title: Host cell restriction factors that limit transcription and replication of human papillomavirus.
abstract: The life cycle of human papillomaviruses (HPV) is tightly regulated by the differentiation state of mucosal and cutaneous keratinocytes. To counteract viral infection, constitutively expressed cellular factors, which are defined herein as restriction factors, directly mitigate viral gene expression and replication. In turn, some HPV gene products target these restriction factors and abrogate their anti-viral effects to establish efficient gene expression and replication programs. Ironically, in certain circumstances, this delicate counterbalance between viral gene products and restriction factors facilitates persistent infection by HPVs. This review serves to recapitulate the current knowledge of nuclear restriction factors that directly affect the HPV infectious cycle.
authors.affiliation: Laboratory of Viral Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, 33 North Drive, MSC3209, Bethesda, MD 20892, USA; Biological Sciences Graduate Program, University of Maryland, University of Maryland, 4066 Campus Drive, College Park, MD 20742, USA.
authors.forename: Samuel S
authors.initials: SS
authors.lastname: Porter
authors.affiliation: Laboratory of Viral Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, 33 North Drive, MSC3209, Bethesda, MD 20892, USA.
authors.forename: Wesley H
authors.initials: WH
authors.lastname: Stepp
authors.affiliation: Laboratory of Viral Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, 33 North Drive, MSC3209, Bethesda, MD 20892, USA.
authors.forename: James D
authors.initials: JD
authors.lastname: Stamos
authors.affiliation: Laboratory of Viral Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, 33 North Drive, MSC3209, Bethesda, MD 20892, USA. Electronic address: amcbride@nih.gov.
authors.forename: Alison A
authors.initials: AA
authors.lastname: McBride
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000235:genetics / Q000378:metabolism; D034961:Antigens, Nuclear / Q000235:genetics / Q000378:metabolism; D001324:Autoantigens / Q000235:genetics / Q000378:metabolism; D002454:Cell Differentiation; D002843:Chromatin / Q000737:chemistry / Q000378:metabolism / Q000821:virology; D056970:Co-Repressor Proteins; D005786:Gene Expression Regulation; D016679:Genome, Viral; D054884:Host-Pathogen Interactions; D006801:Humans; D015603:Keratinocytes / Q000378:metabolism* / Q000821:virology; D018832:Molecular Chaperones; D009687:Nuclear Proteins / Q000235:genetics / Q000378:metabolism; D027383:Papillomaviridae / Q000235:genetics* / Q000254:growth & development / Q000472:pathogenicity; D030361:Papillomavirus Infections / Q000235:genetics / Q000473:pathology / Q000821:virology*; D000071156:Promyelocytic Leukemia Protein / Q000235:genetics / Q000378:metabolism; D014764:Viral Proteins / Q000235:genetics / Q000378:metabolism; D014771:Virion / Q000235:genetics / Q000254:growth & development / Q000472:pathogenicity; D014779:Virus Replication
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D034961:Antigens, Nuclear; D001324:Autoantigens; D002843:Chromatin; D056970:Co-Repressor Proteins; C106985:DAXX protein, human; D018832:Molecular Chaperones; D009687:Nuclear Proteins; D000071156:Promyelocytic Leukemia Protein; D014764:Viral Proteins; C066642:SP100 protein, human; C070576:PML protein, human
keywords: HPV; IFI16; IFIT1; Intrinsic immunity; Restriction factor; Sp100