Peter W. Hunt1,2, Hiroyu Hatano1,2, Elizabeth Sinclair1,2, Tzong-Hae Lee3, Michael P. Busch1,2,3, Jeffrey N. Martin1,2, Joseph M. McCune1,2, and Steven G. Deeks1,2:
Peter W. Hunt, MD, UCSF Positive Health Program, SFGH Bldg 80, Ward 84, 995 Potrero Ave, San Francisco, CA 94110 (email@example.com).
Background. Human immunodeficiency virus (HIV)–-infected individuals maintaining plasma HIV RNA levels <75 copies/mL in the absence of therapy (“HIV controllers”) often maintain high HIV-specific T cell responses, which likely contribute to the control of viral replication. Despite robust immune responses, these individuals never eradicate HIV infection. We hypothesized that HIV-specific CD4+ T cells might serve as target cells for HIV, contributing to viral persistence in this setting.
Methods. We measured frequencies of activated (CD38+ HLA-DR+) and HIV Gag-specific CD4+ and CD8+ T cells and plasma- and cell-associated levels of HIV RNA and DNA in a cohort of 38 HIV controllers.
Results. Although there was no evidence of a relationship between the extent of low-level viremia and the frequency of either activated or HIV-specific CD4+ T cells, controllers with higher HIV-specific CD4+ T cell frequencies had higher cell-associated HIV DNA levels (ρ = 0.53; P = .019). Higher activated CD4+ T cell frequencies were also associated with higher levels of cell-associated DNA (P = .027) and RNA (P = .0096). However, there was no evidence of a relationship between cell-associated HIV RNA or DNA levels and HIV-specific CD8+ T cell frequencies.
Conclusions. These data support a model in which strong HIV-specific CD4+ T cell responses in HIV controllers, while contributing to a potent adaptive immune response, may also contribute to viral persistence, preventing the natural eradication of HIV infection.
My NOTE: Might this apply to XMRV or other infections in ME/CFS ?