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.
A doctor will base a presumptive diagnosis on information provided by the patient and on the physical examination. The characteristic appearance of the herpes sores leaves little doubt about the diagnosis, so the typical appearance of the sores is key to the diagnosis. This appearance helps distinguish oral herpes from oral thrush, shingles, gonorrhea, and syphilis. In addition, chapped or sunburned lips can resemble oral herpes, but the tissue stain (Tzanck smear, see below) shows no virus-induced cell changes. Further testing is usually not necessary but is sometimes done.
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.
Recurrent outbreaks of genital herpes may happen, with some patients having four to six outbreaks in the span of a year. Compared to the first infection, subsequent recurrences are less painful and occur in shorter periods than the first infection. There are some patients, however, who don’t have another outbreak for many years or even once more during their lifetime.11
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.
By boosting the immune system through a healthy diet, making lifestyle changes and being cautious during periods of active breakouts, you can help keep any virus dormant, including herpes. Certain steps can significantly reduce the chances of having having reoccurring herpes symptoms and lower the risk that you’ll pass the virus to someone else. So if you’re wondering how to get rid of herpes, read on to learn the natural ways to keep this virus dormant.
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.

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.
Essential oils that can help treat herpes include clove oil, tea tree oil and myrrh oil. Tea tree oil is one of the most common oils used on the skin for its natural antiviral, antibacterial properties. (3) Simply apply these essential oils three times daily to areas where cold sores are present, being careful to use a very small amount (only one to three drops). If you have sensitive skin, try mixing the essential oils with a carrier oil to dilute their strength a bit, including jojoba or coconut oil.

Consequently, you may already have the virus. A doctor can determine this with a blood test for Herpes 2 (Ig), a type-specific immunoglobulin. If you are already infected, you won’t be at risk for a new infection — you and your boyfriend already share the virus. But knowing your herpes status will tell you whether you are capable of infecting a future partner.
Since genital herpes affects the private parts, people tend to think that the virus acts differently on men and women. However, the symptoms of genital herpes are very similar in males and females. The most important difference is that the virus can cause complications in pregnant women, who can pass the infection on to their babies. Other than that, there is no such thing as a male or female genital herpes virus, the infection is caused by the same virus in both sexes.
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]

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.
Prodrome: Early in the phase of reactivation (also called an outbreak), many people experience an itching, tingling, or painful feeling in the area where their recurrent lesions will develop. This sort of warning symptom – called a “prodrome” – often comes a day or two before lesions appear. To be on the safe side, it’s best to assume virus is active (and, therefore, can be spread through direct skin-to-skin contact) during these times.

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'.
There’s herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2). “HSV-1 and HSV-2 are different but closely related viruses,” says Dr. Christine Johnston, MPH, who is the Associate Medical Director of the Virology Research Clinic at the University of Washington. Johnston explains that both are transmitted through close mucosal or skin contact with infected secretions. HSV-1 primarily causes oral outbreaks, also known as cold sores, and HSV-2 usually causes genital outbreaks. But HSV-1 can also cause genital outbreaks through oral-to-genital contact, according to the CDC. According to Johnston, genital HSV-1 is less likely to recur than HSV-2, and there’s less asymptomatic shedding (transmitting the virus without realizing it) with HSV-1 than with HSV-2.

Many HSV-infected people experience recurrence within the first year of infection.[14] Prodrome precedes development of lesions. Prodromal symptoms include tingling (paresthesia), itching, and pain where lumbosacral nerves innervate the skin. Prodrome may occur as long as several days or as short as a few hours before lesions develop. Beginning antiviral treatment when prodrome is experienced can reduce the appearance and duration of lesions in some individuals. During recurrence, fewer lesions are likely to develop and are less painful and heal faster (within 5–10 days without antiviral treatment) than those occurring during the primary infection.[14] Subsequent outbreaks tend to be periodic or episodic, occurring on average four or five times a year when not using antiviral therapy.


Avoid physical contact with anyone who has visible blisters and sores, and don't share towels or anything that may have come into contact with the sores. "It is also important that before you have any intimate contact with anyone you ask them about their sexual health, whether they have a herpes infection or have ever had any other sexually transmitted infection," Michael advises. "This is because statistically, people who have had an STI are more likely to be infected with the herpes virus. Using condoms and dental dams can also help reduce your risk of catching oral herpes."
Although the exact cause of Bell's palsy—a type of facial paralysis—is unknown, it may be related to reactivation of HSV-1.[23] This theory has been contested, however, since HSV is detected in large numbers of individuals having never experienced facial paralysis, and higher levels of antibodies for HSV are not found in HSV-infected individuals with Bell's palsy compared to those without.[24] Antivirals may improve the condition slightly when used together with corticosteroids in those with severe disease.[25]
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