It has been claimed that MHC class I proteins serve as receptors for murine cytomegalovirus (MCMV) and that this interaction is the most important mechanism for virus entry in most cells. This claim is based on the observation that the MHC haplotype contributes to the susceptibility to cytomegalovirus (CMV) infection . Results from studies support the concept that stable expression of correctly folded MHC class I molecules contributes to infection, since the individual properties of MHC class I alleles, the availability of β-microglobulin (βm) and also the degree of peptide charging of the MHC class I heavy chain βm heterodimers determined the infection phenotype of cell lines. To assess the biological relevance of proper MHC class I expression we investigated CMV infection in βm-deficient mice which fail to express ternary MHC class I complexes and lack peripheral CD8 T lymphocytes. We found that organ virus titres and virus clearance kinetics were not altered in βm mutant mice. In addition, there was no indication of diminished virus propagation in βm embryonic fibroblasts. βm mice suffered from the lack of CD8 T lymphocytes that was partially compensated for by the function of CD4 T lymphocytes. An organ-specific anti-virus function of natural killer (NK) cells was observed, independent from the βm deletion. The immune control unique for salivary gland infection was maintained. From the data presented here, we confirm the role of MHC class I molecules in the immune surveillance of CMV infection but question the biological impact of correct MHC class I complexes for productive infection.


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