UL40-mediated NK evasion during productive infection with human cytomegalovirus

摘要

Human cytomegalovirus (HCMV) exploits a range of strategies to evade and modulate the immune response. Its capacity to down- regulate MHC I expression was anticipated to render infected cells vulnerable to natural killer (NK) attack. Kinetic analysis revealed that during productive infection, HCMV strain AD169 first en- hanced and then inhibited lysis of primary skin fibroblasts by a CD94/NKG2A~+NKG2D~+ILT2~+ NK line. The inhibition of cytotoxicity against strain AD169-infected fibroblasts was abolished by prior treatment of targets or effectors with anti-MHC I and anti-CD94 monoclonal antibodies, respectively, implying a CD94/HLA-E- dependent mechanism.