JUN and infection: Therefore, since we were able to detect activation of both JNK and p38, we also investigated the downstream activation of MK2 and c-Jun during TCRV infection—and, indeed, we saw activation of both of these factors late in the infection, consistent with the kinetics of JNK and p38 activation (Figure 2), and also the regulation of apoptotic regulatory factors (Figure 1) [17].