CGAS and HIV infectious disease: The HSV-2's effect on HIV replication in DCs was not dependent on TLR2, TLR3, or IFI16, all three PRRs known to be activated by herpes virus (55), but rather on the activation of the cGAS-STING pathway and subsequent decreased protein levels of several key regulators of HIV infection, i.e., TREX1, SAMHD1, and ABOBEC3G, which could be due to proteolytic degradation.