To reduce the chance of acquiring HSV-1, avoid touching saliva, skin, or mucous membranes of people who have HSV-1 lesions. Prevention of genital HSV may be accomplished by latex condoms, but protection is never 100%. Spermicides do not protect against HSV. Some clinicians recommend using dental dams (small latex squares) during oral sex, but like condoms, they are not 100% protective.
Human herpes virus 3 (HHV3) is also called varicella-zoster virus. HHV3 causes chickenpox. It can also cause a recurrent virus infection of the skin, which is called herpes zoster or shingles. Shingles occurs when dormant varicella-zoster virus from an initial bout of chickenpox becomes reactivated. Like its close relative, HHV1, herpes zoster likes to infect skin cells and nerve cells. This virus may also recur along nerve fibre pathways, causing multiple sores where nerve fibres end on skin cells. Because an entire group of nerve cells is often affected, shingles is generally much more severe than a recurrence of herpes simplex. The lesions generally appear in a band-like or belt-like pattern occurring on one side of the body and are often accompanied by itching, tingling, or even severe pain. Healing usually occurs in 2 to 4 weeks, and scars may remain. Postherpetic neuralgia is a complication of shingles where the pain associated with the infection can persist for months and even years. Most people who experience shingles once do not experience it again.
Until the 1980s serological tests for antibodies to HSV were rarely useful to diagnosis and not routinely used in clinical practice. 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.
Worldwide rates of either HSV-1 or HSV-2 are between 60% and 95% in adults. HSV-1 is usually acquired during childhood. Rates of both increase as people age. Rates of HSV-1 are between 70% and 80% in populations of low socioeconomic status and 40% to 60% in populations of improved socioeconomic status. An estimated 536 million people worldwide (16% of the population) were infected with HSV-2 as of 2003 with greater rates among women and those in the developing world. Most people with HSV-2 do not realize that they are infected. The name is from Greek: ἕρπης herpēs which means "to creep", referring to spreading blisters. The name does not refer to latency.
Diagnosing herpes is made much easier if you present to your clinician at the time that the rash is present and if possible, we can take a sample from that to be sent for Herpes PCR (Polymerase Chain Reaction) studies to confirm the diagnosis. Advanced medical investigative techniques such as this will allow us to differentiate type one from type two herpes regardless of the nature and distribution of the rash.
When herpes flares up again, it is called a "recurrence" or "outbreak." Herpes does not always recur, and if it does recur, the timing and severity are different from person to person. Some people rarely have recurrences. Others have them often. Herpes is most likely to recur in the first year after infection. Recurrences may be more frequent for people with weakened immune systems.
Varicella-zoster is transmitted though the mucosa of the respiratory system, specifically the upper respiratory tract, or the conjunctiva of the eye. Initial replication takes place in the regional lymph nodes, and then the virus spreads and replication begins in the liver and spleen. The virus is then transported to the skin where the rash develops. The incubation period of varicella is about 10 to 21 days.
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.
Traditionally, it was assumed that HSV-1 strictly caused oral sores and blisters, whereas HSV-2 caused genital and/or rectal sores and blisters. However, the virus- or perhaps just our understanding of the virus itself- has evolved in such a way that doctors now recognize that either HSV-1 or HSV-2 can cause genital and/or rectal sores, albeit with HSV-2 causing the majority of sores in the genital or rectal areas.
This content is strictly the opinion of Dr. Josh Axe and is for informational and educational purposes only. It is not intended to provide medical advice or to take the place of medical advice or treatment from a personal physician. All readers/viewers of this content are advised to consult their doctors or qualified health professionals regarding specific health questions. Neither Dr. Axe nor the publisher of this content takes responsibility for possible health consequences of any person or persons reading or following the information in this educational content. All viewers of this content, especially those taking prescription or over-the-counter medications, should consult their physicians before beginning any nutrition, supplement or lifestyle program.
Human herpes virus 5 (HHV5) is the official name of cytomegalovirus (CMV). CMV is also a cause of mononucleosis. In people with healthy immune systems, the virus may not even cause any symptoms. It can be sexually transmitted, can cause problems to newborns, and can cause hepatitis. CMV can be transmitted through sexual contact, breast-feeding, blood transfusions, and organ transplants. CMV infection is one of the most difficult complications of AIDS. It may lead to diarrhea, severe vision problems including blindness, infections of the stomach and intestines, and even death. For a virus that barely causes a problem in most people with healthy immune systems, it can be amazingly nasty in people with damaged immune systems, such as people with AIDS.
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.
Since genital herpes affects the private parts, people tend to think that the virus acts differently on men and women. However, the symptoms of genital herpes are very similar in males and females. The most important difference is that the virus can cause complications in pregnant women, who can pass the infection on to their babies. Other than that, there is no such thing as a male or female genital herpes virus, the infection is caused by the same virus in both sexes.
The U.S. Centers of Disease Control and Prevention explains that pain, itching or tingling in the area where the rashes will eventually appear will occur at least one to five days before the rashes are seen. Once these rashes are visible, they scab for around seven to 10 days and heal within two to four weeks.29 Aside from rashes, symptoms of shingles include fever, chills, headaches, fatigue and an upset stomach.30,31
The risk of transmission from mother to baby is highest if the mother becomes infected around the time of delivery (30% to 60%), since insufficient time will have occurred for the generation and transfer of protective maternal antibodies before the birth of the child. In contrast, the risk falls to 3% if the infection is recurrent, and is 1–3% if the woman is seropositive for both HSV-1 and HSV-2, and is less than 1% if no lesions are visible. Women seropositive for only one type of HSV are only half as likely to transmit HSV as infected seronegative mothers. To prevent neonatal infections, seronegative women are recommended to avoid unprotected oral-genital contact with an HSV-1-seropositive partner and conventional sex with a partner having a genital infection during the last trimester of pregnancy. Mothers infected with HSV are advised to avoid procedures that would cause trauma to the infant during birth (e.g. fetal scalp electrodes, forceps, and vacuum extractors) and, should lesions be present, to elect caesarean section to reduce exposure of the child to infected secretions in the birth canal. The use of antiviral treatments, such as aciclovir, given from the 36th week of pregnancy, limits HSV recurrence and shedding during childbirth, thereby reducing the need for caesarean section.
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 symptoms commonly show in or around the mouth. Sores may also occur at the back of the throat, causing the lymph nodes in the neck to swell. Mouth herpes is very common in children, as their parents or relatives can pass it on to them easily by a greeting or goodnight kiss. To get a better understanding of oral herpes, let us take a look at its causes.
The most effective method of avoiding genital infections is by avoiding vaginal, oral, and anal sex. Condom use decreases the risk. Daily antiviral medication taken by someone who has the infection can also reduce spread. There is no available vaccine and once infected, there is no cure. Paracetamol (acetaminophen) and topical lidocaine may be used to help with the symptoms. Treatments with antiviral medication such as aciclovir or valaciclovir can lessen the severity of symptomatic episodes.
The broader issue is whether, if you do get infected, herpes will ultimately harm your health. Although I don’t want to trivialize this infection, in your general scheme of health, it probably will not. The major concern is that if you are pregnant and develop a new outbreak of herpes, the virus can be transmitted to the fetus, especially during vaginal delivery. What’s more, people with genital herpes have a much greater risk of acquiring HIV if they are exposed. (It’s theorized that the lesion causes microscopic breaks in the skin, allowing HIV to enter the body.)
In order to diagnose herpes, a health care provider can swab an area of visibly active herpes infection or, if symptoms aren’t active, a blood test can be given that measures the number of herpes antibodies present in the body. The antibodies don’t indicate herpes itself, but rather show the immune system’s response to the presence of the virus in the body. It’s important to note that sometimes a swab can give false negative results since herpes lesions need to be large enough to yield enough detectable virus and if the outbreak is already healing it also may not be detected in a swab. (6)
Canker sores are sometimes thought to be caused by HSV, but this is not true. Canker sores occur only inside the mouth, on the tongue, and on the soft palate (roof of mouth), not on skin surfaces. Although they reoccur, they are not contagious, usually are self-limiting, and have almost no complications. Canker sores are caused by substances that irritate the lining of the mouth.
Worldwide rates of either HSV-1 and/or HSV-2 are between 60 and 95% in adults. HSV-1 is more common than HSV-2, with rates of both increasing as people age. HSV-1 rates are between 70% and 80% in populations of low socioeconomic status and 40% to 60% in populations of improved socioeconomic status. An estimated 536 million people or 16% of the population worldwide were infected with HSV-2 as of 2003 with greater rates among women and in those in the developing world. Rates of infection are determined by the presence of antibodies against either viral species.
When we say, “herpes” many of us are thinking about genital herpes, famously known as an incurable inconvenience. But there is more to it than being just a sexually transmitted infection. There are multiple ways that herpes can transmit but genital herpes is usually picked up from sexual contact. Apart from that, herpes can be transmitted when sharing an environment with someone who has the infection as well.
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Oral herpes, commonly referred to as mouth herpes, is a viral infection of the mouth and gums primarily by the Herpes simplex virus type 1 (HSV-1) but may also be due to the genital variant (HSV-2). It is also known as recurrent herpetic stomatitis or acute herpetic gingivostomatitis. The infection of the mouth typically causes small fluid-filled blisters known as vesicles on the roof of the mouth (palate), inside of the cheeks (buccal muscosa), tongue, gums and even the lips (herpes labialis). It may also occur on the skin around the mouth and extend to the nose and into the nasal cavity.
EYES AND VISIONEARS, NOSE AND THROATSKIN, HAIR, NAILSHEART AND VESSELSKIDNEYS AND URINARY TRACTBLOOD AND IMMUNITYLIVER AND GALLBLADDERLUNGS AND AIRWAYSUPPER AND LOWER LIMBWOMEN’S HEALTH AND PREGNANCYWOMEN’S HEALTHKIDS HEALTHMEN’S HEALTHABCD – FIRST AID: INJURIES, POISONINGNEWBORNS BABIESHORMONES AND METABOLISMMEDICATION, SUPPLEMENTSMEDICAL TERMINOLOGYNUTRITIONSURGERY AND OTHER PROCEDURES
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.