However, asymptomatic carriers of the HSV-2 virus are still contagious. In many infections, the first symptom people will have of their own infections is the horizontal transmission to a sexual partner or the vertical transmission of neonatal herpes to a newborn at term. Since most asymptomatic individuals are unaware of their infection, they are considered at high risk for spreading HSV.[47]
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^ Nasser M, Fedorowicz Z, Khoshnevisan MH, Shahiri Tabarestani M (October 2008). "Acyclovir for treating primary herpetic gingivostomatitis". The Cochrane Database of Systematic Reviews (4): CD006700. doi:10.1002/14651858.CD006700.pub2. PMID 18843726. (Retracted, see doi:10.1002/14651858.cd006700.pub3. If this is an intentional citation to a retracted paper, please replace {{Retracted}} with {{Retracted|intentional=yes}}.)
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]
Although it's rare, pregnant women can pass on the herpes infection to their child. This can result in a serious and sometimes deadly infection in the baby. That's why taking steps to prevent an outbreak at time of delivery is recommended starting at 34 weeks into the pregnancy. If you have signs of an active viral infection when it's time to deliver, your doctor will likely recommend a cesarean section for delivery.
Once a person is infected, there are no symptoms for anywhere between 2 days to 2 weeks. This is known as the incubation period and is the time during which the virus multiplies profusely. The first symptoms that are seen are the small fluid-filled blisters known as vesicles. This arises as the virus starts destroying cells at the site and causes intense localized inflammation. These small vesicles or sometimes the larger bullae may either burst resulting in ulcer or heal completely with no scarring. The virus may also travel from the site of infection and “hides” by the sensory dorsal root. Here it remains latent until is it is reactivated.
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,[92] keratitis,[93] in immunocompromised (transplant) patients,[94] or disseminated herpes zoster.[95] The original compounds used were 5-iodo-2'-deoxyuridine, AKA idoxuridine, IUdR, or(IDU) and 1-β-D-arabinofuranosylcytosine or ara-C,[96] later marketed under the name cytosar or cytarabine. The usage expanded to include topical treatment of herpes simplex,[97] zoster, and varicella.[98] Some trials combined different antivirals with differing results.[92] 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,[99] trifluorothymidine (TFT),[100] Ribivarin,[101] interferon,[102] Virazole,[103] and 5-methoxymethyl-2'-deoxyuridine (MMUdR).[104] The introduction of 9-(2-hydroxyethoxymethyl)guanine, AKA aciclovir, in the late 1970s[105] raised antiviral treatment another notch and led to vidarabine vs. aciclovir trials in the late 1980s.[106] 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.[107] 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.[107] However, aciclovir seems to inhibit antibody response, and newborns on aciclovir antiviral treatment experienced a slower rise in antibody titer than those on vidarabine.[107]
Oral herpes is also known commonly as cold sores and fever blisters but is different entity from oral canker sores although canker sores may sometimes be associated with HSV infection. Canker sores occur solely inside the mouth. Oral herpes occurs inside and around the mouth. Most of the time HSV-1 causes mouth symptoms and in a minority of cases it may also be responsible for genital symptoms. The opposite is true for HSV-2 – it causes genital symptoms in the majority of cases while only a few cases of HSV-2 infection will result in mouth symptoms. HSV-1 infection may be seen in all ages, including children, but when genital herpes is seen in children, sexual abuse needs to be a consideration.
Human herpes virus 1 (HHV1) is also known as herpes simplex virus 1 (HSV1). It is typically the cause of cold sores around the mouth. HHV1 can also lead to infection in the genital area causing genital herpes usually through oral-genital contact, such as during oral sex. HHV1 infections are contagious and are usually spread from skin-to-skin contact with an infected person through small breaks in the skin or mucous membrane. The HHV1 virus is more likely to be spread through things like sharing eating utensils, razors, and towels from a person who has an active lesion.
EYES AND VISIONEARS, NOSE AND THROATSKIN, HAIR, NAILSHEART AND VESSELSKIDNEYS AND URINARY TRACTBLOOD AND IMMUNITYLIVER AND GALLBLADDERLUNGS AND AIRWAYSUPPER AND LOWER LIMBWOMEN’S HEALTH AND PREGNANCYWOMEN’S HEALTHKIDS HEALTHMEN’S HEALTHABCD – FIRST AID: INJURIES, POISONINGNEWBORNS BABIESHORMONES AND METABOLISMMEDICATION, SUPPLEMENTSMEDICAL TERMINOLOGYNUTRITIONSURGERY AND OTHER PROCEDURES
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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