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- W2011445764 abstract "RNase L helps mediate the antiviral state induced by type I interferons (IFNαβ). Although herpes simplex virus (HSV) encodes inhibitors of the IFNαβ-induced antiviral response, the IFNαβ system serves the body as a first line of defense against HSV. We investigated whether RNase L limits HSV-2 replication and virulence. RNaseL −/− and wild-type C57BL/6 mice were infected intravaginally with HSV-2 strain 333. Although initial replication in the genital epithelium was similar, mice lacking RNase L developed less severe genital and neurologic disease than wild-type mice, survived longer, and contained lower viral titers in the nervous system. CD4 + T cell infiltration into the genital tract and spinal cord of RNase L −/− mice was reduced, suggesting that a restricted inflammatory response may account for reduction in disease. Thus, RNase L does not play a significant role in control of HSV-2 infection in vivo; instead, RNase L may regulate aspects of the inflammatory response that contribute to disease." @default.
- W2011445764 created "2016-06-24" @default.
- W2011445764 creator A5007183341 @default.
- W2011445764 creator A5014880617 @default.
- W2011445764 date "2007-04-01" @default.
- W2011445764 modified "2023-10-14" @default.
- W2011445764 title "Herpes simplex virus type 2-mediated disease is reduced in mice lacking RNase L" @default.
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- W2011445764 doi "https://doi.org/10.1016/j.virol.2006.10.042" @default.
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