Herpes infection can cause sores or breaks in the skin or lining of the mouth, vagina, and rectum. This provides a way for HIV to enter the body. Even without visible sores, having genital herpes increases the number of CD4 cells (the cells that HIV targets for entry into the body) found in the lining of the genitals. When a person has both HIV and genital herpes, the chances are higher that HIV will be spread to an HIV-uninfected sex partner during sexual contact with their partner’s mouth, vagina, or rectum.
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.
A scary finding is that more cases of genital herpes than ever before are now being caused by HSV-1 (the type most people assume only causes mouth sores), and about 85 percent of people with genital herpes don’t even know it. (7) Studies show that about 50 percent of the new genital herpes infections in young adults are due to HSV-1 and about 40 percent in older adults. The fact that most people don’t ever find out they’re infected is one of the reasons that transmission rates are steadily climbing.
Diagnosing herpes is made much easier if you present to your clinician at the time that the rash is present and if possible, we can take a sample from that to be sent for Herpes PCR (Polymerase Chain Reaction) studies to confirm the diagnosis. Advanced medical investigative techniques such as this will allow us to differentiate type one from type two herpes regardless of the nature and distribution of the rash.
No method eradicates herpes virus from the body, but antiviral medications can reduce the frequency, duration, and severity of outbreaks. Analgesics such as ibuprofen and paracetamol (acetaminophen) can reduce pain and fever. Topical anesthetic treatments such as prilocaine, lidocaine, benzocaine, or tetracaine can also relieve itching and pain.
The cell this virus targets is the B lymphocyte. These cells mature in the bone marrow and are a type of mononuclear leukocyte cells - white blood cells with a one-lobed nucleus. The incubation period for the Epstein – Barr Virus (EBV) is about 30 to 50 days, and patients typically have enlarged lymph nodes and spleens. Some patients have signs of hepatitis.
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.
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...
The U.S. Centers of Disease Control and Prevention explains that pain, itching or tingling in the area where the rashes will eventually appear will occur at least one to five days before the rashes are seen. Once these rashes are visible, they scab for around seven to 10 days and heal within two to four weeks.29 Aside from rashes, symptoms of shingles include fever, chills, headaches, fatigue and an upset stomach.30,31
Herpes simplex is a viral infection caused by the herpes simplex virus. Infections are categorized based on the part of the body infected. Oral herpes involves the face or mouth. It may result in small blisters in groups often called cold sores or fever blisters or may just cause a sore throat. Genital herpes, often simply known as herpes, may have minimal symptoms or form blisters that break open and result in small ulcers. These typically heal over two to four weeks. Tingling or shooting pains may occur before the blisters appear. Herpes cycles between periods of active disease followed by periods without symptoms. The first episode is often more severe and may be associated with fever, muscle pains, swollen lymph nodes and headaches. Over time, episodes of active disease decrease in frequency and severity. Other disorders caused by herpes simplex include: herpetic whitlow when it involves the fingers, herpes of the eye, herpes infection of the brain, and neonatal herpes when it affects a newborn, among others.
After exposure to the virus, many people experience a so called primary infection which is typically associated with sores on or around the genitals or the anus. During a primary infection some people experience pain in the groins or a mild fever. Not all infected individuals experience a primary infection or show any symptoms at all, but they can still pass the disease on to other people.