These data clearly indicated that the virus suppression phenotype in the bzip60-2 mutant arise from the loss-of-function of bZIP60 S. Consistently, two different double mutants of IRE1A and IRE1B, in which bZIP60 U splicing was blocked, displayed reduced levels of viral RNA accumulation and suppressed viral symptom development like the bzip60-2 mutant (Figs 3 and 8), suggesting that bZIP60 S, not bZIP60 U, plays a crucial function in favoring virus infection. The gene discussed is ERN1; the disease is viral infectious disease.