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An acutely and latently expressed herpes simplex virus 2 viral microRNA inhibits expression of ICP34.5, a viral neurovirulence factor
- Tang, Shuang, Bertke, Andrea S., Patel, Amita, Wang, Kening, Cohen, Jeffrey I., Krause, Philip R.
- Proceedings of the National Academy of Sciences of the United States of America 2008 v.105 no.31 pp. 10931-10936
- humans, Human alphaherpesvirus 2, ganglia, peripheral nervous system, microRNA, viruses, sensory neurons, herpes simplex, guinea pigs
- Latency-associated transcript (LAT) sequences regulate herpes simplex virus (HSV) latency and reactivation from sensory neurons. We found a HSV-2 LAT-related microRNA (miRNA) designated miR-I in transfected and infected cells in vitro and in acutely and latently infected ganglia of guinea pigs in vivo. miR-I is also expressed in human sacral dorsal root ganglia latently infected with HSV-2. miR-I is expressed under the LAT promoter in vivo in infected sensory ganglia. We also predicted and identified a HSV-1 LAT exon-2 viral miRNA in a location similar to miR-I, implying a conserved mechanism in these closely related viruses. In transfected and infected cells, miR-I reduces expression of ICP34.5, a key viral neurovirulence factor. We hypothesize that miR-I may modulate the outcome of viral infection in the peripheral nervous system by functioning as a molecular switch for ICP34.5 expression.