Initial infection with the virus occurs during close contact between an infected person, currently shedding the virus, and a susceptible person. The virus gains entry into the host through breaks in the skin or the oral cavity’s mucous membranes. The viral envelope fuses with the host cell membrane, which initiates the HSV DNA’s shuttling into the nucleus. From there, the virus can replicate and spread to nearby dermal/epidermal cells and local neurons. A transient viremia can occur before the host immune response fully activates. Acantholysis (loss of intercellular connections) occurs in the skin, giving rise to the characteristic vesicles. Clusters of  vesicles can coalesce to form a large, painful ulcer. As the healing process begins, the ulcer will crust over and eventually scab. After resolution of symptoms, the virus establishes latency in a nerve, commonly the trigeminal ganglia. Reactivation leads to viral replication in the ganglia and infection of cells at the nerve’s dermal end, repeating the cycle of blister formation.15

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