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.

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.
Consider designating a special, brightly colored bracelet or visual designator that you will wear only during active viral periods: this will serve as a visual cue, reminding you each time that you eat or drink that food and/or beverage sharing is not an option during this time: this subtle cue will remind you to not engage in a high-risk behavior during an active viral period.
But I was wrong, on so many levels. I did find love again. And I wasn’t alone — very far from it, in fact. Herpes is extremely common, with statistics showing that as many as one in six people ages 14 to 49 in the U.S. has herpes caused by the herpes simplex-2 virus (and since herpes simplex-1 virus also causes herpes, that number is likely even higher).
Neonatal herpes simplex is a HSV infection in an infant. It is a rare but serious condition, usually caused by vertical transmission of HSV-1 or -2) from mother to newborn. During immunodeficiency, herpes simplex can cause unusual lesions in the skin. One of the most striking is the appearance of clean linear erosions in skin creases, with the appearance of a knife cut.[20] Herpetic sycosis is a recurrent or initial herpes simplex infection affecting primarily the hair follicles.[21]:369 Eczema herpeticum is an infection with herpesvirus in patients with chronic atopic dermatitis may result in spread of herpes simples throughout the eczematous areas.[21]:373
Herpes, whether on the mouth or genitals, is caused by a family of over 70 related viruses. These viral infections cause small, fluid-filled blisters to develop on the skin and mucous membranes. There are actually eight different types of herpes simplex viruses that both children and adults can acquire, but two are by far the most common: HSV-1 and HSV-2.

Herpes virus type 1 (HSV-1) is the cause of cold sores or fever blisters around the mouth. Usually, the sores or blisters can show up on the outside of the mouth or on the lips. But sometimes, they can be inside the mouth, on the face, nose, cheeks or fingers. HSV-1 can also lead to infection of the genitals, called genital herpes. This occurs when you have a cold sore and perform oral sex on another person. HSV-1 infections are highly contagious. Apart from oral-genital contact, they can be spread through skin-to-skin contact. If you come into contact with a person or a thing that carries HSV-1, you will be likely to get it, too. Often, people get HSV-1 from kissing someone with a cold sore or when they share eating utensils, razors, or towels.
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.
JJ 55 is right. We are almost always here, I always look at my thread at least 3 times an hour on my days off and I am on here more when I am at work. It's ok to be scared. I still cry about it. I am on antibiotics right now, I go back to the doctor on Tuesday for more humiliating actions. (Pap smear) I will find out about daily medications then. Oh crap sorry I tend to babble. We are here for you, but you will also need to read everything you can get your hands on. I just met JJ55 last night and it seems that we tend to do the same threads together. I am here for you as well. Soon we will have our own little group...
Although it’s not caused by either the HSV-1 or HSV-2 virus, herpes zoster falls under the umbrella of herpes diseases. Also known as shingles, it’s an infection caused by the varicella-zoster virus, and is characterized by the development of painful skin rashes on one side of the face or body.23 These rashes are red patches of fluid-filled blisters that tend to crack easily.24,25

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.
Essential oils that can help treat herpes include clove oil, tea tree oil and myrrh oil. Tea tree oil is one of the most common oils used on the skin for its natural antiviral, antibacterial properties. (3) Simply apply these essential oils three times daily to areas where cold sores are present, being careful to use a very small amount (only one to three drops). If you have sensitive skin, try mixing the essential oils with a carrier oil to dilute their strength a bit, including jojoba or coconut oil.

Following active infection, herpes viruses establish a latent infection in sensory and autonomic ganglia of the nervous system. The double-stranded DNA of the virus is incorporated into the cell physiology by infection of the nucleus of a nerve's cell body. HSV latency is static; no virus is produced; and is controlled by a number of viral genes, including latency-associated transcript.[70]


If you find out your partner has genital herpes, support him or her, and protect yourself. Genital herpes is so common and it may involve more than the virus itself. You can catch the disease from your partner through sexual contact. Without treatment, genital herpes can go away on its own. But, your partner needs medications to stop symptoms and prevent transmission. If you think the disease is harming your relationship, talk to your doctor for help.
As of 2017, there is not currently a herpes vaccine available to prevent HSV-1 or HSV-2. (There is a vaccine available for another virus, herpes zoster; however, despite the similar name, it actually refers to the shingles virus. And, in fact, shingles occurs due to the reactivation of yet another virus, varicella zoster, which causes chicken pox.)
The flares are caused when your immune system falters. This can be due to a number of reasons. Anything from daily stressors, lack of sleep, poor nutrition, weight gain, concurrent illnesses etc may cause your immune system to be distracted from the Herpes Simplex Virus (HSV) infection. The moment that happens, the virus will flare resulting in rashes, cold sores, ulcers or blisters on your body.
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.
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]
Herpes “triggers” (determining exactly what leads to an outbreak) are highly individual, but with time, many people learn to recognize, and sometimes avoid, factors that seem to reactivate HSV in their own bodies. Illness, poor diet, emotional or physical stress, friction in the genital area, prolonged exposure to ultraviolet light (commonly for oral herpes, such as a beach trip or skiing weekend), surgical trauma, and steroidal medication (such as asthma treatment) may trigger a herpes outbreak.
“You don’t want an infant delivered through infected birth canal or vulva because the infant can be infected,” Cullins explains. A neonatal herpes infection is a real risk because it can cause problems with brain development and eye and skin infections, or even be fatal. And since there is more risk for transmission from mother to baby during an initial outbreak than during a recurrent outbreak, the CDC stresses that it’s incredibly important for pregnant women to avoid contracting a new herpes infection.
This means they cannot function independently outside the living cell. Once inside, however, they provide a far different picture. They are parasitic. This means they live off the host at the host’s expense. Unless you have already been exposed to a particular virus, your body is essentially unable temporarily to prevent viral multiplication inside your body.
Although it's rare, pregnant women can pass on the herpes infection to their child. This can result in a serious and sometimes deadly infection in the baby. That's why taking steps to prevent an outbreak at time of delivery is recommended starting at 34 weeks into the pregnancy. If you have signs of an active viral infection when it's time to deliver, your doctor will likely recommend a cesarean section for delivery.
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