Current Thinking on Genital Herpes

Annika M. Hofstetter; Susan L. Rosenthal; Lawrence R. Stanberry

Disclosures

Curr Opin Infect Dis. 2014;27(1):75-83. 

In This Article

Primary Infection and Latency

A broad understanding of the pathogenesis of genital herpes infection and disease is necessary for advancing prevention and treatment strategies. Following skin–skin or skin–mucosa contact, HSV enters epithelial cells in the mid-to-basal epidermis, where it replicates and spreads to adjacent cells. HSV is then transported via sensory neuronal axons to the neuronal cell bodies of dorsal root ganglia,[36,37] where it again replicates and spreads to neighbouring neurons. Thereafter, virus either establishes latent infection or is transported back to mucocutaneous sites where it is released and replicates, potentially leading to cell lysis and the characteristic vesicular and/or ulcerative lesions of primary genital herpes.[38,39] Recent data demonstrate that most primary infections (74% of HSV-1; 63% of HSV-2) are asymptomatic.[33]

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