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.
Cullins explains that even if you’ve never had an outbreak, if you’ve been exposed to herpes, it lies dormant in your body. A blood test could reveal antibodies for HSV-1 and/or HSV-2, which means that you have been exposed to the infection in your past, you have been infected, and you have developed antibodies because your body has or is fighting the infection.
OK, so the majority of people have it. Just this year, the World Health Organization released a study that estimates two thirds of people in the world (67%) have the HSV-1 strain of the herpes simplex virus — that’s approximately 3.7 billion people worldwide. While HSV-1 typically refers to oral herpes infections, it also includes some genital infections. The new report estimates that half of the HSV-1 infections in people between the ages of 15–49 are actually genital infections transmitted via oral-to-genital contact. The Center For Disease Control (CDC) estimates that 1 in 6 people have genital herpes.
Herpesviral encephalitis and herpesviral meningitis Herpes simplex encephalitis (HSE) is a rare life-threatening condition that is thought to be caused by the transmission of HSV-1 either from the nasal cavity to the brain's temporal lobe or from a peripheral site on the face, along the trigeminal nerve axon, to the brainstem. Despite its low incidence, HSE is the most common sporadic fatal encephalitis worldwide. HSV-2 is the most common cause of Mollaret's meningitis, a type of recurrent viral meningitis.
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.
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 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.
Homeopathic medicines can also be used to avoid any adverse effects of allopathic drugs and assist the body’s own healing mechanism. They are approved by FDA and are custom made by the medic in the right proportion to provide immediate relief. One such complete natural product is Herpeset which is to be sprayed on the affected areas especially the tongue. The natural components are quickly absorbed in the blood stream.
The frequency and severity of recurrent outbreaks vary greatly between people. Some individuals' outbreaks can be quite debilitating, with large, painful lesions persisting for several weeks, while others experience only minor itching or burning for a few days. Some evidence indicates genetics play a role in the frequency of cold sore outbreaks. An area of human chromosome 21 that includes six genes has been linked to frequent oral herpes outbreaks. An immunity to the virus is built over time. Most infected individuals experience fewer outbreaks and outbreak symptoms often become less severe. After several years, some people become perpetually asymptomatic and no longer experience outbreaks, though they may still be contagious to others. Immunocompromised individuals may experience longer, more frequent, and more severe episodes. Antiviral medication has been proven to shorten the frequency and duration of outbreaks. Outbreaks may occur at the original site of the infection or in proximity to nerve endings that reach out from the infected ganglia. In the case of a genital infection, sores can appear at the original site of infection or near the base of the spine, the buttocks, or the back of the thighs. HSV-2-infected individuals are at higher risk for acquiring HIV when practicing unprotected sex with HIV-positive persons, in particular during an outbreak with active lesions.
A 2004 study in the New England Journal of Medicine found that suppressive therapy decreases the risk of HSV-2 transmission from symptomatic, infected partners to uninfected partners by 48%. So “the risk of transmission is significantly reduced, but cannot be eliminated even with suppressive therapy,” Johnston explains, and she stresses that the virus can be passed along even without signs or symptoms.