Host cell restriction factors that limit transcription and replication of human papillomavirus

被引:32
作者
Porter, Samuel S. [1 ,2 ]
Stepp, Wesley H. [1 ,3 ]
Stamos, James D. [1 ]
McBride, Alison A. [1 ]
机构
[1] Natl Inst Hlth, Viral Dis Lab, Natl Inst Allergy & Infect Dis, 33 North Dr,MSC3209, Bethesda, MD 20892 USA
[2] Univ Maryland, Biol Sci Grad Program, 4066 Campus Dr, College Pk, MD 20742 USA
[3] Univ N Carolina, North Carolina Jaycee Burn Ctr, Dept Surg, Sch Med, 160 Dent Circle, Chapel Hill, NC 27599 USA
关键词
HPV; Sp100; IFI16; IFIT1; Restriction factor; Intrinsic immunity; DNA-DAMAGE RESPONSE; INTERFERON-INDUCIBLE PROTEIN; SIMPLEX-VIRUS TYPE-1; MINOR CAPSID PROTEIN; NUCLEAR DOMAIN 10; PRIMARY HUMAN KERATINOCYTES; EARLY GENE-EXPRESSION; VIRAL LIFE-CYCLE; PROMYELOCYTIC LEUKEMIA; C/EBP-BETA;
D O I
10.1016/j.virusres.2016.11.014
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
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. Published by Elsevier B.V.
引用
收藏
页码:10 / 20
页数:11
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