Pathogenesis

Lesions begin with infection of a group of epithelial cells that are lysed following viral replication, creating small fluid-filled blisters or vesicles containing large numbers of infectious virions. Rupture of the vesicles produces painful ulcerations. Latency of the disease is incompletely understood. The viral DNA exists within nerve cells in a circular, non-infectious form during times when there are no symptoms. In this state, only a small portion of the HSV genome is transcribed. At times, however, the entire viral chromosome can be transcribed and complete infectious virions replicated. These reinfect the area supplied by the nerve and cause a recurrence. The mechanisms by which the latent infection is maintained or reactivated are not known in detail, but they probably depend on cellular immunity. ■ latent infections, p. 463 Genital herpes can pose a serious risk to newborn babies. If the mother has a primary infection near the time of delivery, the baby has about a one in three risk of acquiring the infection. The baby often dies from overwhelming infection or is permanently disabled by it. To prevent contact with the infected birth canal, these babies must be delivered by cesarian section. If the mother has recurrent disease, the risk to the baby is very low, presumably because transplacental anti-HSV antibody from the mother protects the baby, but physicians will often do a cesarian section to minimize the risk.

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