Susceptibility to fatal Pichinde virus infection in the Syrian hamster.

The data presented in this paper suggest that the susceptible MHA hamster strain possesses a spleen target cell for Pichinde virus replication which is minimally expressed in the resistant strain. This target cell co-purifies with cells mediating NK activity, raising the possibility that the NK cell itself may be the additional target cell for Pichinde virus replication in the susceptible hamster strain. We hypothesize that early virus replication in the spleens of IP-inoculated hamsters leads to an overwhelming proliferation of virus. In contrast, a footpad inoculation of Pichinde virus retards virus spread into the spleen, and the host's immune response can effectively clear the relatively low amount of virus. In addition, data have been presented that show that a footpad inoculation of Pichinde virus elicits swelling in resistant hamster strains at eight days after infection, but fails to evoke a response in the susceptible MHA hamster strain. The response is controlled by a single autosomal dominant gene, and suggests that the MHA hamster strain has a defective delayed-type hypersensitivity response. The gene responsible for footpad swelling appears to be distinct from the single autosomal dominant gene that controls virus replication in the popliteal lymph nodes of footpad-injected hamsters. The phenotype of survival, then, may be the result of either limited virus replication early in infection, or an effective anti-viral cell-mediated immune response, or both.