Abstract
Host-parasite relationships of the virus of LCM and the common mouse (Mus musculus) are influenced by several factors, some of which are (1) age of mouse at time of infection (2) mildness of the original infection (severe infections artificially induced tend to be followed by long persistance of the virus), (3) site of injn. (subcut. injn. tends to produce inapparent or very mild infection, intraperitoneal and intraven. injn. cause severe illness, and intracerebral inoculation with much smaller quantities of virus usually has fatal outcome). The incubation period is relatively constant for any given route of injn. and dose of virus, but shortening can be achieved by repeated injns. at frequent intervals (superinfection). The accelerated type of infection is most notable where subcut. injn. (normally causing no detectable illness) is followed on the 3rd day by intracerebral injn.: mice so super-infected either die in about half the time that would be required for intracerebral injn. alone, or they survive entirely. Virus development in normal mouse brain following intracerebral injn. is marked by presence of little or no demonstrable virus during the first 6 hrs. after intracerebral injn., with marked increase by the 24th hr. In brains removed immediately after injn., and kept in vitro, there is gradual decline in virus over several days, with no immediate lag. In mice hyperlmmunlzed by 2 subcut. injns. of live virus, and challenged intracerebrally, virus development parallels that in non-immune mice, but the hyperimmune mouse survives, despite the virus in its brain, while the non-immune dies. In subcut. injected mice challenged after surviving an intracerebral injn., there was little or no recovery of demonstrable virus after the Ist post-inoculation hr. If brains were kept in vitro after injn., the pattern of virus survival was the same whether mice were non-immune, subcut. immunized, or had survived intracerebral challenge.
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