The papillomavirus life cycle

Doorbar, John

doi:10.1016/j.jcv.2004.12.006

Cited by 686 publications

(690 citation statements)

References 76 publications

(87 reference statements)

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“…In squamous epithelium, the productive cycle of HPV is intimately linked with differentiation factors expressed within various layers of the host epithelial cell [3,5]. HPV cannot be cultured but only recently, an efficient virus propagation in vitro has been introduced [6].…”

Section: Hpv Life Cyclementioning

confidence: 99%

“…This could explain the patchy distribution of HPV DNA detected with in situ hybridization and the low amount of viral transcripts only detectable by highly-sensitive techniques. HPVs critically depend on the cellular machinery for the replication of their genome [3,5]. During the course of infection in proliferating basal cells or in transformed cell systems, HPVs establish their genomes as low-copy-number, autonomously replicating episomes [3,5,19,20].…”

Section: Hpv Replication In Basal Cellsmentioning

confidence: 99%

“…HPVs critically depend on the cellular machinery for the replication of their genome [3,5]. During the course of infection in proliferating basal cells or in transformed cell systems, HPVs establish their genomes as low-copy-number, autonomously replicating episomes [3,5,19,20]. HPV DNA replicates during the S phase, in synchrony with the host cell chromosome, and the mechanism of initiation of replication is fundamentally the same as that of eukaryotic chromosomes [19].…”

Section: Hpv Replication In Basal Cellsmentioning

confidence: 99%

“…E1 interacts with several cellular genes to synchronize the viral replication to host cell replication and is critical for G1/S transition and S phase. E1 also has an important role in retaining the episomal state of the viral molecule, i.e., keeping it separate from the host cell chromosome [3,5,19,20].…”

Section: Hpv Replication In Basal Cellsmentioning

confidence: 99%

“…Hence, the HPVs, especially viral proteins E5, E6 and E7, have developed strategies to subvert cellular growth regulatory pathways and are able to uncouple cellular proliferation and differentiation [3,5,19,20]. E7 is the most important driver of the cell cycle deregulation (Fig.…”

Section: Viral Genome Amplificationmentioning

confidence: 99%

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Biology of Human Papillomavirus Infections in Head and Neck Carcinogenesis

Rautava

Syrjänen

2012

Head and Neck Pathol

127

135

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Section: Hpv Life Cyclementioning

confidence: 99%

Section: Hpv Replication In Basal Cellsmentioning

confidence: 99%

Section: Hpv Replication In Basal Cellsmentioning

confidence: 99%

Section: Hpv Replication In Basal Cellsmentioning

confidence: 99%

Section: Viral Genome Amplificationmentioning

confidence: 99%

See 3 more Smart Citations

Biology of Human Papillomavirus Infections in Head and Neck Carcinogenesis

Rautava

Syrjänen

2012

Head and Neck Pathol

127

135

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Analyzing the Human Papillomavirus (HPV) Life Cycle in Primary Keratinocytes with a Quantitative Colony‐Forming Assay

et al. 2014

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Papillomavirus genomes replicate as extrachromosomal plasmids within infected keratinocytes, requiring the regulated expression of early viral gene products to initially amplify the viral genomes and subvert cell growth checkpoints as part of a complex path to immortalization. Building on contemporary keratinocyte transfection and culture systems, the methods described in this unit form a detailed approach to analyzing critical events in the human papillomavirus (HPV) life cycle, utilizing physiologic levels of viral gene products expressed from their native promoter(s) in the natural host cells for HPV infection. A quantitative colony-forming assay permits comparison of the capacities of various transfected HPV types and mutant HPV genomes to initially form colonies and immortalize human keratinocytes. In conjunction with additional methods, these protocols enable examination of genomic stability, viral and cellular gene expression, viral integration, and differentiation patterns influenced by HPV persistence in clonal human keratinocytes that effectively mimic early events in HPV infection.

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Construction of a Transcription Map for Papillomaviruses using RACE, RNase Protection, and Primer Extension Assays

Wang

Zheng

2016

CP Microbiology

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Papillomaviruses are a family of small, non-enveloped DNA tumor viruses. Knowing a complete transcription map of each papillomavirus genome can provide guidance for various papillomavirus studies. This unit provides detailed protocols to construct a transcription map of human papillomavirus type 18. The same approach can be easily adapted to other transcription map studies of any other papillomavirus genotype due to the high degree of conservation in genome structure, organization, and gene expression among papillomaviruses. The focused methods are 5-and 3-rapid amplification of cDNA ends (RACE), which are techniques commonly used in molecular biology to obtain fulllength RNA transcript or to map a transcription start site (TSS) or an RNA polyadenylation (pA) cleavage site. Primer walking RT-PCR is a method for studying the splicing junction of RACE products. In addition, RNase protection assay and primer extension are also introduced as alternative methods in the mapping analysis.

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The papillomavirus life cycle

Cited by 686 publications

References 76 publications

Biology of Human Papillomavirus Infections in Head and Neck Carcinogenesis

Biology of Human Papillomavirus Infections in Head and Neck Carcinogenesis

Analyzing the Human Papillomavirus (HPV) Life Cycle in Primary Keratinocytes with a Quantitative Colony‐Forming Assay

Construction of a Transcription Map for Papillomaviruses using RACE, RNase Protection, and Primer Extension Assays

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