Expression of extremely low levels of thymidine kinase from an acyclovir-resistant herpes simplex virus mutant supports reactivation from latently infected mouse trigeminal ganglia

Michael I. Besecker, Caroline L. Furness, Donald M. Coen, Anthony Griffiths

    Research output: Contribution to journalArticlepeer-review

    17 Scopus citations

    Abstract

    A single-cytosine-deletion in the herpes simplex virus gene encoding thymidine kinase (TK) was previously found in an acyclovir-resistant clinical isolate. A laboratory strain engineered to carry this mutation did not generate sufficient TK activity for detection by plaque autoradiography, which detected 0.25% wild-type activity. However, a drug sensitivity assay suggested that extremely low levels of TK are generated by this virus. The virus was estimated to express 0.09% of wild-type TK activity via a ribosomal frameshift 24 nucleotides upstream of the mutation. Remarkably, this appeared to be sufficient active TK to support a low level of reactivation from latently infected mouse trigeminal ganglia.

    Original languageEnglish (US)
    Pages (from-to)8356-8360
    Number of pages5
    JournalJournal of virology
    Volume81
    Issue number15
    DOIs
    StatePublished - Aug 2007

    ASJC Scopus subject areas

    • Microbiology
    • Immunology
    • Insect Science
    • Virology

    Fingerprint

    Dive into the research topics of 'Expression of extremely low levels of thymidine kinase from an acyclovir-resistant herpes simplex virus mutant supports reactivation from latently infected mouse trigeminal ganglia'. Together they form a unique fingerprint.

    Cite this