The gammaherpesvirus thymidine kinase

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Herpesviruses are ubiquitous infections and cause many clinical problems in immunosuppressed patients. The most effective treatment to date has been anti-viral drugs such as aciclovir, which exploit a viral enzyme called thymidine kinase (TK). The gamma-herpesviruses have this enzyme, but it is a much weaker enzyme than that of alpha-herpesviruses, against which aciclovir was developed. We suspect that the gamma-herpesvirus TK has different functions, and might therefore best be attacked through different types of drugs.The human gamma-herpesviruses only infect primates, making many experiments impractical. We are therefore defining what the gamma-herpesvirus TK does using a related murine virus, called MHV-68. We know that the MHV-68 TK is important for viral replication in mice. We aim now to work out why, specifically whether it works in the same way as the alpha-herpesvirus TK, or whether it has very different functions that would be best inhibited in different ways. By understanding how the MHV-68 TK works, we should be able to provide a basis for effective TK-based therapies in gamma-herpesvirus infections.