The causes of reactivation are uncertain, but several potential triggers have been documented. A 2009 study showed the protein VP16 plays a key role in reactivation of the dormant virus.[71] Changes in the immune system during menstruation may play a role in HSV-1 reactivation.[72][73] Concurrent infections, such as viral upper respiratory tract infection or other febrile diseases, can cause outbreaks. Reactivation due to other infections is the likely source of the historic terms 'cold sore' and 'fever blister'.
It can be pretty similar to having flu, Michael says. "When you are infected with herpes you can experience symptoms like fever, muscle aches, swollen lymph nodes, and a general feeling of being unwell." However, many people will not have any symptoms at all - which means until someone notices blisters or sores, they might not realise they have a herpes infection.

A scary finding is that more cases of genital herpes than ever before are now being caused by HSV-1 (the type most people assume only causes mouth sores), and about 85 percent of people with genital herpes don’t even know it. (7) Studies show that about 50 percent of the new genital herpes infections in young adults are due to HSV-1 and about 40 percent in older adults. The fact that most people don’t ever find out they’re infected is one of the reasons that transmission rates are steadily climbing.

The causes of reactivation are uncertain, but several potential triggers have been documented. A 2009 study showed the protein VP16 plays a key role in reactivation of the dormant virus.[71] Changes in the immune system during menstruation may play a role in HSV-1 reactivation.[72][73] Concurrent infections, such as viral upper respiratory tract infection or other febrile diseases, can cause outbreaks. Reactivation due to other infections is the likely source of the historic terms 'cold sore' and 'fever blister'.
It should not be confused with conditions caused by other viruses in the herpesviridae family such as herpes zoster, which is caused by varicella zoster virus. The differential diagnosis includes hand, foot and mouth disease due to similar lesions on the skin. Lymphangioma circumscriptum and dermatitis herpetiformis may also have a similar appearance.
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.[citation needed] 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.[37] 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.[citation needed] Herpes simplex is a double-stranded DNA virus.[38]
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]
^ McNeil DG. Topical Tenofovir, a Microbicide Effective against HIV, Inhibits Herpes Simplex Virus-2 Replication Archived 2017-04-09 at the Wayback Machine. NY Times. Research article: Andrei G; Lisco A; Vanpouille C; et al. (October 2011). "Topical Tenofovir, a Microbicide Effective against HIV, Inhibits Herpes Simplex Virus-2 Replication". Cell Host. 10 (4): 379–89. doi:10.1016/j.chom.2011.08.015. PMC 3201796. PMID 22018238.
The cell this virus targets is the B lymphocyte. These cells mature in the bone marrow and are a type of mononuclear leukocyte cells - white blood cells with a one-lobed nucleus. The incubation period for the Epstein – Barr Virus (EBV) is about 30 to 50 days, and patients typically have enlarged lymph nodes and spleens. Some patients have signs of hepatitis.

Genital herpes is an incurable disease. But, there are medications to relieve symptoms and prevent recurrent outbreaks. Prosurx is the best and most common treatment option for genital herpes. It can give your partner immediate relief and stop their outbreak before it starts. Prosurx can also reduce your partner’s risks of spreading the virus to you. So, ask your partner to apply Prosurx 2-3 times a day to get rid of genital herpes.
Laboratory testing is often used to confirm a diagnosis of genital herpes. Laboratory tests include culture of the virus, direct fluorescent antibody (DFA) studies to detect virus, skin biopsy, and polymerase chain reaction to test for presence of viral DNA. Although these procedures produce highly sensitive and specific diagnoses, their high costs and time constraints discourage their regular use in clinical practice.[39]
Although it’s not caused by either the HSV-1 or HSV-2 virus, herpes zoster falls under the umbrella of herpes diseases. Also known as shingles, it’s an infection caused by the varicella-zoster virus, and is characterized by the development of painful skin rashes on one side of the face or body.23 These rashes are red patches of fluid-filled blisters that tend to crack easily.24,25

The annual incidence in Canada of genital herpes due to HSV-1 and HSV-2 infection is not known (for a review of HSV-1/HSV-2 prevalence and incidence studies worldwide, see Smith and Robinson 2002). As many as one in seven Canadians aged 14 to 59 may be infected with herpes simplex type 2 virus[85] and more than 90 per cent of them may be unaware of their status, a new study suggests.[86] In the United States, it is estimated that about 1,640,000 HSV-2 seroconversions occur yearly (730,000 men and 910,000 women, or 8.4 per 1,000 persons).[87]
If abstinence is not possible, using a sexual barrier (such as a condom or dental dam) can reduce the likelihood of transmission, although there is still a risk that these methods will not be sufficient to prevent the spread of the virus. It’s also a good idea to keep a visual reminder of your infection at hand to avoid any accidental food or beverage sharing.
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