Previous studies have shown that several viruses express a viral protein which mimics human CD200 and down-regulates host immunity to the virus following interaction with a human CD200 receptor on host cells (39) (40) (41) . Whether viral infection itself affects the expression of CD200 in host is an issue which remains to be explored. Intranasal infection of A/J mice with the coronavirus murine hepatitis virus strain 1 (MHV-1) has been described to induce pulmonary pathology with features reminiscent of severe acute respiratory syndrome (SARS) (33) . To examine the correlation between the viral (MHV-1) infection and expression of CD200 in host we collected lung tissues from MHV-1 susceptible A/J mice and MHV-1-resistant C57BL/6J mice after infection. RT-PCR was performed using a sense primer located in exon 1 and an antisense primer present in exon 3. Interestingly, we observed a reversal of the normal CD200 splicing pattern in lung tissues of A/J mice postinfection ( Figure 7A ). Real-time RT-PCR provided a more accurate result of this phenomenon. We documented that the full-length CD200 was increased after viral infection and was 2-fold higher at 36 h postinfection compared with that before infection ( Figure 7B ). All the susceptible A/J mice were dead at 96 h postinfection. In contrast, the relative ratio of full-length to truncated CD200 did not change in infected C57BL/6J mice ( Figure 7C and D) . Thus, the pattern of alternative splicing of CD200 was correlated with susceptibility of these strains to viral infection.