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. 2016 Jun 24;7:245. doi: 10.3389/fimmu.2016.00245

Figure 1.

Figure 1

Factors affecting HIV infection of the male genital tract. (A) The foreskin consists of a double layer of stratified epithelium that covers the glans/corona and meatus of a flaccid penis. (B) Circumcision results in the removal of the majority of the foreskin epithelium leaving a “dry” keratinized surface that is assumed to be resistant to HIV infection. Non-STI genital microbial populations have been shown to modulate genital inflammation through the antigen recognition, which may result in migration or activation of HIV target cells into the foreskin. Circumcision results in a removal of the moist sub-preputial space and decrease in anaerobic bacterial species, which are likely pro-inflammatory. (C) The foreskin is a stratified epithelium consisting of six epidermal layers namely stratum corneum (SC), stratum granulosum (SG), stratum spinosum (SS), and stratum basale (SB). HIV virions crosses the keratinized (light brown) epithelial border through micro abrasions that occur during sexual intercourse or through the formation of viral synapses between HIV-infected cells and epithelial cells (20). Langerhans’ Cells (LCs) reside within the epidermis where they are the first to encounter the virus (21). Activated LCs migrate into the lower dermal tissues, transferring the virus to resident dermal immune cells such as T cells, macrophages, and epithelial dendritic cells (DCs). Dendritic cells act as professional antigen presenting cells, phagocytosing virions, and migrating to the draining lymph nodes where they present HIV antigens to immature T cells and B cells (22). Intact virus can be trafficked into the lymph nodes by DCs and transferred to CD4+ T cells (23) where the virus replicates and is disseminated throughout the body (24). Asymptomatic STIs do not present clinically but inflammation still occurs on a cellular level. The release of pro-inflammatory cytokines by keratinocytes and dermal immune cells in response to an STI would result in recruitment and activation immune cells to the site of infection. This inflammatory environment would result in an accumulation of HIV target cells and therefore increase the efficiency of viral transmission in the case of an HIV infection.