Herpes virus type 3 is also known as varicella-zoster virus which causes chicken pox. This virus can also lead to a recurrent infection called herpes zoster or shingles. It occurs when the virus becomes reactivated after causing chicken pox and infects the skin. So if you have had chicken pox as a child, you may get shingles afterwards. Shingles and chicken pox cause blisters anywhere on the body. They are contagious and can be spread by direct contact with fluid from the blisters.
Human herpes virus 6 (HHV6) is a recently observed agent found in the blood cells of a few patients with a variety of diseases. It causes roseola (a viral disease causing high fever and a skin rash in small children) and a variety of other illnesses associated with fever in that age group. This infection accounts for many of the cases of convulsions associated with fever in infancy (febrile seizures).
Signs and symptoms of dehydration usually warrant going to a hospital's emergency department. Infants, especially under 6 weeks of age or if the infant appears to slow urine output or decrease fluid intake, should be evaluated by their pediatrician or in an emergency center if oral sores appear. Individuals with immune suppression (for example, patients undergoing chemotherapy, HIV patients, or cancer patients) should contact their doctors if they suspect a HSV-1 infection.
Human herpes virus 2 (HHV2) is also called herpes simplex virus 2 (HSV2). It typically causes genital herpes, a sexually transmitted infection. However, it can also cause cold sores in the facial area. Like HHV1, the HHV2 infection is contagious and is spread by skin-to-skin contact. The main route of transmission is through sexual contact, as the virus does not survive very long outside the body.
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.
Following active infection, herpes viruses establish a latent infection in sensory and autonomic ganglia of the nervous system. The double-stranded DNA of the virus is incorporated into the cell physiology by infection of the nucleus of a nerve's cell body. HSV latency is static; no virus is produced; and is controlled by a number of viral genes, including latency-associated transcript.
Because the herpes virus is so common most people who have either genital or oral herpes do not know that they have it. Additionally, the symptoms of HSV1 or 2 may be mild or at time, may not appear for days, weeks, or even years and sometimes no symptoms of herpes are present at all. It is important to note that symptoms do not have to be present in order to contract this virus, so it is important that you prevent transmission through proper hygiene and awareness.
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
"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."