Infection with MERS-NS4bNLSmut also did not result inincreased rRNA degradation, as expected given previous work demonstrating cytoplasmic PDElocalization mediates RNase L antagonism (34).However, infection with MERS-ΔNS4a also did not induce increased rRNA degradationrelative to WT MERS-CoV, indicating that the absence of NS4a alone is not enough toactivate RNase L in this cell type (Fig. 8).Infection with MERS-ΔNS4ab did not induce more robust rRNA degradation thanMERS-NS4bH182R, suggesting that NS4a does not play a significant role inantagonism of RNase L during MERS-CoV infection. The gene discussed is RNASEL; the disease is infection.