Competition and complementation between thymidine kinase-negative and wild-type herpes simplex virus during co-infection of mouse trigeminal ganglia

Shih Heng Chen, Yu Wen Lin, Anthony Griffiths, Wen Yen Huang, Shun Hua Chen

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    9 Scopus citations

    Abstract

    Laboratory strains of herpes simplex virus lacking thymidine kinase (TK) cannot replicate acutely to detectable levels in mouse trigeminal ganglia and do not reactivate from latency. However, many pathogenic clinical isolates that are resistant to the antiviral drug acyclovir are heterogeneous populations of TK-negative (TK-) and TK-positive (TK+) viruses. To recapitulate this in vivo, mice were infected with mixtures of wild-type virus and a recombinant TK- mutant in various ratios. Following co-infection, the replication, number of latent viral genomes and reactivation efficiency of TK+ virus in trigeminal ganglia were reduced in a manner related to the amount of TK- virus in the inoculum. TK+ virus did not always complement the acute replication or increase the number of latent viral genomes of TK- mutant in mouse ganglia. Even so, TK+ virus could still confer the pathogenic phenotype to a TK- mutant, somehow providing sufficient TK activity in trans to permit a TK- mutant to reactivate from latently infected ganglia.

    Original languageEnglish (US)
    Pages (from-to)3495-3502
    Number of pages8
    JournalJournal of General Virology
    Volume87
    Issue number12
    DOIs
    Publication statusPublished - Dec 1 2006

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    ASJC Scopus subject areas

    • Virology

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