CMV Mutant Effects on Host Immune Systems
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Cytomegalovirus (CMV) infection within immunosupressed hosts has caused a documented increase in fatality rate. Research aimed at increasing immune response rate and effectiveness has revealed a number of genes responsible for viral immune evasion. A mutant virus with the deletion of the ml52 (Rae 1-Y) gene was injected to immunocapable and immunoincapable hosts to test for mortality rate. In both immunocapable and incapable hosts, the mutant ,Aml52 virus strain showed a decreased mortality rate. A similar immune response within wild type (WT) and Ami52 infected mice was found using CD8 T-cell concentration analysis indicating the mutant virus' potential for vaccine use. In addition, administering the mutant Ami52 viral form post WT infection increased speed and effectiveness of the immune response. These results suggest that the less virulent mutant of CMV is a viable viral derivative to be studied for human application of a CMV vaccine. Although additional analysis is required for comprehension of CMV immunoevasion protein expression targeting the NKG2D receptors upon viral infection, the discovery of the Ami52 viral derivative will form the basis for the analysis of the human CMV strain.