You should stop having sexual contact as soon as you feel warning signs of an outbreak. Warning signs may include a burning, itching, or tingling feeling on the genitals or around the mouth. Do not have vaginal, anal, or oral sex — even with a condom — until seven days after the warning signs stop or the sore heals. The virus can spread from sores not covered by the condom. It can also spread in sweat or vaginal fluids to places the condom doesn't cover.
Laboratory testing is often used to confirm a diagnosis of genital herpes. Laboratory tests include culture of the virus, direct fluorescent antibody (DFA) studies to detect virus, skin biopsy, and polymerase chain reaction to test for presence of viral DNA. Although these procedures produce highly sensitive and specific diagnoses, their high costs and time constraints discourage their regular use in clinical practice.[39]
There are two types of herpes simplex virus, type 1 (HSV-1) and type 2 (HSV-2).[1] HSV-1 more commonly causes infections around the mouth while HSV-2 more commonly causes genital infections.[2] They are transmitted by direct contact with body fluids or lesions of an infected individual.[1] Transmission may still occur when symptoms are not present.[1] Genital herpes is classified as a sexually transmitted infection.[1] It may be spread to an infant during childbirth.[1] After infection, the viruses are transported along sensory nerves to the nerve cell bodies, where they reside lifelong.[2] Causes of recurrence may include: decreased immune function, stress, and sunlight exposure.[2][3] Oral and genital herpes is usually diagnosed based on the presenting symptoms.[2] The diagnosis may be confirmed by viral culture or detecting herpes DNA in fluid from blisters.[1] Testing the blood for antibodies against the virus can confirm a previous infection but will be negative in new infections.[1]
In all cases, HSV is never removed from the body by the immune system. Following a primary infection, the virus enters the nerves at the site of primary infection, migrates to the cell body of the neuron, and becomes latent in the ganglion.[14] As a result of primary infection, the body produces antibodies to the particular type of HSV involved, preventing a subsequent infection of that type at a different site. In HSV-1-infected individuals, seroconversion after an oral infection prevents additional HSV-1 infections such as whitlow, genital herpes, and herpes of the eye. Prior HSV-1 seroconversion seems to reduce the symptoms of a later HSV-2 infection, although HSV-2 can still be contracted.
The causes of reactivation are uncertain, but several potential triggers have been documented. A 2009 study showed the protein VP16 plays a key role in reactivation of the dormant virus.[71] Changes in the immune system during menstruation may play a role in HSV-1 reactivation.[72][73] Concurrent infections, such as viral upper respiratory tract infection or other febrile diseases, can cause outbreaks. Reactivation due to other infections is the likely source of the historic terms 'cold sore' and 'fever blister'.
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.
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