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Cervicovaginal mucins (CVM) are high-molecular-weight, heavily O-glycosylated proteins that serve as the primary structural and functional components of the mucus layer lining the female reproductive tract (Gipson, 2001). This complex mixture includes secreted gel-forming mucins, predominantly MUC5B and MUC5AC, which provide the viscoelastic properties necessary for lubrication and selective filtration, as well as membrane-associated mucins like MUC1, MUC4, and MUC16 that form the glycocalyx (Hanisch et al., 2007; Lacroix et al., 2020). CVM acts as a critical innate immune barrier, trapping pathogens such as HIV, HSV, and HPV through steric hindrance and biochemical interactions, while also regulating sperm transport in a cycle-dependent manner (Wang et al., 2014). In clinical contexts, alterations in CVM rheology or glycosylation are linked to increased susceptibility to infections, bacterial vaginosis, and obstetric complications like preterm birth (Borgdorff et al., 2016). Pharmacologically, CVM is a target for mucoadhesive drug delivery systems designed to prolong the residence time of microbicides and for engineered "muco-trapping" antibodies that enhance the barrier's ability to neutralize viral threats (Newby et al., 2017).
Mucoadhesion to increase drug residence time, barrier enhancement to trap pathogens, and mucolysis to alter rheological properties.
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