![]() In the case of sexual exposure to HIV, there are numerous soluble factors and cells in genital and rectal secretions as well as in saliva that comprise the first line of defense against the virus. During ovulation the mucus plug is, however, more permissive to passage, and likely allows also free virus particles and HIV-infected leukocytes to passage to the upper genital tract regions. The FGT is further protected from microbes by a cervical mucus plug that normally inhibits seminal fluid and microbes from entering the upper genital tract. In the FGT, a layer of mucus is firmly attached to parts of the epithelial surface and functions as a barrier to HIV transmission. Female Genital Secretions Mediate both Antiviral and Inflammatory Activity Natural resistance to HIV infection and the inflammatory status are also critically influenced by physical and chemical external and intrinsic factors, including pH, presence of bacterial vaginosis, STIs, hormonal factors, seminal fluid and ruptions of the epithelial barrier. The balance between a pro- and an anti-inflammatory status of the mucosa may be one of the factors that determines the HESN status. ![]() The altered expression of any of these factors may influence the susceptibility to HIV infection. Here, a host of immune cells, antibodies, antimicrobial peptides, cytokines and chemokines may block the virus from attaching to epithelial surfaces and HIV target cells in the submucosa. ![]() In the case of sexual exposure to HIV, there are numerous soluble factors and cells in genital secretions that comprise the first line of defense against HIV. A layer of mucus is firmly attached to the epithelial surface of the vagina and ectocervix, and constitutes a physical barrier to HIV transmission. The human female genital tract mucosa is covered by epithelial cells arranged in either a single layer (endocervix, endometrium) or multiple layers (ectocervix, vagina). Model of factors that can protect from HIV infection in the female genital tract. In Figure 5.1, both external and intrinsic factors that can affect the genital mucosal surface and thereby contribute to its susceptibility to virus infection are illustrated.įIGURE 5.1. Thus, innate or adaptive immune responses to semen and/or HIV in HESN subjects, especially in female genital secretions, may play a key role in altering HIV susceptibility at the FGT. Clearly, inflammatory immune signals likely influence the ability of HIV to target mucosal cells for replication, and/or transmission out of the mucosal compartment. Thus, the route and dose of HIV exposure are issues that need to be considered when interpreting study results. Additionally, HIV binds to C-type lectins and pattern recognition receptors (PRR) on both epithelial and antigen-presenting cells, and can result in activation of the immune system in a dose-dependent manner. Furthermore, semen triggers induction of a local inflammatory response, induces dendritic cell projections to the luminal surface and promotes attraction of HIV target cells, including Langerhans cells, in the human FGT. Semen also acts as a buffer of the low pH in the female genital tract, and thereby counteracts this natural antimicrobial defense. It was recently shown that specific proteins in seminal fluid, such as semen derived enhancer of virus infection (SEVI), can induce fibril structures promoting the physical contact between the virus and epithelial surfaces, and thereby promote virus infection. HIV can thus be transmitted to mucosal target cells, including dendritic cells, macrophages and T cells. Semen is the main vector for HIV dissemination worldwide, and contains free HIV particles, virions associated to spermatozoa, and HIV-infected leukocytes.
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