Herpes “triggers” (determining exactly what leads to an outbreak) are highly individual, but with time, many people learn to recognize, and sometimes avoid, factors that seem to reactivate HSV in their own bodies. Illness, poor diet, emotional or physical stress, friction in the genital area, prolonged exposure to ultraviolet light (commonly for oral herpes, such as a beach trip or skiing weekend), surgical trauma, and steroidal medication (such as asthma treatment) may trigger a herpes outbreak.
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.
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.
“Someone having HSV doesn't mean that they were reckless or irresponsible with their sex life,” says Sara, age 30. “I used condoms with all my partners, and I still caught it.” For Jamie, who contracted herpes from her husband three years into their monogamous relationship, he was her first and only sexual partner. And she says that he contracted it from one of his very first sexual encounters. No matter how and why someone contracted the virus, it doesn't erase their humanity and right to respect.
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.
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. 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. 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. Herpes simplex is a double-stranded DNA virus.
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.
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.
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.
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.
If you think you have or have been exposed to herpes you should see your primary care provider for follow up, screening, and possible treatment. Many providers today will not test unless you have symptoms of an outbreak, as often tests come back as false positive and the CDC has concluded that false positives cause psychological trauma to those tested. There is much debate on if you should test without symptoms or not, others say it is unethical to not be aware of your current STD status and risk infecting other people.
At the other end of the spectrum, there is a possibility of a herpetic flare up taking a sinister turn and leading to herpetic encephalitis. It is estimated to affect at least 1 in 500,000 individuals per year. The mechanism of this is not fully understood, but it is believed that the infection occurs through direct transmission of the virus via nerves from other parts of the body to the brain. In such cases, a person may complain of fever, headache, and lethargy, followed by confusion or delirium. In some cases, some people even develop seizures. This requires immediate medical attention and treatment.
Some people have recurrent outbreaks with the so-called “classic” blister-like herpes lesions that crust over, or with painful sores. In recurrent herpes, however, this process usually takes about half the time it does in first episodes. In addition, many people have very subtle forms of recurrent herpes that heal up in a matter of days. And lastly, herpes is capable of reactivating without producing any visible lesions (asymptomatic reactivation).
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.
Avoid touching any sores you have. If you do, wash your hands with soap and water. You should avoid sex while you have sores, and use a male or female condom or dental dam with your partner if sex occurs despite intentions to not have sex. Herpes is most contagious during an outbreak, but it’s also possible to spread herpes when no symptoms are present.
Although there is no cure for herpes, treatments can relieve the symptoms. Medication can decrease the pain related to an outbreak and can shorten healing time. They can also decrease the total number of outbreaks. Drugs including Famvir, Zovirax, and Valtrex are among the drugs used to treat the symptoms of herpes. Warm baths may relieve the pain associated with genital sores.
Although herpes treatment is helpful, there is no cure. However, in most cases, outbreaks become fewer, less painful, and weaker over the course of a few years. If you have herpes, you can take certain medications to help manage the infection. Using herpes treatments is usually very effective in speeding up the healing of sores and preventing them from returning frequently.