A significant number of medical institutions place the incidence of oral herpes (HSV-1), which is commonly called cold sores, between 50 and 80 percent among the American population in the fifth decade of life. The overall HSV-1 seroprevalence is dropping a few points per decade in the US, as in all industrialized countries. Blacks and immigrants from undeveloped countries typically have HSV-1 rates in adolence that two or three times higher than Whites. As a result of lower HSV-1 seroprevalence, more Americans (westerners) are entering marriage/sexual activity/child bearing years seronegative for HSV-1. The Absence of antibody to HSV-1 from a prior oral HSV-1 infection leaves them susceptible to primary HSV-1 genital infections. This brings with it a serious risk of vertical transmission to the neonate if contracted in the third trimester, not allowing time for full seroconversion before childbirth. The seronegative mother without antibodies has up to a 57% chance of conveying the infection to her child, whereas a recurrent infection in a woman seropositive for both HSV-1 and HSV-2 is thought to be around 1-3%.
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. African Americans, people with multiple sexual partners, women, and those who become sexually active at a young age are all higher-risk populations for the transmission of HSV-2. [1][2][3][4] 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 mistaken for another condition. [2]
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 or 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 infects the trigeminal ganglia that provides sensation to the lips, lower mouth and neck; while HSV-2 often infects 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 their 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 (kissing, touching, and possibly from objects such as shared drinking glasses.[citation needed]) 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.
While both oral and genital herpes are characteristically "nuisance infections" that are not life-threatening, they can cause rare severe or fatal disease if they disseminate to the eyes or brain. This is a particular concern for newborns who might be infected by genital herpes during passage through the birth canal (the risk of this occurring is by far higher when the mother has a primary infection just prior to birth and lacks protective antibodies that would otherwise reduce viable virus shedding). HSV-1 genital herpes has been shown to be more infectious in primary episodes than HSV-2. Both oral and genital herpes infections have periods of active cold sore disease lasting 2-10 days and then remission when the cold sores disappear. The majority of cases however are asymptomatic, but asymptomatic shedding has been shown to occur. Over time, periods of remission generally increase in length, and the duration of cold sores decrease, until the person rarely has active disease. This is regulated by specific immunity developed by the patient against the virus. A previous HSV-1 infection tends to ameliorate the symptoms of a subsequent HSV-2 infection. The virus infection is, however, life-long and can be retriggered in some individuals by specific events, such as sunburn, ultraviolet light, wind, trauma, surgery, stress or other infections. Being that the virus is present but held in check by antibodies in an immunocompetent person, the weakening of the immune system in HIV or transplant patients can frequently triggers serious HSV infections such as keratitis in transplant patients.
The ways in which herpes simplex infections manifest themselves vary tremendously among individuals. The following are general descriptions of the courses outbreaks may take in the oral and genital regions.
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