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Laboratory evidence suggests that Carrageenan (an inexpensive gelling agent that is non-toxic and safe in animals and humans) is a potent HPV infection inhibitor. Inhibition occurred against all high and low oncogenic risk HPV types. Recently, carrageenan was shown to inhibit genital transmission of HPV in mice and in monkeys. Other than vaccination, which confers partial protection and whose immunity benefits may wane, there is no other intervention against HPV infection. Furthermore, screening generates very high costs to society because of the need to manage and treat all precancerous lesions that are found and the fertility problems that occur post-treatment. As a primary prevention approach, a carrageenan-based strategy would minimize these negative public health consequences of screening. Carrageenan has the desirable properties of efficacy and safety that could make it one of the most effective strategies against genital HPV infection and associated diseases.



Scientific basis for studying Carrageenan

Carrageenan is an anionic polymer that is naturally derived from three species of red algae. It has a long history of human use and has been employed extensively in the food, pharmaceutical, and cosmetics industries as stabilizer and emulsifier. Three major chains of Carrageenans exist: iota, lambda and kappa. All act as extremely potent HPV inhibitors. The principal mechanism by which Carrageenan blocks HPV infection is via the direct binding of Carrageenan to the viral capsid thus blocking its attachment to cell-surface Heparan Sulfate Proteoglycans (HSPG) acting as cell receptors. This blockage seems to last long enough to allow natural inactivation of the pathogens by the normal innate defences within the genital tract. In addition to blocking the initial interaction between HPV virions and HSPGs, laboratory studies show that Carrageenan also exerts a second HSPG-independent inhibitory effect via occlusion of virion surfaces involved in binding to cellular proteins involved in the infectious process; or alternately, by interference with the development of needed conformational changes within the virion. Additionally, in vitro studies have shown that HPV capsids bind to sperm cells at two distinct sites along the sperm head, suggesting that this may promote dispersal and mucosal penetration of HPV in the female genital tract. Carrageenan also blocks this binding. The existence of more than one inhibition mechanism increases the likelihood that Carrageenan might ultimately be effective as a topical microbicide against HPVs.

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