Mechanism of resistance to virus challenge in mice infected with Brucella abortus

Summary

Mice infected intraperitoneally or intravenously with liveB. abortus showed increased resistance to intraperitoneal infection with Mengo virus. The resistant state lasted for at least 3 weeks.When the bacteria were given by the intraperitoneal route, passage of virus from the peritoneal cavity to the circulation was inhibited. By analogy to findings with polycarboxylate-treated mice, it was concluded that this trapping of virus in the peritoneal cavity contributed to the development of resistance to virus infection.

In mice which were protected by intravenous injection of brucellae, passage of the challenge virus from the peritoneal cavity to the blood was not inhibited. Replication of virus in the spleens of these mice was decreased. However, no interferon was detectable in the sera or spleens, and no increased interf eron response to Mengo virus was observed, suggesting that interferon was not responsible for the observed inhibition of virus replication. It is proposed thatB. abortus infection potentiated phagocytic and virucidal activity of reticuloendothelial cells and thereby depressed apparent virus production in the spleen. This view was supported by the observation that uptake and subsequent clearance of a non-replicating picornavirus (poliovirus) were enhanced in the spleens ofB. abortus-infected mice.