Reid William, Abdelwahab Sayed, Sadowska Mariola, Huso David, Neal Ashley, Ahearn Aaron, Bryant Joseph, Gallo Robert C, Lewis George K, Reitz Marvin
Division of Basic Science, University of Maryland, Baltimore, MD 21201, USA.
Virology. 2004 Mar 30;321(1):111-9. doi: 10.1016/j.virol.2003.12.010.
HIV-1 infection leads to impaired antigen-specific T cell proliferation, increased susceptibility of T cells to apoptosis, progressive impairment of T-helper 1 (Th1) responses, and altered maturation of HIV-1-specific memory cells. We have identified similar impairments in HIV-1 transgenic (Tg) rats. Tg rats developed an absolute reduction in CD4+ and CD8+ T cells able to produce IFN-gamma following activation and an increased susceptibility of T cells to activation-induced apoptosis. CD4+ and CD8+ effector/memory (CD45RC- CD62L-) pools were significantly smaller in Tg rats compared to non-Tg controls, although the converse was true for the naïve (CD45RC+ CD62L+) T cell pool. Our interpretation is that the HIV transgene causes defects in the development of T cell effector function and generation of specific effector/memory T cell subsets, and that activation-induced apoptosis may be an essential factor in this process.