Target peptide sequence within infectious human immunodeficiency virus type 1 does not ensure envelope-specific T-helper cell reactivation: influences of cysteine protease and gamma interferon-induced thiol reductase activities.

Recent clinical trials have shown that the presence of a robust human immunodeficiency virus type 1 (HIV-1)-specific T-cell response may not be sufficient to prevent or control HIV-1 infection. Studies of antigen processing in the context of infectious HIV-1 are therefore warranted. Envelope-specific, major histocompatibility complex class II-restricted murine T-cell hybridomas were tested for responsiveness to splenic antigen-presenting cells exposed to HIV-1-infected GHOST cells. Interleukin-2 assays showed that the presence of a peptide within HIV-1 did not ensure the reactivation of peptide-specific T cells. Further experiments defined the impact of gamma interferon-induced thiol reductase and cysteine proteases on the processing of HIV-1 peptides. The results highlight potential influences of peptide context on T-cell reactivation by HIV-1 and encourage the continued study of antigen processing as support for improved vaccine design.