During sexual intercourse, the virus enters the normal cells through direct contact between the normal human skin mucosal surface and the patient’s skin mucosal surface or secretions, and the virus multiplies and expands within the cells; this process, the acute infection phase, can be without any conscious symptoms. Local multiplication of the virus leads to infection of the sensory nerve endings, and then the virus runs through the sensory nerves to the neurons against the axons and enters the dorsal root ganglion, and enters the latent infection state after a brief replication (2-3 days). At this time, the infected cells do not die; the viral genes exist in a suppressed state within the infected cells, and cell survival and function are unaffected and can be maintained for years or even for life. Under the right conditions, such as trauma, menstruation and immunosuppression, the virus can be activated and released from the dorsal root ganglion, infecting and destroying skin or mucosal cells and forming ulcers. Since the virus is infected through intercellular infection and can be latent in the dorsal root ganglion, it can evade the body’s immune response to a large extent, thus causing recurrent lesions. The pattern of latent HSV infection may be that after HSV enters neurons, the expression of α genes with important transcriptional regulation is suppressed, and multiple stimuli can activate the latent viral genome to enter the replication cycle, which requires the participation of host transcription factors in addition to an increase in viral DNA copy number to fully activate the viral genome, while the ability of viral replication activation to lead to infection depends on The ability of viral replication to lead to infection depends on whether the strain has all the genes necessary for replication and whether the expression of these genes is adequate. The replication of DNA is a decisive factor in the activation of latent viruses.