Stress keratin 17 and estrogen support viral persistence and modulate the immune environment during cervicovaginal murine papillomavirus infection

Significance Using a murine papillomavirus as a model for human papillomavirus (HPV) infection, this report reveals that two host factors, estrogen and stress keratin 17, cooperatively support viral persistence and disease progression in papillomavirus-induced cervicovaginal lesions at least in part by modulating distinct populations of immune cells. This study provides insight into underlying mechanisms of papillomavirus-induced cervical carcinogenesis and reveals two different host persistence factors that may potentially serve as new or complementary therapeutic targets in the treatment of cervical neoplastic disease and cancer.

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