| First Author | Walder CE | Year | 1989 |
| Journal | Proc Soc Exp Biol Med | Volume | 190 |
| Issue | 1 | Pages | 70-8 |
| PubMed ID | 2536182 | Mgi Jnum | J:25990 |
| Mgi Id | MGI:73830 | Doi | 10.3181/00379727-190-42831 |
| Citation | Walder CE, et al. (1989) Peritoneal barrier to the spread of Semliki forest virus in mice. Proc Soc Exp Biol Med 190(1):70-8 |
| abstractText | The LD50 for encephalitis caused by Semliki forest virus in 6- to 8-week-old mice is 1 plaque-forming unit (PFU) in C3H/Ten strain of mice when injected intracerebrally, iv, or in the footpad; however, the LD50 by the ip route is 4 x 10(3) PFU. In the ICR strain of mice at the same age, the LD50 for the intracerebral route is 1 PFU, 10(3) PFU for the iv and footpad routes, and 4 x 10(3) PFU for the ip route. A number of in vivo and in vitro experiments were done to explain the relative resistance to Semliki forest virus injection by the ip route. The results suggest that the viruses are adsorbed to and enter adherent cells of the peritoneal cavity but do not replicate and release progeny virus. After inoculation with the virus, viral antigens could only be observed in methanol-treated cells as a halo by immunofluorescence at or just below the plasma membrane of only a small fraction (less than 0.5%) of peritoneal adherent cells. Naturally occurring interferon-alpha/beta (less than 1 unit/ml) was found to probably play a marginal role, if any, in the resistance. |
