidence suggests that HIV infection could enable HERV expression by disrupting the normal controls that keep HERV in check. In some HIV-infected individuals this induces infection fighting T cells to target HERV expressing cells.
The scientists looked at 29 individuals recently infected with HIV from the University of California San Francisco OPTIONS Project and 13 HIV-negative individuals and 3 hepatitis C infected, HIV-negative individuals from Toronto. In the group recently infected with HIV, researchers found a relationship between increased T-cell response to HERV and decreased levels of HIV virus present in patients blood.
The investigators also compared the T cells that recognize HERV to other types of T cells including those that recognize HIV. They found that T cells recognizing HERV were different from T cells that recognize HIV.
“HERV-specific CD8+ T cells have characteristics consistent with an important role in the response to HIV-1 infection: a phenotype similar to that of T cells responding to an effectively controlled virus (cytomegalovirus), an inverse correlation with HIV-1 plasma viral load, and the ability to lyse cells presenting their target peptide,” wrote the team.
“These characteristics suggest that elicitation of antiHERV-specific immune responses is a novel approach to immunotherapeutic vaccination. As endogenous retroviral sequences are fixed in the human genome, they provide a stable target, and HERV-specific T cells could recognize a cell infected by any HIV-1 viral variant,” the researchers concluded in their paper published in the November 9 issue of PLoS Pathogens. The work was performed by scientists at the University of Toronto and UCSF.