“I kind of can't stand when people tell me how ‘brave’ I am for talking about it,” says Lachrista Greco, 30, who was diagnosed with herpes almost two year ago. That kind of narrative can actually perpetuate the stigma around the virus. By insinuating that talking about something makes someone brave, the implication is that that thing shouldn’t be talked about at all.
Most people with genital herpes have no symptoms, have very mild symptoms that go unnoticed, or have symptoms but do not recognize them as a sign of infection. Genital herpes symptoms include blisters, sharp pain or burning feelings if urine flows over sores, an inability to urinate if severe swelling of sores blocks the urethra (tube from the bladder to outside the vagina), itching, open sores, and pain in the infected area.
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.
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.
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.
We usually do this for short durations of time. Not something that can be taken as lifelong therapy. I know it might not make sense to some of you. You’re probably asking why it is that we can’t just take the suppressive antiviral medications for the rest of our lives and with that, have no flares of herpes? Well basically, we know that having a high viral load is not the definitive factor in determining a herpetic flare. It is how the body is coping with the virus. So ultimately, you can be taking medications for months on end with your body in good shape to contain the virus so that there are no breakouts but that does not mean that the virus is eliminated from your body.
HSV-1 has been proposed as a possible cause of Alzheimer's disease. In the presence of a certain gene variation (APOE-epsilon4 allele carriers), HSV-1 appears to be particularly damaging to the nervous system and increases one's risk of developing Alzheimer's disease. The virus interacts with the components and receptors of lipoproteins, which may lead to its development.
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.
Condoms offer moderate protection against HSV-2 in both men and women, with consistent condom users having a 30%-lower risk of HSV-2 acquisition compared with those who never use condoms. A female condom can provide greater protection than the male condom, as it covers the labia. The virus cannot pass through a synthetic condom, but a male condom's effectiveness is limited because herpes ulcers may appear on areas not covered by it. Neither type of condom prevents contact with the scrotum, anus, buttocks, or upper thighs, areas that may come in contact with ulcers or genital secretions during sexual activity. Protection against herpes simplex depends on the site of the ulcer; therefore, if ulcers appear on areas not covered by condoms, abstaining from sexual activity until the ulcers are fully healed is one way to limit risk of transmission. The risk is not eliminated, however, as viral shedding capable of transmitting infection may still occur while the infected partner is asymptomatic. The use of condoms or dental dams also limits the transmission of herpes from the genitals of one partner to the mouth of the other (or vice versa) during oral sex. When one partner has a herpes simplex infection and the other does not, the use of antiviral medication, such as valaciclovir, in conjunction with a condom, further decreases the chances of transmission to the uninfected partner. Topical microbicides that contain chemicals that directly inactivate the virus and block viral entry are being investigated.
I am so scared. My boyfriend is the only person I have ever had unprotected sex with 4 times. We had a herpes scare. He got tested. They swabbed him and gave him a blood test and his results for Herpes 1 and 2 came back negative. I went to the doctor but the lumps on my vagina healed and they said come back when you have a lesion. I told my BF but he still wanted to have sex, I told him what the doctor said and I told him we should not have sex or use a condom. He said it does not matter because if he did not have herpes I did not have Herpes. He said ok and put the condom on but when we were done he started to laugh and said he took the condom off. Since then we have had sex twice. I went to the doctor and they gave me a blood test. They said if something was wrong they would send a letter to the house. Since they never sent the letter to the house I thought I was fine and I never had any other lumps since then and my boy friend never had any symptoms I thought I was fine.Today something told me to go to the doctor. I went and they said they never ordered the test. I AM So ANGRY. What Should I do? If I do have it shouldn't it have been in his blood from me? I am so scared that I may have it? I am also worried that one day he may get symptoms because his test was wrong and think I gave it to him when he was the one who may have given it to me if my blood test comes back positive. I have only had sex once with a condom before him. What should I do? He has had other a few partners. What is the likely hood that I may have given him herpes?
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.
Oral herpes (HSV-1) infection (or exposure without noticeable infection) is common. About 65% of the U.S. population has detectable antibodies to HSV-1 by age 40. This article will focus on HSV-1, or oral herpes, not on HSV-2, also commonly known as genital herpes. Genital herpes is considered to be a sexually transmitted disease (STD). In addition, HSV-2 virus should not be confused with human papillomavirus (HPV), the cause of genital warts, and some cervical and other cancer types.
If not treated immediately, it has potential spread to other parts of the body. Being highly contagious in nature it gets readily transmitted by sharing utensils, clothes, and toothbrush. Maintaining sexual contact, kissing and touching also leads to the spread of virus. It is likely to spread more when the virus is present with physical outbursts. It is less contagious if the virus is present without any outward physical signs.
Not every person with a herpes infection actually experiences breakouts of cold sores throughout his or her lifetime or even after initially becoming infected. How often someone has a herpes cold sore outbreak, how severe the outbreaks are, how contagious someone is after infection and how long the sores take to heal all depend on someone’s individual immune response.
Although the exact cause of Bell's palsy—a type of facial paralysis—is unknown, it may be related to reactivation of HSV-1. This theory has been contested, however, since HSV is detected in large numbers of individuals having never experienced facial paralysis, and higher levels of antibodies for HSV are not found in HSV-infected individuals with Bell's palsy compared to those without. Antivirals may improve the condition slightly when used together with corticosteroids in those with severe disease.