In RSV infection, stark differences are evident in regard to the effect of UPR modulation on replication in vitro and in vivo. For instance, deletion of the UPR-suppressing RSV SH protein is dispensable in tissue but accompanies a 10-fold decrease in replication efficiency in the upper respiratory tract of mice . RSV infection induces ER stress-mediated apoptosis through the caspase-12 and caspase-3 pathway . However, RSV also utilises its SH protein to partially suppress ER-mediated apoptosis, a protective effect that may help the virus avoid host immune detection .