Characterization of immune cell infiltrates in condyloma acuminata: implications for HIV transmission
Bohnert, Lindsay Amanda
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Condyloma acuminata, or genital warts, is the clinical manifestation of a human papillomavirus (HPV) infection, with low-risk subtypes HPV-6 and HPV-11 causing 90% of genital warts. The incidence rate of visible condyloma acuminata is about 1% in the sexually active population and growing, while genital HPV infection has prevalence rates as high as 10-20% in the United States. These lesions are friable, bleed easily, and occur on locations engaged during sexual intercourse. Our focus was to describe the composition of the immune cell infiltrates present in these lesions, while exploring the possibility that HIV-target cells may be present among these infiltrates. We studied genital warts from men and women, using immunohistochemistry to identify cell types associated with HIV infection: CD1a+ dendritic cells, CD68+ macrophages, CD3+, CD4+, and COB+ lymphocytes, CD15+ granulocytes, and cells expressing HIV coreceptors CCR5 and CXCR4. Concentrations of CD1a+, CD3+, CD4+, and CD8+ cells were much higher in condyloma tissue compared to normal control tissue in both genders. The CD1a+ dendritic cells were distributed throughout the epithelium, with a number also present in the dermis. CD3+, CD4+, and CDS+ lymphocytes were scattered throughout the dermis and dermal papillae, and were often found in focal accumulations. These cells were also found throughout the epithelium, which was not seen in control tissue. We observed an increased presence of CD68' and CXCR4+ cells in most of the condyloma tissues, but their distribution varied. CD68' macrophages were found in greater numbers throughout the dermis and dermal papillae, and were also present in small numbers in the epithelium. CXCR4ˉ cells were present in the dermis and epithelium in many of the samples. A few condyloma tissues contained some CD15+ or CCR5+ cells, but no cells expressing these markers were found in control tissue. This striking increase in CD1a', C068+, and CD4' HIV target cells in condyloma acuminata provides evidence that genital warts are highly susceptible sites for HIV transmission. Additionally, the unique distribution of these cells could promote infection from HIV-infected individuals to HIV-negative partners. This risk would be further exacerbated by any breaks in the epithelial barrier, which is feasible due to the structural characteristics of these lesions. Our study suggests that measures to prevent and treat genital warts, such as HPV vaccination and wart removal, could decrease the sexual transmission of HIV.
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