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

The copyright holder for this preprint (which was not peer-reviewed) is the author/funder. . https://doi.org/10.1101/852194 doi: bioRxiv preprint KO cells compared to both WT and OAS3 KO cells, but to a lesser degree than during 254 ZIKV infection ( Figure 4F) . Overall, absence of OAS3-dependent RNase L activity had a 255 greater impact on ZIKV genome localization and expression compared to that of DENV 256 and KUNV, which agrees with its minimal effects on DENV and KUNV RFs and viral titers. The copyright holder for this preprint (which was not peer-reviewed) is the author/funder. . https://doi.org/10.1101/852194 doi: bioRxiv preprint right panel). In RNase L KO cells, dsRNA was detectable, validating that absence of 277 dsRNA in WT cells was due to RNase L specifically and not from other antiviral responses 278 induced by pIC ( Figure 5B ). In OAS3 KO cells, pIC transfection before ZIKV infection 279 had no effect on dsRNA expression, further demonstrating that RNase L was not 280 activated in the absence of OAS3 (Figure 5C) . 281