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

¹ Institute of Basic Medical Sciences and Department of Microbiology and Immunology, Medical College, National Cheng Kung University, Tainan 70101, Taiwan, Republic of China
² Department of Virology and Immunology, Southwest Foundation for Biomedical Research, 7620 NW Loop 410, San Antonio, TX 78227, USA

Correspondence
Shun-Hua Chen
shunhua{at}mail.ncku.edu.tw

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.

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