CD8+ T cell responses to human immunodeficiency viruses type 2 (HIV‐2) and type 1 (HIV‐1) gag proteins are distinguishable by magnitude and breadth but not cellular phenotype

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Abstract
The mechanisms underlying the relatively slow progression of human immunodeficiency virus type 2 (HIV‐2) compared with HIV‐1 infection are undefined and could be a result of more effective immune responses. We used HIV‐2 and HIV‐1 IFN‐γ enzyme‐linked immunospot assays to evaluate CD8+ T cell responses in antiretroviral‐naive HIV‐2‐ (‘HIV‐2+’) and HIV‐1‐infected (‘HIV‐1+’) individuals. Gag‐specific responses were detected in the majority of HIV‐2+ and HIV‐1+ subjects. Overlapping gag peptide analysis indicated a significantly greater magnitude and breadth of responses in the HIV‐1+ cohort, and this difference was attributable to low responses in HIV‐2+ subjects with undetectable viral load (medians 2107 and 512 spot‐forming units per 106 PBMC, respectively, p=0.007). We investigated the phenotype of viral epitope‐specific CD8+ T cells identified with HLA‐B53‐ and HLA‐B58‐peptide tetramers (8 HIV‐2+, 11 HIV‐1+ subjects). HIV‐2‐specific CD8+ T cells were predominantly CD27+ CD45RA–, and only a minority expressed perforin. The limited breadth and low frequency of CD8+ T cell responses to HIV‐2 gag in aviremic HIV‐2+ subjects suggests that these responses reflect antigen load in plasma, as is the case in HIV‐1 infection. Immune control of HIV‐2 does not appear to be related to the frequency of perforin‐expressing virus‐specific CD8+ T cells.

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