Murine cytomegalovirus (MCMV) encodes three immune evasion genes (m04, m06, and m152) that interfere with MHC class I antigen presentation to CD8 T cells. Although not required for viral persistence, these genes are evolutionarily conserved, suggesting an important role in immune modulation. This dissertation characterizes the individual and combined effects of these immune evasion genes on antigen-specific CD8 T cell responses. Coordinated expression of all three genes potently inhibits CD8 T cell–mediated killing of infected cells, whereas loss of any single gene partially restores lysis. The findings demonstrate that reduced total MHC class I levels, rather than complete absence of cognate peptide, weaken T cell–target interactions and impair effective cytotoxic responses, revealing a key mechanism by which MCMV evades antiviral immunity.
