Peritoneal Barrier to the Spread of Semliki Forest Virus in Mice

Abstract

Abstract

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 × 10³ PFU. In the ICR strain of mice at the same age, the LD₅₀ for the intracerebral route is 1 PFU, 10³ PFU for the iv and footpad routes, and 4 × 10³ 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 (<0.5%) of peritoneal adherent cells. Naturally occurring interferon-α/β (<1 unit/ml) was found to probably play a marginal role, if any, in the resistance.