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T cells target APOBEC3 proteins in human immunodeficiency virus type 1-infected humans and simian immunodeficiency virus-infected Indian rhesus macaques. 2013
Stéphane Champiat, and
Keith E Garrison, and
Rui André Saraiva Raposo, and
Benjamin J Burwitz, and
Jason Reed, and
Ravi Tandon, and
Vanessa A York, and
Laura P Newman, and
Francesca A Nimityongskul, and
Nancy A Wilson, and
Rafael R Almeida, and
Jeffrey N Martin, and
Steven G Deeks, and
Michael G Rosenberg, and
Andrew A Wiznia, and
Gerald E Spotts, and
Christopher D Pilcher, and
Fredrick M Hecht, and
Mario A Ostrowski, and
Jonah B Sacha, and
Douglas F Nixon
Division of Experimental Medicine, Department of Medicine, University of California San Francisco, San Francisco, California, USA.
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.
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