Acute necrotizing inflammatory disease after intracerebral injection of LCM virus is largely dependent on the host immune response to the virus and is controlled, in part, by a dominant gene which is closely linked to the H-2 locus. The F1 hybrid (H-2q/k) from mating a susceptible SWR/J mouse (H-2q/q) to a resistant C3H/HeJ mouse (H-2k/k) is susceptible to LCM virus disease. When such hybrids (H-2q/k) are backcrossed to susceptible parents (H-2q/q), all F2 offspring (H-2q/q, H-2q/k) are highly susceptible. In contrast, hybrid (H-2q/k) backcross to resistant parents (H-2k/k) results in half of the F2 offspring being susceptible (H-2q/k) while the other half are resistant (H-2k/k). Similarly, in congenic H-2q/q and H-2k/k mice, H-2q/q mice are relatively susceptible to acute LCM disease, whereas H-2k/k are resistant.

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