Abstract
In vitro assays indicate that both major histocompatibility complex (MHC) class I and II-restricted cytotoxic T lymphocytes are important for recognition of varicella-zoster virus (VZV)-infected cells. This study demonstrates that infection of human fibroblasts with wild-type or recombinant-derived strain Oka VZV results in down-regulation of surface expression of class I MHC heavy chains. Radioactive labeling of infected cells indicated that the amount of newly synthesized class I antigen was similar in uninfected and VZV-infected cells. In addition, immunoblotting showed that the amount of total cellular class I MHC heavy chains was unaffected by VZV infection. These results suggest that the reduction of class I heavy chains on the surface of VZV-infected cells is due to a defect in posttranslational processing. The down-regulation of class I MHC antigens in VZV-infected cells may provide a mechanism for the virus to escape the host immune response.
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