After observing the disconnect between IFIT1 transcript levels and protein levels in the C7/10-derived virus infections, we hypothesized that the C7/10-derived virus is shutting off host translation sooner and preventing the translation of these transcripts, thus explaining the disconnect between transcript levels and protein levels as well as how the C7/10-derived virus is able to replicate better in the presence of more IFN-β and ISG mRNAs. The gene discussed is IFIT1; the disease is viral infectious disease.