| First Author | Conrady CD | Year | 2011 |
| Journal | J Virol | Volume | 85 |
| Issue | 4 | Pages | 1625-33 |
| PubMed ID | 21147921 | Mgi Jnum | J:168790 |
| Mgi Id | MGI:4938236 | Doi | 10.1128/JVI.01715-10 |
| Citation | Conrady CD, et al. (2011) Loss of the type I interferon pathway increases vulnerability of mice to genital herpes simplex virus 2 infection. J Virol 85(4):1625-33 |
| abstractText | The mouse model of genital herpes relies on medoxyprogesterone treatment of female mice to render the vaginal lumen susceptible to inoculation with herpes simplex virus 2 (HSV-2). In the present study, we report that mice deficient in the A1 chain of the type I interferon receptor (CD118(-/-)) are susceptible to HSV-2 in the absence of medroxyprogesterone preconditioning. In the absence of hormone pretreatment, 2,000 PFU of a clinical isolate of HSV-2 was sufficient to establish a productive infection in the vagina of 75% +/- 17% and in the spinal cord of 71% +/- 14% of CD118(-/-) mice, whereas the same dose of HSV-2 replicated to detectable levels in only 13% +/- 13% of vaginal samples and 0% of spinal cord samples from wild-type mice, as determined at day 5 postinfection. The susceptibility to HSV-2 infection in the CD118(-/-) mice was associated with a significant reduction in the infiltration of HSV-specific cytotoxic T lymphocytes into the vaginal tissue, the local production of gamma interferon (IFN-gamma), and the expression of T cell-recruiting chemokines CCL5, CXCL9, and CXCL10. Collectively, the results underscore the significant contribution of type I IFNs in resistance to genital HSV-2 infection. |
