Researchers Document Process of Herpes Latency
Herpes latency established and maintained through production of microRNAs
THURSDAY, July 3 (HealthDay News) -- The hypothesis that herpes viruses utilize microRNAs (miRNAs) to initiate and maintain latency was supported by a finding that herpes viruses are capable of downregulating key viral immediate early proteins, according to an article published online July 2 in Nature.
Jennifer Lin Umbach, Ph.D., of Duke University Medical Center in Durham, N.C., and colleagues used molecular genetic, Northern and Western blotting techniques to examine Herpes simplex virus 1 (HSV-1) from the dissected trigeminal ganglia of mice latently infected with HSV-1 strain. HSV-1 establishes latency in neurons of sensory ganglia and researchers are able to measure a gene product, the latency associated transcript (LAT).
The investigators found that LAT coded four distinct miRNAs in HSV-1 infected cells. One of these miRNAs is miR-H2-3p, which inhibits ICP0 protein expression, a transcriptional activator that is important for productive HSV-1 replication in the sensory ganglia. LAT also codes for miR-H6, which inhibits expression of ICP4, also required for expression of HSV-1 genes during infection, the report indicates.
"HSV-1 expresses at least two primary miRNA precursors in latently infected neurons that may facilitate the establishment and maintenance of viral latency by post-transcriptionally regulating viral gene expression," the authors conclude.