Herpes simplex is a viral infection caused by the herpes simplex virus. Infections are categorized based on the part of the body infected. Oral herpes involves the face or mouth. It may result in small blisters in groups often called cold sores or fever blisters or may just cause a sore throat. Genital herpes, often simply known as herpes, may have minimal symptoms or form blisters that break open and result in small ulcers. These typically heal over two to four weeks. Tingling or shooting pains may occur before the blisters appear. Herpes cycles between periods of active disease followed by periods without symptoms. The first episode is often more severe and may be associated with fever, muscle pains, swollen lymph nodes and headaches. Over time, episodes of active disease decrease in frequency and severity. Other disorders caused by herpes simplex include: herpetic whitlow when it involves the fingers, herpes of the eye, herpes infection of the brain, and neonatal herpes when it affects a newborn, among others.
For mild infections, self-care may be adequate for treatment. Other treatments termed "home remedies" are not considered cures but can ease or hasten recovery. These remedies include aloe vera gel, cornstarch paste, and tea or mint leaves. A cool compress may reduce pain. There is no cure for the infection. People with severe infection symptoms, especially children, should be evaluated by a medical caregiver.
According to Gina*, 21, “A herpes diagnosis is very shaking and it gives you the opportunity to look inward and really find what you love about yourself.” Gina says she has even better self-esteem than prior to finding out she had HSV. She explains, “You learn not to lower your standards, because you start to pick out who it is worth disclosing to and who isn't.”
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 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.
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.