| Literature DB >> 23536679 |
Stéphane Champiat1, Keith E Garrison, Rui André Saraiva Raposo, Benjamin J Burwitz, Jason Reed, Ravi Tandon, Vanessa A York, Laura P Newman, Francesca A Nimityongskul, Nancy A Wilson, Rafael R Almeida, Jeffrey N Martin, Steven G Deeks, Michael G Rosenberg, Andrew A Wiznia, Gerald E Spotts, Christopher D Pilcher, Fredrick M Hecht, Mario A Ostrowski, Jonah B Sacha, Douglas F Nixon.
Abstract
APOBEC3 proteins mediate potent antiretroviral activity by hypermutating the retroviral genome during reverse transcription. To counteract APOBEC3 and gain a replicative advantage, lentiviruses such as human immunodeficiency virus type 1 (HIV-1) and simian immunodeficiency virus (SIV) have evolved the Vif protein, which targets APOBEC3 proteins for proteasomal degradation. However, the proteasome plays a critical role in the generation of T cell peptide epitopes. Whether Vif-mediated destruction of APOBEC3 proteins leads to the generation and presentation of APOBEC3-derived T cell epitopes on the surfaces of lentivirus-infected cells remains unknown. Here, using peptides derived from multiple Vif-sensitive APOBEC3 proteins, we identified APOBEC3-specific T cell responses in both HIV-1-infected patients and SIV-infected rhesus macaques. These results raise the possibility that these T cell responses may be part of the larger antiretroviral immune response.Entities:
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Year: 2013 PMID: 23536679 PMCID: PMC3648095 DOI: 10.1128/JVI.00579-12
Source DB: PubMed Journal: J Virol ISSN: 0022-538X Impact factor: 5.103