Herpes Testing Blog

This article has the point of dispelling some common myths about genital herpes, and also of  spreading the news about prevention.

Herpes is a very common virus: the CDC estimates that as many as 45 million people ages 12 and older are infected with genital herpes.  This is about one in five adolescents and adults.  This means that it is very likely that you or someone you know have this virus.

Many people that have genital herpes may not know that they have it because they either have very mild symptoms or they mistake the symptoms – such as painful urination in women – for another condition such as a yeast infection.

Just by taking some simple precautions, including using a condom and taking anti-herpetic medicine, you can protect yourself and your partner from getting the virus. Another way, possibly the most effective way, to prevent herpes (or any other STD) transmission is for you and your partner to be tested and known to be uninfected.

What is genital herpes?

Genital herpes is caused by herpes simplex virus type 2 (HSV-2), which can invade the body through a crack in the skin or through the mucosa of the mouth or genital areas. Signs of a HSV-2 infection are usually one or more blisters on or around the rectum or genitals. When the blisters eventually break, they leave tender ulcers or sores. Those can take two to four weeks to heal after the first breakout. Typically future breakouts will be less severe and have a shorter healing time.

Viral activity tends to decrease with time. This means that as time progresses, somebody with herpes will have less frequent and less severe outbreaks.

Did you know?

Genital herpes can spread whether or not there are symptoms present or if there have never been signs or symptoms.
Herpes is likely to be spread 3-5 days before a breakout.
Having genital herpes can make you two to five times more susceptible to HIV infection.
Condoms do not fully protect you against HSV-2 because the virus can infect areas not covered by the condom.
Even if you are not having a herpes outbreak, you may still “shed” the virus.

How can you protect yourself and your partner?

Abstinence is the only 100 percent effective way to ensure against the spread of any STD including genital herpes. Herpes can also be spread without the presence of signs or symptoms. Condoms act as a physical barrier against the spread of the virus, but they are only effective at protecting the area that it covers, which is probably not the only part of you that is coming in contact with your partner when you are having sex.

There are also over-the-counter as well as prescription medicines that one can take to suppress the frequency and severity of the outbreaks.  In doing so, they also reduce the risk of transmitting the virus. If you are interested in this, the best thing to do would be to ask you doctor about your options

Because such a high number of people are unaware that they are infected with genital herpes, testing for herpes is the best way to determine your status. A long-term mutually monogamous relationship with a partner who has been tested and is known to be uninfected is one of the best ways to remain disease-free.

*For the original article, please refer to http://www.hivtestingblog.com/original-articles/

New research helps explain why infection with herpes simplex virus-2 (HSV-2), which causes genital herpes, increases the risk for HIV infection even after successful treatment heals the genital skin sores and breaks that often result from HSV-2.

Scientists have uncovered details of an immune-cell environment conducive to HIV infection that persists at the location of HSV-2 genital skin lesions long after they have been treated with oral doses of the drug acyclovir and have healed and the skin appears normal. These findings are published in the advance online edition of Nature Medicine on Aug. 2.

Led by Lawrence Corey, M.D., and Jia Zhu, Ph.D., of the Fred Hutchinson Cancer Research Center and Anna Wald, M.D., M.P.H., of the University of Washington, both in Seattle, the study was funded mainly by the National Institute of Allergy and Infectious Diseases (NIAID) with support from the Eunice Kennedy Shriver National Institute of Child Health and Human Development, both part of the National Institutes of Health.

“The findings of this study mark an important step toward understanding why HSV-2 infection increases the risk of acquiring HIV and why acyclovir treatment does not reduce that risk,” says NIAID Director Anthony S. Fauci, M.D. “Understanding that even treated HSV-2 infections provide a cellular environment conducive to HIV infection suggests new directions for HIV prevention research, including more powerful anti-HSV therapies and ideally an HSV-2 vaccine.”

One of the most common sexually transmitted infections worldwide, HSV-2 is associated with a two- to three-fold increased risk for HIV infection. Some HSV-2-infected people have recurring sores and breaks in genital skin, and it has been hypothesized that these lesions account for the higher risk of HIV acquisition. However, recent clinical trials, including an NIAID-funded study completed last year, demonstrated that successful treatment of such genital herpes lesions with the drug acyclovir does not reduce the risk of HIV infection posed by HSV-2 . The current study sought to understand why this is so and to test an alternative theory.

“We hypothesized that sores and breaks in the skin from HSV-2 are associated with a long-lasting immune response at those locations, and that the response consists of an influx of cells that are a perfect storm for HIV infection,” says Dr. Corey, co-director of the Vaccine and Infectious Diseases Institute at The Hutchinson Center and head of the Virology Division in the Department of Laboratory Medicine at the University of Washington. “We believe HIV gains access to these cells mainly through microscopic breaks in the skin that occur during sex.”

The research team took biopsies of genital skin tissue from eight HIV-negative men and women who were infected with HSV-2. These biopsies were taken at multiple time points: when the patients had genital herpes sores and breaks in the skin, when these lesions had healed, and at two, four and eight weeks after healing. The researchers also took biopsies from four of the patients when herpes lesions reappeared and the patients underwent treatment with oral acyclovir. The scientists continued to take biopsies at regular intervals for 20 weeks after the lesions had healed. For comparison, the investigators also took biopsies from genital tissue that did not have herpes lesions from the same patients.

Previous research has demonstrated that immune cells involved in the body’s response to infection remain at the site of genital herpes lesions even after they have healed. The scientists conducting the current study made several important findings about the nature of these immune cells. First, they found that CD4+ T cells—the cells that HIV primarily infects—populate tissue at the sites of healed genital HSV-2 lesions at concentrations 2 to 37 times greater than in unaffected genital skin. Treatment with acyclovir did not reduce this long-lasting, high concentration of HSV-2-specific CD4+ T cells at the sites of healed herpes lesions.

Second, the scientists discovered that a significant proportion of these CD4+ T cells carried CCR5 or CXCR4, the cell-surface proteins that HIV uses (in addition to CD4) to enter cells. The percentage of CD4+ T cells expressing CCR5 during acute HSV-2 infection and after healing of genital sores was twice as high in biopsies from the sites of these sores as from unaffected control skin. Moreover, the level of CCR5 expression in CD4+ T cells at the sites of healed genital herpes lesions was similar for patients who had been treated with acyclovir as for those who had not.

Third, the scientists found a significantly higher concentration of immune cells called dendritic cells with the surface protein called DC-SIGN at the sites of healed genital herpes lesions than in control tissue, whether or not the patient was treated with acyclovir. Dendritic cells with DC-SIGN ferry HIV particles to CD4+ T cells, which the virus infects. The DC-SIGN cells often were near CD4+ T cells at the sites of healed lesions—an ideal scenario for the rapid spread of HIV infection.

Finally, using biopsies from two study participants, the scientists found laboratory evidence that HIV replicates three to five times as quickly in cultured tissue from the sites of healed HSV-2 lesions than in cultured tissue from control sites.

All four of these findings help explain why people infected with HSV-2 are at greater risk of acquiring HIV than people who are not infected with HSV-2, even after successful acyclovir treatment of genital lesions.

“HSV-2 infection provides a wide surface area and long duration of time for allowing HIV access to more target cells, providing a greater chance for the initial ’spark’ of infection,” the authors write. This spark likely ignites once HIV penetrates tiny breaks in genital skin that commonly occur during sex. “Additionally,” the authors continue, “the close proximity to DC-SIGN-expressing DCs [dendritic cells] is likely to fuel these embers and provide a mechanism for more efficient localized spread of initial infection.” The investigators conclude that reducing the HSV-2-associated risk of HIV infection will require diminishing or eliminating the long-lived immune-cell environment created by HSV-2 infection in the genital tract, ideally through an HSV vaccine. Further, they hypothesize that other sexually transmitted infections (STIs) may create similar cellular environments conducive to HIV infection, explaining why STIs in general are a risk factor for acquiring HIV.