Immune evasion by herpes simplex viruses

Abstract

Herpes simplex viruses and humans have co-existed for tens of thousands of years. This long relationship has translated into the evolution and selection of viral determinants to evade the host immune response and reciprocally the evolution and selection of host immune components for limiting virus infection and damage. Currently there are no vaccines available to avoid infection with these viruses or therapies to cure them. Herpes simplex viruses are neurotropic and reside latently in neurons at the trigeminal and dorsal root ganglia, occasionally reactivating. Most viral recurrences are subclinical and thus, unnoticed. Here, we discuss the initial steps of infection by herpes simplex viruses and the molecular mechanisms they have developed to evade innate and adaptive immunity. A better understanding of the molecular mechanisms evolved by these viruses to evade host immunity should help us envision novel vaccine strategies and therapies that limit infection and dissemination. Keywords. Author Keywords:Genital infection; innate immune evasion; adaptive immune evasion; latency; reactivation . KeyWords Plus:DOUBLE-STRANDED-RNA; SEXUALLY-TRANSMITTED-DISEASES; DEPENDENT PROTEIN-KINASE; RECURRENT GENITAL HERPES; VARICELLA-ZOSTER-VIRUS; HUMAN DENDRITIC CELLS; NATURAL-KILLER-CELLS; NF-KAPPA-B; T-CELLS; GLYCOPROTEIN-D