PubMed1990
We found that susceptibility to Murine Hepatitis Virus, type 3 (MHV3)-induced paralysis is controlled by genes of the H-2 complex. In this article, we compared MHV3 antigen specific cellular reactions, in congenic mice harbouring different H-2 genes (or gene). In a first set of experiments, paralysis susceptible (B10.A x A/J)F1, partly susceptible (B10.AQR x A/J)F1 and resistant (B10.Q x A/J)F1 hybrids were infected with live MHV3. Three weeks or more post-infection (p. i.), the spleens and peritoneal exudate (PE) cells from the mice were put into culture. Killed MHV3 was added to cultures, and antigen specific lymphokine production and utilization were measured: IL-1 production by PE cells after 24 hr in culture, IL-2 production by splenocytes after 24 hr in culture, IL-2 utilization (as appraised by splenocyte proliferation) after 96 hr in culture. No clearcut difference, resulting from genetic disparity, could be observed in the antigen-specific responses. In a second set of experiments, mice were primed with ultra-violet radiation killed MHV3. In that case, increases of IL-1 production by PE cells, of IL-2 production by splenocytes and splenocyte proliferation were always observed, compared to PE cells and splenocytes from non-primed (control) donor mice. However, in latter case, addition of MHV3 antigen to cultures did not result in augmentation of antigen specific IL-2 production and utilization. Here again, no genetic effect was observed. We conclude from these results that MHV3 infection elicited strong lymphokine responses, but that antigen-specific IL-1 and IL-2 production did not correlate with the susceptibility to MHV3-induced paralysis.