Following active infection, herpes viruses establish a latent infection in sensory and autonomic ganglia of the nervous system. The double-stranded DNA of the virus is incorporated into the cell physiology by infection of the nucleus of a nerve's cell body. HSV latency is static; no virus is produced; and is controlled by a number of viral genes, including latency-associated transcript.[70]
HSV-2 is contracted through forms of sexual contact with a person who has HSV-2. An estimated 20 percent of sexually active adults in the United States are infected with HSV-2, according to the American Academy of Dermatology (AAD). HSV-2 infections are spread through contact with a herpes sore. In contrast, most people get HSV-1 from an infected person who is asymptomatic, or does not have sores.
A 2004 study in the New England Journal of Medicine found that suppressive therapy decreases the risk of HSV-2 transmission from symptomatic, infected partners to uninfected partners by 48%. So “the risk of transmission is significantly reduced, but cannot be eliminated even with suppressive therapy,” Johnston explains, and she stresses that the virus can be passed along even without signs or symptoms.
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