Herpes (types 1 and 2) can be transmitted through skin to skin contact, kissing, sexual intercourse, and oral sex. The mucous membranes (mouth, nose, ears, throat, genitals, and anus) are most susceptible to infection with HSV. The cervix and urethra are also high target areas. Also susceptible are any areas that may be subject to abrasion, and warm, moist areas such as the upper thighs, underarms, hairline, lower back, perineum, scrotum, and buttocks - any areas when sweating is common.
Herpes is most easily passed through inoculation from active lesions. The virus may also spread during times when there are no symptoms, and from sites that are seemingly inactive. Most incidences of genital Herpes occur during sexual intercourse. There is, however, a significant percentage of genital herpes infections resulting from oral to genital sexual contact. Most of these oral to genital transmissions will be of the type 1 variety, although type 2 incidence is not uncommon. Many times the partner who carries the virus is not even aware of an outbreak. In most cases, however, close examination may reveal a history of some of the symptoms listed previously.
Inoculation and autoinoculation (self-infection) of genital Herpes occurs primarily through vigorous intercourse, masturbation, anal sex, and oral sex with an infected member. Herpes can be passed via the use of sexual stimulators such as vibrators.
Inoculation and autoinoculation can occur by transferring the virus from one part of the body to another, usually via touching a sore with a hand and then touching another susceptible area, such as the mouth or eyes. This complication is more common during a first episode because of higher amounts of virus present during that time. Herpes is also more likely to spread to compromised epithelial tissue - skin that has suffered cuts, abrasions, scrapes, etc.
In studies of transmission of genital Herpes in couples, the annual risk of transmission averaged 5 to 10% per year for those abstaining from sex during outbreaks. The risk of acquisition was much higher (16.9%) for women, but somewhat lower for those who already had HSV-1. There is some evidence that people who have HSV-1 are more resistant to the HSV-2. This should not be interpreted as immunity but rather as a higher resistance factor. The transmission rate was also lower for those who used condoms. The greater risk of acquisition for women may be due partly to anatomy, and partly because, generally, men tend to have more frequent outbreaks, while women tend to have more severe outbreaks. More frequent outbreaks means more times there is virus on the surface of the skin, and hence a greater the risk of transmission.
The best way to avoid transmission is to abstain from sexual activity during prodrome and outbreaks, and to use condoms the rest of the time. While consistent use of condoms (particularly in conjunction with nonoxynol-9, a spermicide that also disables HSV) affords some measure of protection, the nature of HSV is such that condoms may not cover the site of active virus, and therefore condoms are not a guarantee against transmission of the virus.
The risk of transmission for HSV-1 from the oral to the genital area is much higher than the risk of transmission of HSV-2 from the genital to the oral area. In addition, the recurrence and shedding rate for genital HSV-1 is much less than for HSV-2 - this is why getting a culture to determine the viral type can come in handy. And although HSV-2 can be transmitted to the mouth, because HSV-2 "prefers" the genitals, the recurrence rate of oral HSV-2 is statistically very low - about once every ten years.
Once infected, the Herpes virus stays in the body. After outbreak, the virus goes into "latency." While latent, HSV lives in a kind of state of suspended animation, in the nerve centers in the spine: genital HSV in the sacral nerve roots (ganglia) at the base of the spine, and oral-facial HSV in the trigeminal nerve roots at the base of the neck. When reactivated, HSV begins to replicate, and travels the nerve pathways to the surface of the skin.
Once infected with any type of Herpesvirus, the carrier remains capable of transmitting virus for the rest of their life even when showing no symptoms due to a process called viral shedding. Shedding means that the virus is active on the skin, and risk of transmission is high. HSV sheds at prodrome, during outbreaks, during healing periods after outbreaks, but also at random times where there may be no noticeable symptoms at all. This is called "subclinical shedding" or "asymptomatic shedding."
Asymptomatic Shedding is the release of the virus on the skin when there are no symptoms. These asymptomatic shedding episodes occur (according to studies) typically 3 to 10 days in the year, so although the risk is minimal it does exist, because one can't tell when those days are. During an episode of asymptomatic shedding, virus often sheds from several different sites in the area concurrently. And there is new research suggesting that shedding occurs more frequently than previously thought. In a recently published study, researchers found that half of the episodes of subclinical shedding of HSV occurred within seven days of a symptomatic recurrence. Asymptomatic shedding is not detectable by any accessible procedure. It should be noted that for the first 6 months to a year after a primary episode, shedding may occur much more frequently. The incidence of asymptomatic shedding is greatest during the first year or two after infection.
Shedding occurs randomly and sporadically and seems to some degree influenced by sites of infection and viral type, severity and frequency of outbreaks, though studies remain unclear. Thus, the more outbreaks one has, the more severe one's outbreaks are, the higher the incidence of shedding. HSV-2 seems to shed more often than HSV-1, particularly in genital infections. Medical experts believe asymptomatic shedding is responsible for most cases of transmission. Suppressive acyclovir therapy has been shown in some studies to reduce the rate of shedding by up to 95%.