Herpes Testing Blog

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.

 People who use condoms regularly can reduce their risk of getting genital herpes by 30 percent, a new study finds. The herpes simplex virus 2 (HSV-2) causes genital herpes, which is a chronic, lifelong viral infection. Although studies have found that regular condom use reduces the spread of HIV and other sexually transmitted diseases (STDs) such as chlamydia and gonorrhea, whether they prevent the transmission of HSV-2 has been less certain, the researchers noted.

“Condoms work for herpes,” said study author Emily T. Martin, a postdoctoral fellow with the Seattle Children’s Hospital Research Institute. “Even though the decrease is smaller than you would see with some other STDs, the evidence from previous studies has been unclear whether using a condom to prevent getting herpes was going to be effective, but this shows that it is,” she said.

Using condoms reduces herpes transmission by only 30 percent because, unlike other STDs, herpes is transmitted by skin-to-skin contact, Martin explained. “Transmission has a lot to do with where the virus is being shed at the time,” she said. “If someone with herpes is shedding virus for an area that is not covered by a condom, we speculate the virus will spread whether or not they are using a condom.” The study is published in the July 13 issue of Archives of Internal Medicine.

For the study, Martin’s team looked at data from six HSV-2 studies that dealt with the effectiveness of condoms in preventing herpes. The studies included 5,384 men and women who did not have herpes when the studies began. During the follow-up period, which ranged from 12 to 19 months, 415 people had contracted the herpes virus. But people who used condoms 100 percent of the time reduced the risk of catching the virus by 30 percent, the researchers found.

In addition, the risk of getting herpes was reduced 7 percent “every additional 25 percent of the time that condoms were used during anal or vaginal sex,” the researchers wrote. The risk of getting herpes increased with the frequency of unprotected sex, and there was no significant difference between men and women in the effectiveness of condoms in preventing herpes transmission, they add.

Martin said using a condom not only reduces the odds of getting herpes, but of other STDs as well. “If you don’t know the STD status of your partner, a condom is always a good idea,” she said. Dr. Jeffrey D. Klausner, director of STD Prevention and Control Services at the San Francisco Department of Public Health, said the study provides more evidence that condoms work.

“We know condoms can prevent the spread of sexually transmitted infections like HIV, herpes, warts, hepatitis, gonorrhea, chlamydia and syphilis, but it’s always been hard to show that in research studies,” Klausner said. “If condoms can hold air and water, I never understood why folks thought they would not prevent the spread of germs, which are much, much larger than air or water molecules,” he said.

Klausner said that the study provides scientific evidence that condoms work and should help in efforts to get condoms into the hands of sexually active teenagers and adults.

For the full article, please refer to http://www.healthscout.com/news/1/628978/main.html

Pro-medics.com, the online pharmaceutical company, announced their sales addition of the new herpes medication, Generic Valtrex. This innovative drug treatment has just recently become FDA approved for the prevention and treatment of Genital Herpes.

Valtrex is an anti-viral medication that has been medically proven to treat both cold sores and shingles, as well as shorten the length of Herpes treatment time.

Ralphe Rowe, Company Product manager explained, “Unfortunately, Genital Herpes has been currently increasing in appearance amongst the American public, involving a series of embarrassing and uncomfortable symptoms.” “Pro-medics online is proud to offer its customers a discreet and medically effective solution to treating the virus.”

Pro-medics online, offers its clientele free anonymous phone consultations, providing customers with live medical advice and support. This unique form of customer service alleviates the requirement of a prior prescription or potentially embarrassing visit to the doctor.

Pro-medics pharmaceuticals is known for offering its customers first rate service and quality medications at highly discounted prices. The company therefore stocks the preferred generic version of Valacyclovir, otherwise referred to as Generic Valtrex. Generic Valtrex is just as effective as its name brand counterpart, only it’s available at less than half the original drug’s price.

Regarding this decision, Pro-medics President of Sales, Sarah Tenne, explained “Our Company places an emphasis on bringing its customers quality drugs at discount prices. We see no reason for product quality to come at the expense of customer affordability”.

About Pro-Medics
Pro-Medics.com is an online pharmacy website, offering customers popularly prescribed prescription drugs. Pro-Medics also specializes in erectile dysfunction and diet pills, offering a full line of both popular brand name medications as well as their discounted generic counterparts.

For the complete article, please refer to http://www.prweb.com/releases/2009/07/prweb2610284.htm.