期刊
CURRENT OPINION IN VIROLOGY
卷 50, 期 -, 页码 76-86出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.coviro.2021.07.010
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资金
- U.S. National Institutes of Health [R01 CA207368, R21 DE028652, P30 CA118100, R01 GM136853, P30 CA023074]
HPV infects and replicates in differentiating mucosal and cutaneous epithelium. Most infections are asymptomatic, but persistent infections by oncogenic types can progress to cancer. HPV particles interact with host proteins during infectious entry into keratinocytes, leading to uncoating of the viral genome and eventual transcription in the nucleus.
Human papillomaviruses (HPVs) infect and replicate in differentiating mucosal and cutaneous epithelium. Most HPV infections are asymptomatic or cause transient benign neoplasia. However, persistent infections by oncogenic HPV types can progress to cancer. During infectious entry into host keratinocytes, HPV particles interact with many host proteins, beginning with major capsid protein L1 binding to cellular heparan sulfate and a series of enzymatic capsid modifications that promote infectious cellular entry. After utilizing the endosomal pathway to uncoat the viral genome (vDNA), the minor capsid protein L2/vDNA complex is retrograde trafficked to the Golgi, and thereafter, to the nucleus where viral transcription initiates. Post-Golgi trafficking is dependent on mitosis, with L2-dependent tethering of vDNA to mitotic chromosomes before accumulation at nuclear substructures in G1. This review summarizes the current knowledge of the HPV entry pathway, the role of cellular proteins in this process, and notes many gaps in our understanding.
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