Herpes simplex virus interference with immunity: Focus on dendritic cells

Herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) are highly prevalent in the human population. These viruses cause lifelong infections by establishing latency in neurons and undergo sporadic reactivations that promote recurrent disease and new infections. The success of HSVs in persisting in infected individuals is likely due to their multiple molecular determinants involved in escaping the host antiviral and immune responses. Importantly, HSVs infect and negatively modulate the function of dendritic cells (DCs), key immune cells that are involved in establishing effective and balanced immunity against viruses. Here, we review and discuss several molecular and cellular processes modulated by HSVs in DCs, such as autophagy, apoptosis, and the unfolded protein response. Given the central role of DCs in establishing optimal antiviral immunity, particular emphasis should be given to the outcome of the interactions occurring between HSVs and DCs.

Automated summary

HSV-1 and HSV-2 are highly prevalent in humans, causing lifelong infections by establishing latency in neurons and undergoing sporadic reactivations. These viruses possess molecular determinants that help them evade host antiviral and immune responses, including modulating the function of dendritic cells. The interactions between HSVs and DCs play a crucial role in determining optimal antiviral immunity.