Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 5869-5873 |
| Journal | Journal of Immunology |
| Volume | 166 |
| DOIs | |
| Publication status | Published - 2001 |
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