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Journal of Global Infectious Diseases / Jan-Mar 2012 / Vol-4 / Issue-1 T evidence that male circumcision (MC) reduces the risk of human immunodeficiency virus (HIV) in men is substantial,[1-3] but a biologically plausible explanation for this effect remains elusive. The pathogenesis is more complex than previously thought, and may involve several different mechanisms acting in concert to activate mucosal immunity and disrupt the barrier function of the epithelium. Earlier studies focused on the differential thickness between the inner and outer keratin layers. Tissue studies have shown that the inner foreskin, frenulum, and urethra are less keratinized than the outer foreskin and glans.[4] There is also evidence of an increased density of HIV target cells (Langerhans cells, macrophages, and CD4 cells) in the foreskin.[5] It has been postulated that the thinner anatomical barrier between the dendritic projections of the Langerhans cells and the vaginal secretions at the inner foreskin allow a more effective uptake of the virus. Other studies, however, challenge this theory. Analyses of the foreskins of Chinese men and boys following elective circumcision have found a thicker inner foreskin compared to the outer surface in adults and children with a history of penile infections.[6] Another recent study has reported no significant difference in the thickness between the inner and outer keratin layers, using a novel staining technique of the tissues.[7] All these investigations are limited by small sample sizes, lack of standardized technique to measure keratin, and a possible confounding effect of recurrent infection. Thus, the barrier theory needs further study.

Male circumcision and HIV: Do all roads lead to Rome?