“Herpes is caused by sexual intimacy and contact with a person who is actively shedding the herpes virus,” says Cullins. If you have HSV-1, that shedding could happen through the mouth or a cold sore, which means that the virus can be transmitted through kissing, or just sharing a drink. If you have herpes that affects the genitals, it can be transmitted from sharing sex toys, grinding, or even mutual masturbation — any activity where the virus can be transmitted from one person to another through skin-to-skin or mucosal contact.
To protect yourself from catching genital herpes, you should use condoms during sex. If your partner develops symptoms, it’s necessary to avoid having sex. If the two of you get positive test, you don’t need to worry about the transmission. But, still use condoms every time to avoid other STDs. Condoms can also help stop your infection from getting worse.
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Some people have recurrent outbreaks with the so-called “classic” blister-like herpes lesions that crust over, or with painful sores. In recurrent herpes, however, this process usually takes about half the time it does in first episodes. In addition, many people have very subtle forms of recurrent herpes that heal up in a matter of days. And lastly, herpes is capable of reactivating without producing any visible lesions (asymptomatic reactivation).
Oral herpes is a viral infection mainly of the mouth area and lips caused by a specific type of the herpes simplex virus. Oral herpes is also termed HSV-1, type 1 herpes simplex virus, or herpes labialis. The virus causes painful sores on the upper and lower lips, gums, tongue, roof of the mouth, inside the cheeks or nose, and sometimes on the face, chin, and neck. Infrequently, it may cause genital lesions. It also can cause symptoms such as swollen lymph nodes, fever, and muscle aches. People commonly refer to the infection as "cold sores."
If there is enlargement of the spleen, strenuous physical exercise should be avoided to prevent rupture. With the exception of possible complications, mono is rarely fatal and recovery is complete. Once recovered from the mono, you will usually have lifelong immunity from further infection because the body produces antibodies. If too hasty a departure is made from bed rest, however, a relapse may be experienced.
There are two types of herpes simplex viruses (HSV), they are termed HSV-1 and HSV-2. These two viruses have distinctly different DNA, and both cause oral and genital lesions. However, HSV-1 causes about 80% of all oral lesions and only about 20% of genital lesions while HSV-2 causes the reverse (about 80% genital and 20% oral). Studies also suggest that in adolescents, up to 40% of genital herpes is caused by HSV-1 because of reported increased oral/genital contact (transmission by oral sex).
Herpes virus type 4 is also called Epstein-Barr virus. It typically causes infectious mononucleosis, a “kissing” disease. Symptoms include skin rash, fever, sore throat and swollen lymph glands. The virus can be involved in cancers like nasopharyngeal cancer. Herpes virus type 4 is contagious through bodily fluids, including saliva. Kissing, coughing, sneezing, or sharing utensils can make the infection spread.
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.

Once a person is infected, there are no symptoms for anywhere between 2 days to 2 weeks. This is known as the incubation period and is the time during which the virus multiplies profusely. The first symptoms that are seen are the small fluid-filled blisters known as vesicles. This arises as the virus starts destroying cells at the site and causes intense localized inflammation. These small vesicles or sometimes the larger bullae may either burst resulting in ulcer or heal completely with no scarring. The virus may also travel from the site of infection and “hides” by the sensory dorsal root. Here it remains latent until is it is reactivated.
I do plan on dumping him, but I don't know how. I think I am still with him because I think if my test comes back positive for genital herpes he is the only guy who will ever want me if he did in fact give it to me or I have to stay with him because I may have given it to him. Somedays I feel like I can hand the idea of having herpes for the rest of my life but other days I am not so sure. I am so afraid. Its funny I use to say I never wanted to get married and have kids, but this situation has made me realize how much I want those things and now I may never get the chance. I guess thats life. Funny, as I write this I remember the first time I had sex with him he told me he used a condom but I don't think he did. I am such an idiot. I pray my blood test comes back negative. If it comes back positive life for me will be over.
Primary orofacial herpes is readily identified by examination of persons with no previous history of lesions and contact with an individual with known HSV infection. The appearance and distribution of sores is typically presents as multiple, round, superficial oral ulcers, accompanied by acute gingivitis.[39] Adults with atypical presentation are more difficult to diagnose. Prodromal symptoms that occur before the appearance of herpetic lesions help differentiate HSV symptoms from the similar symptoms of other disorders, such as allergic stomatitis. When lesions do not appear inside the mouth, primary orofacial herpes is sometimes mistaken for impetigo, a bacterial infection. Common mouth ulcers (aphthous ulcer) also resemble intraoral herpes, but do not present a vesicular stage.[39]
While some people realize that they have genital herpes, many do not. It is estimated that one in five persons in the United States has genital herpes; however, as many as 90 percent are unaware that they have the virus. This is because many people have very mild symptoms that go unrecognized or are mistaken for another condition or no symptoms at all.
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]
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.
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