The herpes virus is probably the most well-known virus after influenza (the flu) or the common cold. What most people don’t know is that this nasty little virus can take several different forms, eight to be exact. The most common form of the herpes virus is chicken pox, which is called varicella-zoster. Herpes simplex is the sexually transmitted version of the virus.
There are two types of herpes simplex virus, type 1 (HSV-1) and type 2 (HSV-2). HSV-1 more commonly causes infections around the mouth while HSV-2 more commonly causes genital infections. They are transmitted by direct contact with body fluids or lesions of an infected individual. Transmission may still occur when symptoms are not present. Genital herpes is classified as a sexually transmitted infection. It may be spread to an infant during childbirth. After infection, the viruses are transported along sensory nerves to the nerve cell bodies, where they reside lifelong. Causes of recurrence may include: decreased immune function, stress, and sunlight exposure. Oral and genital herpes is usually diagnosed based on the presenting symptoms. The diagnosis may be confirmed by viral culture or detecting herpes DNA in fluid from blisters. Testing the blood for antibodies against the virus can confirm a previous infection but will be negative in new infections.
Herpes, whether on the mouth or genitals, is caused by a family of over 70 related viruses. These viral infections cause small, fluid-filled blisters to develop on the skin and mucous membranes. There are actually eight different types of herpes simplex viruses that both children and adults can acquire, but two are by far the most common: HSV-1 and HSV-2.
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. Changes in the immune system during menstruation may play a role in HSV-1 reactivation. 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'.
Not every person with a herpes infection actually experiences breakouts of cold sores throughout his or her lifetime or even after initially becoming infected. How often someone has a herpes cold sore outbreak, how severe the outbreaks are, how contagious someone is after infection and how long the sores take to heal all depend on someone’s individual immune response.
Herpes antiviral therapy began in the early 1960s with the experimental use of medications that interfered with viral replication called deoxyribonucleic acid (DNA) inhibitors. The original use was against normally fatal or debilitating illnesses such as adult encephalitis, keratitis, in immunocompromised (transplant) patients, or disseminated herpes zoster. The original compounds used were 5-iodo-2'-deoxyuridine, AKA idoxuridine, IUdR, or(IDU) and 1-β-D-arabinofuranosylcytosine or ara-C, later marketed under the name cytosar or cytarabine. The usage expanded to include topical treatment of herpes simplex, zoster, and varicella. Some trials combined different antivirals with differing results. The introduction of 9-β-D-arabinofuranosyladenine, (ara-A or vidarabine), considerably less toxic than ara-C, in the mid-1970s, heralded the way for the beginning of regular neonatal antiviral treatment. Vidarabine was the first systemically administered antiviral medication with activity against HSV for which therapeutic efficacy outweighed toxicity for the management of life-threatening HSV disease. Intravenous vidarabine was licensed for use by the U.S. Food and Drug Administration in 1977. Other experimental antivirals of that period included: heparin, trifluorothymidine (TFT), Ribivarin, interferon, Virazole, and 5-methoxymethyl-2'-deoxyuridine (MMUdR). The introduction of 9-(2-hydroxyethoxymethyl)guanine, AKA aciclovir, in the late 1970s raised antiviral treatment another notch and led to vidarabine vs. aciclovir trials in the late 1980s. The lower toxicity and ease of administration over vidarabine has led to aciclovir becoming the drug of choice for herpes treatment after it was licensed by the FDA in 1998. Another advantage in the treatment of neonatal herpes included greater reductions in mortality and morbidity with increased dosages, which did not occur when compared with increased dosages of vidarabine. However, aciclovir seems to inhibit antibody response, and newborns on aciclovir antiviral treatment experienced a slower rise in antibody titer than those on vidarabine.
Do everything possible to prevent spreading it to other people. The virus cannot live long when it is not in contact with the skin, so door handles and towels are not likely to spread it. Do not share your personal belongings, like toothbrushes and combs. Wash your hands with soap and water often, and immediately if you touch the sores. This is important so as to minimize the chance of getting ocular herpes (herpes infection of the eye) which is a serious infection. Be especially careful around infants because their immune systems may not be fully developed. Little children often express affection with sloppy wet kisses. This is a common way to spread the herpes virus within the family.
There’s quite a variety, in short. And while genital herpes certainly can and does cause these signs of infection literally on the genitals (the penis or the vulva) it also can produce signs of infection nearby. Herpes sores on or between the buttocks are common (and sometimes slow to heal), as are lesions on the thigh. Herpes can bring about what feels like a tiny fissure around the anus, something easily confused with hemorrhoids. So remember: recurring signs and symptoms in the genital or anal area could well be herpes lesions.
Oral herpes is a viral infection mainly of the mouth area and lips caused by a specific type of the herpes simplex virus. Oral herpes is also termed HSV-1, type 1 herpes simplex virus, or herpes labialis. The virus causes painful sores on the upper and lower lips, gums, tongue, roof of the mouth, inside the cheeks or nose, and sometimes on the face, chin, and neck. Infrequently, it may cause genital lesions. It also can cause symptoms such as swollen lymph nodes, fever, and muscle aches. People commonly refer to the infection as "cold sores."
“Someone having HSV doesn't mean that they were reckless or irresponsible with their sex life,” says Sara, age 30. “I used condoms with all my partners, and I still caught it.” For Jamie, who contracted herpes from her husband three years into their monogamous relationship, he was her first and only sexual partner. And she says that he contracted it from one of his very first sexual encounters. No matter how and why someone contracted the virus, it doesn't erase their humanity and right to respect.
Antibodies that develop following an initial infection with a type of HSV prevents reinfection with the same virus type—a person with a history of orofacial infection caused by HSV-1 cannot contract herpes whitlow or a genital infection caused by HSV-1. In a monogamous couple, a seronegative female runs a greater than 30% per year risk of contracting an HSV infection from a seropositive male partner. If an oral HSV-1 infection is contracted first, seroconversion will have occurred after 6 weeks to provide protective antibodies against a future genital HSV-1 infection. Herpes simplex is a double-stranded DNA virus.
If you are pregnant and have genital herpes, it is very important for you to go to prenatal care visits. Tell your doctor if you have ever had symptoms of, or have been diagnosed with, genital herpes. Also tell your doctor if you have ever been exposed to genital herpes. There is some research that suggests that genital herpes infection may lead to miscarriage, or could make it more likely for you to deliver your baby too early.