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HSV-1 first binds to heparan sulfate on the cell surface, then to a secondary receptor such as nectin. The viral envelope fuses with the host plasma membrane, releasing the capsid and proteins into the cytoplasm. The viral DNA then enters the nucleus, where it circularizes and hijacks host machinery for replication.

Once in the nucleus, viral DNA circularizes and directs a coordinated cascade of immediate-early, early, and late gene expression. This process hijacks host machinery to replicate the viral genome and produce viral mRNA. These mRNAs are translated into viral proteins, which assemble to form nucleocapsids that eventually exit the nucleus.

After replicating in epithelial cells, HSV-1 enters sensory nerve cells and travels to the trigeminal ganglion, where it remains latent. Stress, fever, or immune suppression can trigger reactivation. The virus then travels back to the skin or mucosa, replicates, and causes recurrent lesions.

Transmission occurs through direct contact with infected secretions or mucosal surfaces. Transmission is likely during active lesions, though asymptomatic viral shedding can also transmit infection. Preventive measures include avoiding direct contact with active lesions, practicing good hygiene, and avoiding sharing personal items like lip balm or utensils.

HSV-1 infection is often recognized through characteristic orolabial lesions. Laboratory confirmation may involve polymerase chain reaction (PCR) testing, viral culture, or direct fluorescent antibody assays from lesion samples. Serologic testing for HSV-1 antibodies has limitations and is generally not used as the sole diagnostic approach.

HSV-1 is incurable, but antiviral agents such as acyclovir, valacyclovir, and famciclovir effectively reduce symptom severity and shorten outbreaks by targeting viral DNA polymerase. For recurrent episodes, topical agents like penciclovir or docosanol may be used, though oral therapy is generally more effective. Suppressive antiviral therapy may be considered for frequent recurrences.

HSV-1 is marked by painful skin lesions most commonly around the mouth and causes orolabial infection. In contrast, genital herpes typically affects the genital region. Both are caused by herpes simplex viruses and transmit through direct contact with infected secretions or mucosal surfaces, though transmission routes and affected anatomical sites differ.