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Human immunodeficiency virus (HIV) proteins produced inside infected host cells are processed into peptide fragments that are presented on the cell surface by major histocompatibility complex (MHC) class I and class II molecules. MHC class I molecules display endogenously-synthesized (intracellular) HIV peptides to CD8^+^ cytotoxic T lymphocytes, which can then kill infected cells. MHC class II molecules present exogenous or autophagocytosed HIV antigens to CD4^+^ helper T cells, facilitating broader immune activation. HIV has evolved mechanisms (notably via its *Nef* protein) to impair both class I and II pathways, helping it evade immune detection and perpetuate infection. Modulating these pathways is central to vaccine and immunotherapy research but is not directly druggable in the sense of a typical pharmacological target. As such, this concept is best understood as a cardinal immune process rather than a singular molecular target.
Some antiviral therapies may enhance antigen presentation by upregulating MHC expression or improving antigen processing. Interferon-γ can increase MHC II expression.
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