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Persistent infection with human papillomavirus (HPV) is responsible for nearly all new cervical cancer cases worldwide. In low- and middle-income countries (LMIC), infection with helminths has been linked to increased HPV prevalence. As the incidence of cervical cancer rises in helminth endemic regions, it is critical to understand the interaction between exposure to helminths and the progression of cervical cancer. Here we make use of several cervical cancer cell lines to demonstrate that exposure to antigens from the hookworm  N. brasiliensis  significantly reduces cervical cancer cell migration and global expression of vimentin and N-cadherin. Importantly,  N. brasiliensis  antigen significantly reduced expression of cell-surface vimentin, while decreasing HPV type 16 (HPV16) pseudovirion internalization.  In vivo  infection with  N. brasiliensis  significantly reduced vimentin expression within the female genital tract, confirming the relevance of these  in vitro  findings. Together, these findings demonstrate that infection with the hookworm-like parasite  N. brasiliensis  can systemically alter genital tract mesenchymal markers in a way that may impair cervical cancer cell progression. These findings reveal a possible late-stage treatment for reducing cervical cancer progression using helminth antigens.

scientific reports

Hookworm exposure decreases human papillomavirus uptake and cervical cancer cell migration through systemic regulation of epithelial-mesenchymal transition marker expression