Do everything possible to prevent spreading it to other people. The virus cannot live long when it is not in contact with the skin, so door handles and towels are not likely to spread it. Do not share your personal belongings, like toothbrushes and combs. Wash your hands with soap and water often, and immediately if you touch the sores. This is important so as to minimize the chance of getting ocular herpes (herpes infection of the eye) which is a serious infection. Be especially careful around infants because their immune systems may not be fully developed. Little children often express affection with sloppy wet kisses. This is a common way to spread the herpes virus within the family.
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.
These drugs may stop viral replication in the skin but do not eliminate HSV from the body or prevent later outbreaks (HSV reactivation). These drugs are used more frequently with HSV-2 infections. Most investigators suggest consulting an infectious-disease expert when HSV-infected people need hospitalization. Research findings suggest laser treatments may speed healing and lengthen the time before any sores reappear.
Herpes simplex type 1, which is transmitted through oral secretions or sores on the skin, can be spread through kissing or sharing objects such as toothbrushes or eating utensils. In general, a person can only get herpes type 2 infection during sexual contact with someone who has a genital HSV-2 infection. It is important to know that both HSV-1 and HSV-2 can be spread even if sores are not present.
Herpes type 2 (HSV-2) can cause genital herpes. This is one of the most common sexually transmitted infections (STIs) in the US. It causes sores or painful blisters on the penis, vagina, scrotum, anus and buttocks. Along with blisters, people with HSV-2 may experience tingling, itching or pain. Like HSV-1, HSV-2 infections are highly contagious. They can be spread easily through skin-to-skin contact. Sexual intercourse is the main route of transmission.
According to Cullins, there are no standardized guidelines from the CDC for suppressive therapy through medication, but it is an option that people with HSV should talk to their healthcare providers about. “If a person knows they have had herpes in the past that has affected their genitals, they can take suppressive therapy — for example, 500 mg of valacyclovir daily.” While it won’t prevent outbreaks, it will prevent asymptomatic virus shedding. Preventing exposure to the virus through both medication and a physical barrier can be very effective.
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.
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.