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)
The most common reason that people develop cold sores on their mouths is due to becoming infected with HSV-1. (4) HSV-1 usually causes cold sore breakouts around the lips or mouth, or what some people describe as “fever blisters.” Someone can become infected with HSV-1 starting as a child, and then the virus can lay dormant in the body until the immune system is weakened, at which point symptoms can surface.
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.
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.
However, there is much more to the herpes virus than just chicken pox or genital herpes. For instance, after an active infection, the virus is shed (eliminated) in the urine and feces for up to several months (sometimes years in the case of the cytomegalovirus) after the active infection has resolved. This means the infected person is still contagious, which is what makes this virus so contagious. It can easily be transferred when the patient is asymptomatic.
Although herpes treatment is helpful, there is no cure. However, in most cases, outbreaks become fewer, less painful, and weaker over the course of a few years. If you have herpes, you can take certain medications to help manage the infection. Using herpes treatments is usually very effective in speeding up the healing of sores and preventing them from returning frequently.
“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.
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.