Abstract

The role of herpes simplex virus (HSV) thymidine kinase (TK) expression for HSV neurovirulence and latency has been evaluated by many investigators. Although neurovirulence is complex and involves multiple host and viral factors, in studies with HSV TK-negative (TK) mutants, it seemed that TK expression was an important factor. This was apparent in experimental animal studies, as indicated by decreased replication of TK− HSV mutants in neural tissue and by decreased mortality. Although some virulent TK− HSV mutants have been reported, most investigators, including studies with HSV deletion mutants, have supported an important role for HSV TK expression and neurovirulence.

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