—– Original Message —– From: “M.L.S.” Newsgroups: alt.support.herpes Sent: Thursday, January 08, 2004 11:12 AM Subject: Re: Cold Sores HEALED in 3.6 Days! Second, having sores or outbreaks and being on meds or not on meds has NO correlation to when you are contagious. nothing but just several rashes on scortum.. A month later I’ve had sex again and it has reopened. The herpes simplex virus – or “cold sore virus” – is highly contagious and can be easily passed from person to person by close direct contact. 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. To be effective, these treatments should be applied as soon as the first signs of a cold sore appear – when you feel a tingling, itching or burning sensation around your mouth. 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. In very rare cases, encephalitis, a condition where the brain becomes inflamed and swollen, can be caused by the cold sore virus spreading to the brain. 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. The study was funded mainly by the NIAID with support from the Eunice Kennedy Shriver National Institute of Child Health and Human Development, both part of the National Institutes of Health.