Abstract
Etiology, transmission and protection: Herpes simplex virus-2 (HSV-2) is a leading cause of sexually transmitted infections with recurring manifestations throughout the lifetime of infected hosts. Currently no effective vaccines or prophylactics exist that provide complete protection or immunity from the virus, which is endemic throughout the world. Pathology/Symptomatology: Primary and recurrent infections result in lesions and inflammation around the genital area and the latter accounts for majority of genital herpes instances. Immunocompromised patients including neonates are susceptible to additional systemic infections including debilitating consequences of nervous system inflammation. Epidemiology, incidence and prevalence: More than 500 million people are infected worldwide and most reported cases involve the age groups between 16-40 years, which coincides with an increase in sexual activity among this age group. While these numbers are an estimate, the actual numbers may be underestimated as many people are asymptomatic or do not report the symptoms. Treatment and curability: Currently prescribed medications, mostly nucleoside analogs, only reduce the symptoms caused by an active infection, but do not eliminate the virus or reduce latency. Therefore, no cure exists against genital herpes and infected patients suffer from periodic recurrences of disease symptoms for their entire lives. Molecular mechanisms of infection: The last few decades have generated many new advances in our understanding of the mechanisms that drive HSV infection. The viral entry receptors such as nectin-1 and HVEM have been identified, cytoskeletal signaling and membrane structures such as filopodia have been directly implicated in viral entry, host motor proteins and their viral ligands have been shown to facilitate capsid transport and many host and HSV proteins have been identified that help with viral replication and pathogenesis. New understanding has emerged on the role of autophagy and other innate immune mechanisms that are subverted to enhance HSV pathogenesis. This review summarizes our current understanding of HSV-2 and associated diseases and available or upcoming new treatments.
Highlights
Genital herpes is one of the most common, persistent and highly infectious sexually transmitted viral infections mostly caused by herpes simplex virus-2 (HSV-2) and in many emerging first time cases, by HSV-1 [1]
The viral entry receptors such as nectin-1 and herpes virus entry mediator (HVEM) have been identified, cytoskeletal signaling and membrane structures such as filopodia have been directly implicated in viral entry, host motor proteins and their viral ligands have been shown to facilitate capsid transport and many host and HSV proteins have been identified that help with viral replication and pathogenesis
This review provides an insight into the epidemiology, pathology, our current understanding of the molecular mechanisms of infection and the currently available and upcoming treatments for genital herpes
Summary
Genital herpes is one of the most common, persistent and highly infectious sexually transmitted viral infections mostly caused by herpes simplex virus-2 (HSV-2) and in many emerging first time cases, by HSV-1 [1]. Viral particles were shown to surf along the filopodia and the formation of filopodial structures increased upon HSV infection, possibly due to activation of Rho GTPase signaling during virus attachment to cells. An initial absence of IgG antibodies specific for gG and subsequent development of such antibodies after 12 weeks confirms new HSV infection Clinicians recommend this method to diagnose genital herpes when there are no lesions or the above mentioned detection tests do not provide substantial results. A study showed the effect of a synthetic 3-OS HS specific peptide: G2 in blocking HSV-2 infections in human cervical (HeLa) cell lines This peptide significantly blocked the entry and thereby the spread of the virus [130] and a D-enantiomer of this peptide exhibits higher stability and more promise in inhibiting HSV infection [131]. A study developed a peptide based vaccine: HerpV, which generates CD4+ and CD8+ responses when subjected to HSV-2 challenge [140, 141]
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