Stephane Champiat, Rui André Saraiva Raposo, Nicholas J. Maness, John L. Lehman, Sean E. Purtell, Aaron M. Hasenkrug, Jacob C. Miller, Hansi Dean, Wayne C. Koff, Marisa Ailin Hong, Jeffrey N. Martin, Steven G. Deeks, Gerald E. Spotts, Christopher D. Pilcher, Fredrick M. Hecht, Esper G. Kallas, Keith E. Garrison, Douglas F. Nixon

Translational errors can result in bypassing of the main viral protein reading frames and the production of alternate reading frame (ARF) or cryptic peptides. Within HIV, there are many such ARFs in both sense and the antisense directions of transcription. These ARFs have the potential to generate immunogenic peptides called cryptic epitopes (CE). Both antiretroviral drug therapy and the immune system exert a mutational pressure on HIV-1. Immune pressure exerted by ARF CD8(+) T cells on the virus has already been observed in vitro. HAART has also been described to select HIV-1 variants for drug escape mutations. Since the mutational pressure exerted on one location of the HIV-1 genome can potentially affect the 3 reading frames, we hypothesized that ARF responses would be affected by this drug pressure in vivo.