Herpes simplex virus latent RNA (LAT) is not required for latent infection in the mouse.
Virus latency
Latent Virus
Vero cell
Recombinant virus
DOI:
10.1073/pnas.86.19.7596
Publication Date:
2006-05-31T11:03:53Z
AUTHORS (2)
ABSTRACT
During latent infection by herpes simplex virus (HSV), an abundant latency-associated transcript (LAT) that is antisense to a predominant viral alpha gene (ICP0) found localized in the nucleus of sensory neurons. We disrupted both copies LAT HSV-1 genome insertion Escherichia coli lacZ under promoter control. The resulting recombinant virus, RH142, does not express any detectable either latently or productively infected cells, although beta-galactosidase expression readily neurons mice. Expression was first 3 days postinoculation and continued at approximately same level for entire experimental period (56 days). beta-Galactosidase time during RH142 replication Vero cells. Thus, kinetics cell-type specificity are distinct from other genes expressed productive growth. When trigeminal ganglia were explanted, reactivated latency with efficiency indistinguishable parental wild-type virus. These studies argue against possible regulatory mechanism regulation role LAT-encoded protein establishment maintenance mouse.
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