The induction of IFN response by WT, N36S, 36KN and 36R. NIH3T3 cells were infected with WT, N36S, 36KN or 36R virus at MOI=0.05. At 24 hours post infection, cell supernatant and RNA extracted from the infected cells were analyzed for endogenous IFN-β production by ELISA (left) and transcription level of IFN-β (middle) and Mx1 (right) by q-PCR. For ELISA, samples from three independent experiments were combined and tittered. (B) The multi-step growth curve of WT, N36S, 36KN, and 36R. Samples from two independent experiments were combined, tittered, and shown here. (C) Transcript level of ISGs in the lung after WT or 36S MHV-68 infection examined by q-PCR. Viral genome and cellular actin transcript level were also measured as control. Data are represented as mean + SD. (D) Acute replication in the lung after intranasal infection of the indicated viruses in normal C57BL/6 (left) and IFNAR−/− (right) mice. (E) Latency establishment in the spleen after intranasal infection of the indicated viruses in normal C57BL/6 (left) and IFNAR−/− (right) mice. I.C.: infectious center; sp.: splenocytes. 500 pfu/mouse and 4~5 mice per group and per time point. Data are represented as mean + SD. n.s.: not significant; *, P < 0.05.