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CUTTING EDGE |
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Pediatric Virology and Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, TX 77555; and
Department of Microbiology, University of Western Australia, Queen Elizabeth II Medical Centre, Nedlands, Australia
Herpes simplex causes latent infections that periodically reactivate. Specific immunization attempts are failing to control herpes, prompting a fresh look at which host responses predominate. We report a NK complex-linked genetic locus, Rhs1, whose alleles influence the magnitude of experimental herpes simplex. Rhs1 provided rapid control of primary infection but caused a reciprocal increase in the number of latently infected neurons. Thus, in principle, establishment of latency is a consequence of efficient front line defense against herpesvirus infection. Based on conservation between human and mouse NK complexes, the data predict the presence of a human Rhs1 orthologue on chromosome 12p12–13.
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