Regulation of the life cycle of HPVs by differentiation and the DNA damage response

被引：55

作者：

Hong, Shiyuan ^{[1
]}

Laimins, Laimonis A. ^{[1
]}

机构：

[1] Northwestern Univ, Dept Microbiol Immunol, Feinberg Sch Med, Chicago, IL 60611 USA

来源：

FUTURE MICROBIOLOGY | 2013年 / 8卷 / 12期

关键词：

amplification; ATM; CHK2; differentiation; DNA damage; papillomaviruses; replication foci; STAT-5; HUMAN-PAPILLOMAVIRUS TYPE-16; ATM-DEPENDENT PHOSPHORYLATION; EPITHELIAL DIFFERENTIATION; GENOMIC INSTABILITY; COMPLEX-FORMATION; P53; ACTIVATION; FRAGILE SITES; E1; PROTEIN; E6; REPLICATION;

D O I：

10.2217/fmb.13.127

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

HPVs are the causative agents of cervical and other anogenital cancers. HPVs infect stratified epithelia and link their productive life cycles to cellular differentiation. Low levels of viral genomes are stably maintained in undifferentiated cells and productive replication or amplification is restricted to differentiated suprabasal cells. Amplification is dependent on the activation of the ATM DNA damage factors that are recruited to viral replication centers and inhibition of this pathway blocks productive replication. The STAT-5 protein appears to play a critical role in mediating activation of the ATM pathway in HPV-positive cells. While HPVs need to activate the DNA damage pathway for replication, cervical cancers contain many genomic alterations suggesting that this pathway is circumvented during progression to malignancy.

引用

页码：1547 / 1557

页数：11

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