Herpes of the mouth is a viral infection. The virus HSV-1 may be transmitted by droplet spread – direct contact with saliva or even respiratory droplets. These droplets must make contact with broken skin or the mucous membranes in order to infect a person. The method of spread can involve kissing an infected person or even through touch. It can also be spread through the use of contaminated kitchen utensils. Sexual contact accounts for a small number of cases of HSV-1. Nevertheless it is a consideration when genital lesions are present. HSV-2 on the other hand is usually transmitted through sexual contact.

Both HSV-1 and HSV-2 infections are acquired from direct contact with someone who carries the virus. The infectious secretions that pass on HSV-1 or HSV-2 live on oral, genital or anal mucosal surfaces. They’re passed through skin-to-skin transmission, and any form of direct contact with sores on the mouth, buttocks or genitals can cause the virus to be passed.


Transmission of HSV-1 occurs by direct exposure to saliva or droplets formed in the breath of infected individuals. In addition, skin contact with the lesions on an infected individual can spread the disease to another individual. Although close personal contact is usually required for transmission of the virus, it is possible to transmit HSV-1 when people share toothbrushes, drinking glasses, or eating utensils.
As of 2017, there is not currently a herpes vaccine available to prevent HSV-1 or HSV-2. (There is a vaccine available for another virus, herpes zoster; however, despite the similar name, it actually refers to the shingles virus. And, in fact, shingles occurs due to the reactivation of yet another virus, varicella zoster, which causes chicken pox.)

These drugs may stop viral replication in the skin but do not eliminate HSV from the body or prevent later outbreaks (HSV reactivation). These drugs are used more frequently with HSV-2 infections. Most investigators suggest consulting an infectious-disease expert when HSV-infected people need hospitalization. Research findings suggest laser treatments may speed healing and lengthen the time before any sores reappear.
Herpes infection can be passed from you to your unborn child before birth but is more commonly passed to your infant during delivery. This can lead to a potentially deadly infection in your baby (called neonatal herpes). It is important that you avoid getting herpes during pregnancy. If you are pregnant and have genital herpes, you may be offered anti-herpes medicine towards the end of your pregnancy. This medicine may reduce your risk of having signs or symptoms of genital herpes at the time of delivery. At the time of delivery, your doctor should carefully examine you for herpes sores. If you have herpes symptoms at delivery, a ‘C-section’ is usually performed.
Neonatal herpes simplex is a HSV infection in an infant. It is a rare but serious condition, usually caused by vertical transmission of HSV-1 or -2) from mother to newborn. During immunodeficiency, herpes simplex can cause unusual lesions in the skin. One of the most striking is the appearance of clean linear erosions in skin creases, with the appearance of a knife cut.[20] Herpetic sycosis is a recurrent or initial herpes simplex infection affecting primarily the hair follicles.[21]:369 Eczema herpeticum is an infection with herpesvirus in patients with chronic atopic dermatitis may result in spread of herpes simples throughout the eczematous areas.[21]:373
Stage 3 -- Recurrence: When people encounter certain stresses (also termed triggers), emotional or physical, the virus may reactivate and cause new sores and symptoms. The following factors may contribute to or trigger recurrence: stress, illness, ultraviolet light (UV rays including sunshine), fever, fatigue, hormonal changes (for example, menstruation), immune depression, and trauma to a site or a nerve region where previous HSV infection occurred.
Oral herpes (HSV-1) infection (or exposure without noticeable infection) is common. About 65% of the U.S. population has detectable antibodies to HSV-1 by age 40. This article will focus on HSV-1, or oral herpes, not on HSV-2, also commonly known as genital herpes. Genital herpes is considered to be a sexually transmitted disease (STD). In addition, HSV-2 virus should not be confused with human papillomavirus (HPV), the cause of genital warts, and some cervical and other cancer types.

Primary orofacial herpes is readily identified by examination of persons with no previous history of lesions and contact with an individual with known HSV infection. The appearance and distribution of sores is typically presents as multiple, round, superficial oral ulcers, accompanied by acute gingivitis.[39] Adults with atypical presentation are more difficult to diagnose. Prodromal symptoms that occur before the appearance of herpetic lesions help differentiate HSV symptoms from the similar symptoms of other disorders, such as allergic stomatitis. When lesions do not appear inside the mouth, primary orofacial herpes is sometimes mistaken for impetigo, a bacterial infection. Common mouth ulcers (aphthous ulcer) also resemble intraoral herpes, but do not present a vesicular stage.[39]
However, there is much more to the herpes virus than just chicken pox or genital herpes. For instance, after an active infection, the virus is shed (eliminated) in the urine and feces for up to several months (sometimes years in the case of the cytomegalovirus) after the active infection has resolved. This means the infected person is still contagious, which is what makes this virus so contagious. It can easily be transferred when the patient is asymptomatic.

When a herpes outbreak occurs, you can expect cold sores to take about 10–14 days to heal on average. During this time period, the virus is considered to be active, and you should be very careful to avoid direct contact between a sore and someone else. If after trying the natural remedies for herpes described above you still experience frequent recurrences, talk to your doctor for how to get rid of herpes symptoms. Sometimes immunity is suppressed due to another infection or virus, or even as a side effect of taking some medications, so be sure to rule these causes out.
Primary Infection: This is the first stage wherein the contagion reproduces upon entering from the mucous membrane or skin. Typical symptom is the appearance of oral lesions which may not be present initially resulting in an asymptotic infection. In this case due to lack of symptoms one will be unaware of the presence of an infection. The sores usually takes 21 days to form and become visible, then the blisters will persist up to 10 days before beginning to heal.
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]
Many people wonder if there is a natural cure for herpes or are looking for ways on how to get rid of herpes for good. While technically the virus that causes herpes (whether on the mouth or genital herpes) is not curable, there are many natural herpes remedies that can put herpes into remission. (1) In fact, many people with herpes don’t experience any symptoms at all, especially long term, once they learn to manage triggers of outbreaks. So while there’s no guide for how to get rid of herpes naturally, there is a method for how to get rid of herpes symptoms the natural way and keep breakouts at bay.
While some people realize that they have genital herpes, many do not. It is estimated that one in five persons in the United States has genital herpes; however, as many as 90 percent are unaware that they have the virus. This is because many people have very mild symptoms that go unrecognized or are mistaken for another condition or no symptoms at all.
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]

Herpes sores follow a similar cyclical pattern and appear first like pimples that turn into small vesicles.  Then, the skin becomes crusty, and eventually a scab is formed.  It can take up to several weeks for the lesions to heal, during which time there may be one outbreak followed by another.  Certain risk factors may increase the likelihood of an outbreak, such as: asthma medication, lack of sleep, stress, decreased immunity and ultraviolet rays.


Herpes is contracted through direct contact with an active lesion or body fluid of an infected person.[31] Herpes transmission occurs between discordant partners; a person with a history of infection (HSV seropositive) can pass the virus to an HSV seronegative person. Herpes simplex virus 2 is typically contracted through direct skin-to-skin contact with an infected individual, but can also be contracted by exposure to infected saliva, semen, vaginal fluid, or the fluid from herpetic blisters.[32] To infect a new individual, HSV travels through tiny breaks in the skin or mucous membranes in the mouth or genital areas. Even microscopic abrasions on mucous membranes are sufficient to allow viral entry.

Primary orofacial herpes is readily identified by examination of persons with no previous history of lesions and contact with an individual with known HSV infection. The appearance and distribution of sores is typically presents as multiple, round, superficial oral ulcers, accompanied by acute gingivitis.[39] Adults with atypical presentation are more difficult to diagnose. Prodromal symptoms that occur before the appearance of herpetic lesions help differentiate HSV symptoms from the similar symptoms of other disorders, such as allergic stomatitis. When lesions do not appear inside the mouth, primary orofacial herpes is sometimes mistaken for impetigo, a bacterial infection. Common mouth ulcers (aphthous ulcer) also resemble intraoral herpes, but do not present a vesicular stage.[39]

The cell this virus targets is the B lymphocyte. These cells mature in the bone marrow and are a type of mononuclear leukocyte cells - white blood cells with a one-lobed nucleus. The incubation period for the Epstein – Barr Virus (EBV) is about 30 to 50 days, and patients typically have enlarged lymph nodes and spleens. Some patients have signs of hepatitis.


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]
Primary Infection: This is the first stage wherein the contagion reproduces upon entering from the mucous membrane or skin. Typical symptom is the appearance of oral lesions which may not be present initially resulting in an asymptotic infection. In this case due to lack of symptoms one will be unaware of the presence of an infection. The sores usually takes 21 days to form and become visible, then the blisters will persist up to 10 days before beginning to heal.
If not treated immediately, it has potential  spread to other parts of the body. Being highly contagious in nature it gets readily transmitted by sharing utensils, clothes, and toothbrush. Maintaining sexual contact, kissing and touching also leads to the spread of virus. It is likely to spread more when the virus is present with physical outbursts. It is less contagious if the virus is present without any outward physical signs.
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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