| First Author | Duerst RJ | Year | 2007 |
| Journal | Virology | Volume | 360 |
| Issue | 2 | Pages | 322-8 |
| PubMed ID | 17157346 | Mgi Jnum | J:136747 |
| Mgi Id | MGI:3796930 | Doi | 10.1016/j.virol.2006.10.042 |
| Citation | Duerst RJ, et al. (2007) Herpes simplex virus type 2-mediated disease is reduced in mice lacking RNase L. Virology 360(2):322-8 |
| abstractText | RNase L helps mediate the antiviral state induced by type I interferons (IFNalphabeta). Although herpes simplex virus (HSV) encodes inhibitors of the IFNalphabeta-induced antiviral response, the IFNalphabeta 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. |
