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Abstract: Autophagy is a self-consumption mechanism used by cells to maintain homeostasis inthe body. Some findings suggest that high-risk human papillomavirus (HR-HPV) promotes cervical carcinogenesis by acting on host cell autophagy. HR-HPV can integrate the viral genome into the host DNA, which in turn infects the host cell. HR-HPV L1 and L2 proteins assist viral entry into cells and inhibit the autophagic process by activating the PI3K / AKT / mTOR signalling pathway through interactions with cell-surface receptors on the membrane of the target cell, resulting in the uninterrupted transport of viral particles into the cell. At the end stage of viral infection, HR-HPV L1 and L2 proteins are expressed in the cytoplasm and translocate to the nucleus, assisting viral evasion of immune surveillance by affecting autophagy. Although HPV prophylactic vaccines against HR-HPV L1 and L2 proteins are available, clarifying the specific regulation of autophagy in cervical cancer by HR-HPV L1 and L2 proteins may expand new ideas for cervical cancer prevention and treatment.

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