Evasion of Early Antiviral Responses by Herpes Simplex Viruses

Figure 2

HSVs interfere with cell viability. HSVs encode determinants that modulate cell viability. (a) Within epithelial cells, HSV can extend the survival of cells by blocking apoptosis thanks to viral proteins, such as gD, gJ, UL14, ICP0, and US3. Tetherin, a host antiviral factor involved in blocking virus release from the surface of infected cells, is blocked by HSV vhs. Contrarily, fibroblasts display necrosis upon infection with HSV, which would be mediated by ICP6. (b) Dendritic cells display apoptosis early after infection with HSVs by unknown viral determinants. The autophagosome, which mediates virus control in these and other cells, such as neurons, is inhibited by the viral protein γ34.5. HSV also induces apoptosis of NK cells, albeit through Fas/FasL interactions between these cells and HSV-infected macrophages.

(a)

(b)