The studies reported here show that the relative expression of two isoforms (CD200 and CD200 tr ) is tissue and cell specific and the alternative slicing patterns are different between the pattern in the lymphoid tissues and that of neuronal tissues. The relative expression of the two isoforms of CD200 is of interest, given our recent evidence that the truncated form (CD200 tr ) can antagonize the functional suppression induced by full-length CD200 (27) . Although Borriello et al. (26) reported no change in the alternative splicing pattern of murine CD200 in lymphoid tissue after stimulation by Con A or LPS in vivo, in our in vivo studies of mouse lung tissues before/after infection of MHV-1 virus we observed that, unlike in the natural condition, following viral infection the expression of total CD200 increased in lung of both MHV-1 susceptible A/J mice and MHV-1-resistant C57BL/6 mice. However, the splicing pattern of CD200 is reversed only in A/J mice, with the full-length transcript, capable of inducing immunosuppresion, becoming the predominant one. In contrast, for C57BL/6J, an MHV-1-resistant mouse strain, no change in the splicing pattern of CD200 was seen in the lung. This result importantly demonstrates that only the splicing pattern, but not the total transcription level, of CD200 determines the murine immune response to MHV-1 and is consistent with the hypothesis that the shift in the balance of expression of CD200/CD200 tr to decrease expression of the truncated product allowing CD200 to function in its immunosuppressive role, possibly contributing to the increased susceptibility to MHV-1 in the A/J mice. Further studies showed an increased expression of SF2/ ASF in A/J mice postinfection and the increase in SF2/ ASF occurred prior to increased full-length CD200, strongly suggesting that the regulation of alternative splicing of CD200 is mediated by SF2/ASF. It remains to be determined what viral proteins of MHV-1 have this effect and how the proteins regulate expression of SF2/ASF. Our studies suggest that viruses escape elimination by the host's immune system not only through producing viral proteins which mimic CD200 but also by inducing host CD200 expression and reducing expression of the antagonist CD200 tr . Posttranscriptional regulation, including mRNA stability, plays an important role for gene expression (42) . Whether the increase of full-length CD200 in A/J mice is also due to differential mRNA stability cannot be ruled out.