The incidence of genital herpes (HSV-2) in the US is estimated to be between 25 and 30 percent or about one in four adults. "Although African Americans are more likely to test positively for HSV-2, Caucasians have a higher risk for active genital symptoms, and over the past few years the greatest increase in HSV-2 has been observed in white adolescents." People with multiple sexual partners and those who become sexually active at a young age are also higher-risk populations for the transmission of HSV-2. According to the American Social Health Association (ASHA), most infected people (up to 90%) don’t know they are infected because their symptoms are too mild to notice or are mistaken for another condition. Several estimates suggest that by 2025 up to 40% of all men and half of all women could be infected with genital herpes.
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Herpes simplex 1 and 2 viruses are similar in that they are both transmitted by direct contact and can sometimes cause intensely painful fluid-filled blisters, containing millions of infectious virus particles. The primary difference between the two infections is the principal site of infection—mucous membranes of the lips and nearby oro-facial skin for HSV-1, and the genital skin for HSV-2. After initial infection, these viruses both travel to sensory nerves, where they reside as life-long, latent viruses. HSV-1 often lies dormant in the trigeminal ganglia that provides sensation to the lips, lower mouth and neck; while HSV-2 often resides in the sacral ganglia supplying sensation to the pelvic area including the genitals, perineum and upper legs. When the viruses reactivate to cause symptomatic disease, they travel back to the respective skin areas served by these nerves, leading to the different (oral vs. genital) distributions of cold sores.
Both HSV-1 and HSV-2 are transmitted by contact with a herpetic sore. Transmission of these two viruses can be more complicated in that both HSV-1 and HSV-2 are shed (to a much lesser extent) from persons without active sores.
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