NEW RESEARCH ON HIV and HERPES - NO NEED FOR OPEN SORES FOR TRANSMISSION???
Aug 4, 2009
Dear Dr. Bob: You have been extremely helpful to me over the years and I have donated to support the great work you are doing. I have been somewhat satisfied with being sexually active with women using a condom correctly every time based on everything I have read on your forum - up until today. Now I am suddenly not so comfortable anymore and quite nervous. I just read a short article about this new strain of HIV found in a woman from Cameroon. The second half of the article discussed new research that apparently shows that even people with genital herpes remain at increased risk of HIV infection even after the sores heal!! Everything I have read on this forum and others up until now seemed to clearly state that the only risk (with respect to herpes and HIV transmission) was when you had active herpes infection. That is, there was a direct route into the blood stream through open wounds. I cut and paste the portion of the article I am referring to from "Arab News" below. It includes a chilling quote by Dr. Anthony S. Fauci. I also cut and paste below a fairly recent posting from you saying HIV doesn't pass through intact skin and you directed the response to someone who was concerned about his Herpes infection and HIV transmission. I suppose I have 2 main questions: 1) Are you aware of this new research and do you agree with its conclusions? 2) As the writer below stated, I also have genital herpes at the base of my penis. Since I always use a condom and am reasonably sure the base of my penis is not actually entering women's vaginas (although there may be some moisture from women's vagina coming into contact with the base of my penis on occasion especially when penetrating deeply) - even if the findings of this research are accurate - would I be at greater risk of transmission when I am not having outbreaks or open sores given that the base of my penis is not actually entering the woman? I would much appreciate an answer to this question. The article is very new and I haven't seen anyone post a question about this in July or August on your forum yet. Thanks in advance and for the great work you continue to do! Nervous Again in Asia
"A separate paper, also in Nature Medicine, reports that people with genital herpes remain at increased risk of HIV infection even after the herpes sores have healed and the skin appears normal. Researchers led by Drs. Lawrence Corey and Jia Zhu of the Fred Hutchinson Cancer Research Center in Seattle found that long after the areas where the herpes sores existed seem to be clear, they still have immune-cell activity that can encourage HIV infection. Herpes is marked by recurring outbreaks and has been associated with higher rates of infection with HIV. It had been thought that the breaks in the skin were the reason for higher HIV rates, but a study last year found that treatment of herpes with drugs did not reduce the HIV risk. The researchers tested the skin of herpes patients for several weeks after their sores had healed and found that, compared with other genital skin, from twice to 37 times more immune cells remained at the locations where the sores had been. HIV targets immune cells and in laboratory tests the virus reproduced three to five times faster in tissue from the healed sites as in tissue from other areas. Understanding that even treated (herpes) infections provide a cellular environment conducive to HIV infection suggests new directions for HIV prevention research, commented Dr. Anthony S. Fauci, director of the National Institute of Allergy and Infectious Disease.
From Dr. Bob to writer:
"If the skin wasn't intact enough to prevent the herpes then I guess it couldn't have been intact enough to prevent HIV." If you did "guess" this, your assumption would be completely wrong! The facts are that herpes, like HPV (genital warts), is spread merely by skin-to-skin contact. Therefore even with the skin intact you can contract herpes and HPV. However, HIV is more difficult to transmit. HIV cannot permeate intact skin! HIV can cross intact mucous membranes, such as the lining of the urethra (pee hole), but not skin (the covering of the shaft of the penis, for example). You can read much more about HIV transmission, both sexual and nonsexual, in the archives of this forum. You can also learn more about other STDs and their modes of transmission as well.
Good luck. Dr. Bob.
Response from Dr. Frascino
1. This new research was just presented and consequently I'm learning about it now along with everyone else. I'll post below some more detailed analysis about what we know so far. I'll also urge you to stay tuned, as we promise to keep you up to date as this story evolves.
2. If this research is indeed accurate, yes, there would be a theoretical risk that infectious bodily fluids could transmit the virus to areas of herpetic lesions, even if the lesions are healed or not presently open and active.
U.S. National Institute of Allergy and Infectious Diseases Press Release Scientists Learn Why Even Treated Genital Herpes Sores Boost the Risk of HIV Infection
August 2, 2009
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+ T cells) 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.
For more information about HIV/AIDS research, visit the NIAID HIV/AIDS portal, and for more information about HSV-2 research, go to NIAID's Genital Herpes Web page.
References Zhu et al. Persistence of HIV-1 receptor-positive cells after HSV-2 reactivation is a potential mechanism for increased HIV-1 acquisition. Nature Medicine DOI: 10.1038/nm2006 (2009). C Celum et al. Effect of aciclovir on HIV-1 acquisition in herpes simplex virus 2 seropositive women and men who have sex with men: a randomised, double-blind, placebo-controlled trial. Lancet DOI: 10.1016/S0140-6736(08)60920-4 (2008).
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