RPA2 and infection: While inhibition of RPA32 phosphorylation by TDRL-505 (using the schematic illustrated in Fig 4D) was sufficient to shorten cellular replication forks monitored by IdU and CldU lengths (iRPA samples in Fig 4E,F), these defects on the host replication fork was not enhanced further in the presence of wtAAV2 infection (iRPA + wtAAV2 in Fig 4E,F).