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Abstract
Background HIV-specific CD8 T cells responses rely on the recognition of peptide-MHC-I complexes by cognate T cell receptors. HIV-derived MHC-I epitopes result from the degradation of viral proteins by the cellular processing machinery including proteasomes and aminopeptidases. Interferon gamma changes proteasome composition and peptidase activities. We hypothesize that HIV infection might affect the expression or activities of the antigen processing machinery, either through a direct effect of the virus or indirectly through cellular activation or from the release of cytokines by surrounding infected cells.
Highlights
HIV-specific CD8 T cells responses rely on the recognition of peptide-MHC-I complexes by cognate T cell receptors
HIV-derived MHC-I epitopes result from the degradation of viral proteins by the cellular processing machinery including proteasomes and aminopeptidases
We hypothesize that HIV infection might affect the expression or activities of the antigen processing machinery, either through a direct effect of the virus or indirectly through cellular activation or from the release of cytokines by surrounding infected cells
Summary
HIV-specific CD8 T cells responses rely on the recognition of peptide-MHC-I complexes by cognate T cell receptors. HIV-derived MHC-I epitopes result from the degradation of viral proteins by the cellular processing machinery including proteasomes and aminopeptidases. Interferon gamma changes proteasome composition and peptidase activities. We hypothesize that HIV infection might affect the expression or activities of the antigen processing machinery, either through a direct effect of the virus or indirectly through cellular activation or from the release of cytokines by surrounding infected cells. HIV peptide in extracts from T cells analyzed by mass spectrometry shows differences in epitope production between non-activated and PHA-activated cells
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