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• W2122350335 abstract "Abstract Background Although HIV can infect several cellular subsets, such as CD4 + T lymphocytes and macrophages, it remains unclear whether an HIV infection in macrophages supports cytotoxic T lymphocyte (CTL) escape. Here, we tested two naturally-arising mutations located in the well-conserved polyproline region of Nef for their effects on CTL recognition, Nef's functionality, and viral replication capacity in macrophages. These mutations were selected because they are known to cause CTL escape in the context of T lymphocytes. Findings Monocyte-derived macrophages (MDMs) infected with the wild-type virus, but not with variant viruses, were efficiently killed by CTL clones targeting Nef epitopes, VY8 (VPLRPMTY) and RY11 (RPQVPLRPMTY). The CTL-escape mutation, Arg 75 Thr, or Arg 75 Thr/Tyr 85 Phe double mutation, reduced the HLA class I down-regulation activity and, interestingly, increased the susceptibility of virus-infected MDMs to recognition by CTLs targeting a different epitope. The same mutations reduced the CCR5, but not CD4, down-regulation activity. Moreover, the Nef variants were impaired for Hck activation and enhancement of viral replication in MDMs. Conclusions These results suggest that HIV-infected MDMs are killed by CTLs targeting Nef epitopes, contributing to selection and adaptation of CTL-escape viral variants." @default.
• W2122350335 created "2016-06-24" @default.
• W2122350335 creator A5016741990 @default.
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• W2122350335 date "2011-06-22" @default.
• W2122350335 modified "2023-09-26" @default.
• W2122350335 title "Effects of naturally-arising HIV Nef mutations on cytotoxic T lymphocyte recognition and Nef's functionality in primary macrophages" @default.
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• W2122350335 doi "https://doi.org/10.1186/1742-4690-8-50" @default.
• W2122350335 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3131245" @default.
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