The host antiviral ribonuclease L protein supports Zika virus replication factory formation to enhance infectious virus production

Jillian N Whelan; Joshua Hatterschide; David M. Renner; Beihua Dong; Robert H Silverman; Susan R Weiss

to that of WT cells, we found that dsRNA intensity and circularity were decreased while 165 diameter was increased without RNase L, a similar trend but to a lesser degree than with 166 ZIKV ( Figure 2D&F) . Furthermore, this does not result in a defect in virus release as 167 measured by viral titer, but instead virus titer is enhanced by RNase L KO (Figure 1C The copyright holder for this preprint (which was not peer-reviewed) is the author/funder. We also found that by 48hpi OAS3 KO, which suppresses RNase L activation, 201 restored infectious ZIKV production from reduced levels of RNase L KO cells to that 202 observed during WT cell infection ( Figure 3D ). DENV production, which was limited by 203