Dr. Charles "Pat" Davis, MD, PhD, is a board certified Emergency Medicine doctor who currently practices as a consultant and staff member for hospitals. He has a PhD in Microbiology (UT at Austin), and the MD (Univ. Texas Medical Branch, Galveston). He is a Clinical Professor (retired) in the Division of Emergency Medicine, UT Health Science Center at San Antonio, and has been the Chief of Emergency Medicine at UT Medical Branch and at UTHSCSA with over 250 publications.
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.[citation needed] 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.[37] 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.[citation needed] Herpes simplex is a double-stranded DNA virus.[38]
An important source of support is the National Herpes Resource Center which arose from the work of the American Sexual Health Association (ASHA).[113] The ASHA was created in 1914 to in response to the increase in sexually transmitted diseases that had spread during World War I.[114] During the 1970s, there was an increase in sexually transmitted diseases. One of the diseases that increased dramatically was genital herpes. In response, ASHA created the National Herpes Resource Center in 1979. The HRC was designed to meet the growing need for education and awareness about the virus. One of the projects of The Herpes Resource Center (HRC) was to create a network of local support (HELP) groups. The goal of these HELP groups was to provide a safe, confidential environment where participants can get accurate information and share experiences, fears, and feelings with others who are concerned about herpes.[115][116]
Worldwide rates of either HSV-1 or HSV-2 are between 60% and 95% in adults.[4] HSV-1 is usually acquired during childhood.[1] Rates of both increase as people age.[4] Rates of HSV-1 are between 70% and 80% in populations of low socioeconomic status and 40% to 60% in populations of improved socioeconomic status.[4] An estimated 536 million people worldwide (16% of the population) were infected with HSV-2 as of 2003 with greater rates among women and those in the developing world.[10] Most people with HSV-2 do not realize that they are infected.[1] The name is from Greek: ἕρπης herpēs which means "to creep", referring to spreading blisters.[11] The name does not refer to latency.[12]
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'.

It should not be confused with conditions caused by other viruses in the herpesviridae family such as herpes zoster, which is caused by varicella zoster virus. The differential diagnosis includes hand, foot and mouth disease due to similar lesions on the skin. Lymphangioma circumscriptum and dermatitis herpetiformis may also have a similar appearance.


The herpes simplex virus is probably the most well-known virus of the herpes family, and it is just as contagious. Herpes simplex infects epithelial cells and remains latent in neurons. HSV-1 causes recurrent oropharyngeal lesions, commonly known as “fever blisters" or "cold sores.” It is also the primary cause of sporadic encephalitis (inflammation of the brain), gingivostomatitis (inflammation of the gums and mucous lining of the mouth), and keratoconjunctivitis (severe dryness of the eye that involves the cornea) and dendritic corneal ulcers (also called HSV keratitis) in which the cornea becomes affected by herpetic lesions that look like the dendrites of neurons in the brain.
Dr. Charles "Pat" Davis, MD, PhD, is a board certified Emergency Medicine doctor who currently practices as a consultant and staff member for hospitals. He has a PhD in Microbiology (UT at Austin), and the MD (Univ. Texas Medical Branch, Galveston). He is a Clinical Professor (retired) in the Division of Emergency Medicine, UT Health Science Center at San Antonio, and has been the Chief of Emergency Medicine at UT Medical Branch and at UTHSCSA with over 250 publications.
A scary finding is that more cases of genital herpes than ever before are now being caused by HSV-1 (the type most people assume only causes mouth sores), and about 85 percent of people with genital herpes don’t even know it. (7) Studies show that about 50 percent of the new genital herpes infections in young adults are due to HSV-1 and about 40 percent in older adults. The fact that most people don’t ever find out they’re infected is one of the reasons that transmission rates are steadily climbing.
Herpes simplex viruses -- more commonly known as herpes -- are categorized into two types: herpes type 1 (HSV-1, or oral herpes) and herpes type 2 (HSV-2, or genital herpes). Most commonly, herpes type 1 causes sores around the mouth and lips (sometimes called fever blisters or cold sores). HSV-1 can cause genital herpes, but most cases of genital herpes are caused by herpes type 2. In HSV-2, the infected person may have sores around the genitals or rectum. Although HSV-2 sores may occur in other locations, these sores usually are found below the waist.
^ Xu, Fujie; Fujie Xu; Maya R. Sternberg; Benny J. Kottiri; Geraldine M. McQuillan; Francis K. Lee; Andre J. Nahmias; Stuart M. Berman; Lauri E. Markowitz (2006-10-23). "Trends in Herpes Simplex Virus Type 1 and Type 2 Seroprevalence in the United States". JAMA. 296 (8): 964–73. doi:10.1001/jama.296.8.964. PMID 16926356. Archived from the original on 2010-04-24.
HSV asymptomatic shedding occurs at some time in most individuals infected with herpes. It can occur more than a week before or after a symptomatic recurrence in 50% of cases.[33] Virus enters into susceptible cells by entry receptors[34] such as nectin-1, HVEM and 3-O sulfated heparan sulfate.[35] Infected people who show no visible symptoms may still shed and transmit viruses through their skin; asymptomatic shedding may represent the most common form of HSV-2 transmission.[33] Asymptomatic shedding is more frequent within the first 12 months of acquiring HSV. Concurrent infection with HIV increases the frequency and duration of asymptomatic shedding.[36] Some individuals may have much lower patterns of shedding, but evidence supporting this is not fully verified; no significant differences are seen in the frequency of asymptomatic shedding when comparing persons with one to 12 annual recurrences to those with no recurrences.[33]
In order to diagnose herpes, a health care provider can swab an area of visibly active herpes infection or, if symptoms aren’t active, a blood test can be given that measures the number of herpes antibodies present in the body. The antibodies don’t indicate herpes itself, but rather show the immune system’s response to the presence of the virus in the body. It’s important to note that sometimes a swab can give false negative results since herpes lesions need to be large enough to yield enough detectable virus and if the outbreak is already healing it also may not be detected in a swab. (6)
Evidence is insufficient to support use of many of these compounds, including echinacea, eleuthero, L-lysine, zinc, monolaurin bee products, and aloe vera.[68] While a number of small studies show possible benefit from monolaurin, L-lysine, aspirin, lemon balm, topical zinc, or licorice root cream in treatment, these preliminary studies have not been confirmed by higher-quality randomized controlled studies.[69]

A person may show symptoms within days after contracting genital herpes, or it may take weeks, months, or years. Some people may have a severe outbreak within days after contracting the virus while others may have a first outbreak so mild that they do not notice it. Because of these possibilities, it can be difficult for people to know when and from whom they may have contracted the virus.
The “classic” symptoms that most people associate with genital herpes are sores, vesicles, or ulcers – all of which can also be called “lesions.” (The scientific literature on herpes uses the term “lesion” to describe any break or irregularity in the skin.) These classic lesions of genital herpes often resemble small pimples or blisters that eventually crust over and finally scab like a small cut. These lesions may take anywhere from two to four weeks to heal fully.
The herpes virus can be shed from an infected person even when there are no lesions visible. So caution is important. Some may wish to take the daily prophylactic oral drug Valtrex (an antiviral oral medication) to help cut down on shedding. Herpes can also be transmitted on any skin: fingers, lips, etc. Depending on sexual practices, herpes simplex can be transferred to genitals and or buttocks from the lips of someone who has fever blisters. Honesty between partners is very important so these issues can be discussed openly.
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