Herpes virus type 4 is also called Epstein-Barr virus. It typically causes infectious mononucleosis, a “kissing” disease. Symptoms include skin rash, fever, sore throat and swollen lymph glands. The virus can be involved in cancers like nasopharyngeal cancer. Herpes virus type 4 is contagious through bodily fluids, including saliva. Kissing, coughing, sneezing, or sharing utensils can make the infection spread.
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]
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.
Until the 1980s serological tests for antibodies to HSV were rarely useful to diagnosis and not routinely used in clinical practice.[39] The older IgM serologic assay could not differentiate between antibodies generated in response to HSV-1 or HSV-2 infection. However, a glycoprotein G-specific (IgG) HSV test introduced in the 1980s is more than 98% specific at discriminating HSV-1 from HSV-2.[40]
Pain, sore lips, burning sensation, tingling, or itching occurs at the infection site before the sores appear. These are the early symptoms (prodrome). Sometimes these symptoms happen prior to the appearance of sores, bumps, pimple-like lesions, or blisters (herpes or herpetic stomatitis). Thereafter, clusters or groups of painful blisters (also termed fever blisters) or vesicles erupt or ooze with a clear to yellowish fluid that may develop into a yellowish crust. These blisters break down rapidly and appear as tiny, shallow gray ulcers on a red base. Fever blisters are smaller than canker sores. A few days later, they become crusted or scabbed and appear drier and more yellow.
A herpes infection is caused by the herpes simplex virus (HSV). It has 2 main types, including HSV-1 and HSV-2. While HSV-1 can cause oral herpes, HSV-2 can be responsible for genital herpes. Oral herpes is also known as cold sores or fever blisters. It mainly occurs on the lips, around the mouth. Genital herpes is usually referred to as herpes. It mostly affects the genitals and anal area. Genital herpes is considered to be a sexually transmitted disease. It’s extremely contagious and can be spread through sexual intercourse.
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