T cells target APOBEC3 proteins in human immunodeficiency virus type 1-infected humans and simian immunodeficiency virus-infected indian rhesus macaques

Stéphane Champiat, 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. SachaDouglas F. Nixon

Research output: Contribution to journalArticle

3 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)6073-6080
Number of pages8
JournalJournal of virology
Volume87
Issue number11
DOIs
StatePublished - Jun 2013

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

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