ABSTRACT
Human herpesviruses are enveloped viruses with double-stranded linear DNA genomes highly prevalent in the human population. These viruses are subdivided into three subfamilies, namely alphaherpesvirinae (herpes simplex virus type 1, HSV-1; herpes simplex virus type 2, HSV-2; and varicella-zoster virus, VZV), betaherpesvirinae (human cytomegalovirus, HCMV; human herpesvirus 6, HHV-6; and human herpesvirus 7, HHV-7) and gammaherpesvirinae (Epstein-Barr virus, EBV; and Kaposi's sarcoma-associated herpesvirus, KSHV). Besides encoding numerous molecular determinants to evade the host antiviral responses, these viruses also modulate cellular metabolic processes to promote their replication. Here, we review and discuss existing studies describing an interplay between carbohydrate metabolism and the replication cycle of herpesviruses, altogether highlighting potentially new molecular targets based on these interactions that could be used to block herpesvirus infections.
ABSTRACT
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.