Evasion of Early Antiviral Responses by Herpes Simplex Viruses

Figure 1

HSVs interfere with host detection of viral determinants. Immune and nonimmune cells express an array of pathogen recognition receptors intended to detect microbes, which ultimately lead to NF-κB and IRF translocation into the nucleus and secretion of antiviral molecules, such as interferons and cytokines. A: Host cells can sense HSV determinants through TLR2, although the specific viral elements detected by this receptor are currently unknown. Intracellular signaling through TLR2 can occur with the help of integrin -binding after this receptor binds with the HSV complex gH/gL. B: Alternatively, integrin can signal intracellularly on its own after gH/gL binding. This process can be interfered by ICP0 C: TLR3, D: TLR7, and E: TLR9 engagement by activating ligands, such as polyI:C, imiquimod (IM), and CpG-ODN, respectively, have been shown to play favorable roles against HSV infection by inducing activating pathways within cells that lead to the secretion of antiviral molecules. F: Nucleic acids generated during HSV infection can also be detected by host intracellular sensors, such as DAI, cGAS, and IFI16. G: The RIG-1/MDA5 complex can also detect virus-derived nucleic acids; however its function is blocked by viral vhs. H: Finally, the inflammasome is activated by HSV determinants, although HSV ICP0 can counteract its activity and negatively modulate its function.