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.
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With the first outbreak of herpes virus infection, an individual may also experience nonspecific flu-like symptoms like fever, swollen lymph nodes, headache, and muscle aches. It is also possible to have herpes virus infection without having any symptoms or signs, or having signs and symptoms that are so mild that the infection is mistaken for another condition.
That being said, if on paper the HSV titres are high, indicating a high viral load in the body, this can be an indicator of an impending flare. Knowing this, we can prescribe antiviral medications with the aim of suppressing the virus activity. The idea is that we reduce the viral load of HSV, therefore helping the body’s immunity better contain the virus.
According to Cullins, there are no standardized guidelines from the CDC for suppressive therapy through medication, but it is an option that people with HSV should talk to their healthcare providers about. “If a person knows they have had herpes in the past that has affected their genitals, they can take suppressive therapy — for example, 500 mg of valacyclovir daily.” While it won’t prevent outbreaks, it will prevent asymptomatic virus shedding. Preventing exposure to the virus through both medication and a physical barrier can be very effective.
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. Virus enters into susceptible cells by entry receptors such as nectin-1, HVEM and 3-O sulfated heparan sulfate. 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. 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. 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.
“You don’t want an infant delivered through infected birth canal or vulva because the infant can be infected,” Cullins explains. A neonatal herpes infection is a real risk because it can cause problems with brain development and eye and skin infections, or even be fatal. And since there is more risk for transmission from mother to baby during an initial outbreak than during a recurrent outbreak, the CDC stresses that it’s incredibly important for pregnant women to avoid contracting a new herpes infection.
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.
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.
Herpes is transmitted via skin-to-skin contact, not through blood or saliva. Cullins explains that someone with HSV can be shedding the herpes virus without having an outbreak (known as asymptomatic virus shedding), and infect somebody that way. Suppressive antiviral medications, like acyclovir or valacyclovir, inhibit HSV replication, which decreases shedding but does not completely eliminate it, says Johnston.
To reduce the chance of acquiring HSV-1, avoid touching saliva, skin, or mucous membranes of people who have HSV-1 lesions. Prevention of genital HSV may be accomplished by latex condoms, but protection is never 100%. Spermicides do not protect against HSV. Some clinicians recommend using dental dams (small latex squares) during oral sex, but like condoms, they are not 100% protective.
Herpes infection can cause sores or breaks in the skin or lining of the mouth, vagina, and rectum. This provides a way for HIV to enter the body. Even without visible sores, having genital herpes increases the number of CD4 cells (the cells that HIV targets for entry into the body) found in the lining of the genitals. When a person has both HIV and genital herpes, the chances are higher that HIV will be spread to an HIV-uninfected sex partner during sexual contact with their partner’s mouth, vagina, or rectum.
Herpes has been known for at least 2,000 years. Emperor Tiberius is said to have banned kissing in Rome for a time due to so many people having cold sores. In the 16th-century Romeo and Juliet, blisters "o'er ladies' lips" are mentioned. In the 18th century, it was so common among prostitutes that it was called "a vocational disease of women". The term 'herpes simplex' appeared in Richard Boulton's A System of Rational and Practical Chirurgery in 1713, where the terms 'herpes miliaris' and 'herpes exedens' also appeared. Herpes was not found to be a virus until the 1940s.
When herpes flares up again, it is called a "recurrence" or "outbreak." Herpes does not always recur, and if it does recur, the timing and severity are different from person to person. Some people rarely have recurrences. Others have them often. Herpes is most likely to recur in the first year after infection. Recurrences may be more frequent for people with weakened immune systems.
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. Herpetic sycosis is a recurrent or initial herpes simplex infection affecting primarily the hair follicles.: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.:373
Worldwide rates of either HSV-1 and/or HSV-2 are between 60 and 95% in adults. HSV-1 is more common than HSV-2, with rates of both increasing as people age. HSV-1 rates are between 70% and 80% in populations of low socioeconomic status and 40% to 60% in populations of improved socioeconomic status. An estimated 536 million people or 16% of the population worldwide were infected with HSV-2 as of 2003 with greater rates among women and in those in the developing world. Rates of infection are determined by the presence of antibodies against either viral species.
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.
"When you are having an outbreak of oral herpes, symptoms usually start with a burning, itching or tingling sensation on your lips," Michael says. "This will intensify until a small rash, and then blisters, appear. These sores are commonly called 'cold sores'. The blisters are usually filled with a clear or slightly yellow liquid. Over a short time, these blisters will burst leaving a painful, raw area. These will then dry and scab over. The scabs will generally fall off after a week or two, leaving fresh clear skin beneath."