Coronavirus induction of class I major histocompatibility complex expression in murine astrocytes is virus strain specific

Perhaps one of the more interesting findings in these studies is the prevalence of K b expression over that of D b after MHV infection, and to a lesser extent, IFN-3" treatment. Differential modulation of H-2K and H-2D molecules has been reported to follow in vitro JHMV infection in mouse brain endothelial cells, and the data indicate that the nature of the regulation was dependent on the mouse strain and did not necessarily correlate with susceptibility to JHMV-induced CNS disease (64) . Thus, K was decreased and D increased in endothelial cells from susceptible BALB/c mice, but both were upregulated in susceptible B10.S and (BALB/c x SJL)F1 and resistant SJL endothelial cells. Differential expression of K and D molecules has not always been observed after virus infection of neural cells; both K and D molecules appear to be equally enhanced by West Nile virus infection in astrocytes from CBA/H mice (65) , and the murine neuroblastoma C1300 does not show differential K and D expression when persistently infected with measles virus (66) . However, the possibility that differential modulation of class I molecules may be linked to CNS disease, or may be a marker of susceptibility to virus-induced CNS disease, is suggested by studies using Theiler's murine encephalomyelitis virus (TMEV; 67, 68). After i.c. TMEV inoculation, resistant B10 mice showed minimal class I expression in the CNS that did not differ between K and D, whereas susceptible B10.Q and B10.RBQ mice showed a greater increase in D expression compared with that of K (67) .