Papillomavirus genome structure, expression, and post-transcriptional regulation
Top Cited Papers
- 1 January 2006
- journal article
- review article
- Published by IMR Press in Frontiers in Bioscience-Landmark
- Vol. 11 (1), 2286-302
- https://doi.org/10.2741/1971
Abstract
Papillomaviruses are a group of small non-enveloped DNA tumor viruses whose infection usually causes benign epithelial lesions (warts). Certain types of HPVs, such as HPV-16, HPV-18, and HPV-31, have been recognized as causative agents of cervical cancer and anal cancer and their infections, which arise via sexual transmission, are associated with more than 95% of cervical cancer. Papillomaviruses infect keratinocytes in the basal layer of stratified squamous epithelia and replicate in the nucleus of infected keratinocytes in a differentiation-dependent manner. Viral gene expression in infected cells depends on cell differentiation and is tightly regulated at the transcriptional and post-transcriptional levels. A noteworthy feature of all papillomavirus transcripts is that they are transcribed as a bicistronic or polycistronic form containing two or more ORFs and are polyadenylated at either an early or late poly(A) site. In the past ten years, remarkable progress has been made in understanding how this complex viral gene expression is regulated at the level of transcription (such as via DNA methylation) and particularly post-transcription (including RNA splicing, polyadenylation, and translation). Current knowledge of papillomavirus mRNA structure and RNA processing has provided some clues on how to control viral oncogene expression. However, we still have little knowledge about which mRNAs are used to translate each viral protein. Continuing research on post-transcriptional regulation of papillomavirus infection will remain as a future focus to provide more insights into papillomavirus-host interactions, the virus life-cycle, and viral oncogenesis.Keywords
This publication has 69 references indexed in Scilit:
- Epidemiologic Classification of Human Papillomavirus Types Associated with Cervical CancerThe New England Journal of Medicine, 2003
- Selective silencing of viral gene expression in HPV-positive human cervical carcinoma cells treated with siRNA, a primer of RNA interferenceOncogene, 2002
- Early Polyadenylation Signals of Human Papillomavirus Type 31 Negatively Regulate Capsid Gene ExpressionJournal of Virology, 2001
- The E8 Domain Confers a Novel Long-Distance Transcriptional Repression Activity on the E8^E2C Protein of High-Risk Human Papillomavirus Type 31Journal of Virology, 2001
- The E8^E2C Protein, a Negative Regulator of Viral Transcription and Replication, Is Required for Extrachromosomal Maintenance of Human Papillomavirus Type 31 in KeratinocytesJournal of Virology, 2000
- The sCYMV1 hairpin ribozyme: targeting rules and cleavage of heterologous RNAGene Therapy, 1999
- AU-rich mRNA instability elements on human papillomavirus type 1 late mRNAs and c-fos mRNAs interact with the same cellular factorsOncogene, 1997
- In vitro cleavage of HPV16 E6 and E7 RNA fragments by synthetic ribozymes and transcribed ribozymes from RNA-trimming plasmidsFEBS Letters, 1993
- Cleavage of Cottontail Rabbit Papillomavirus E7 RNA with an anti-E7 RibozymeBiochemical and Biophysical Research Communications, 1993
- Expression and splicing patterns of human papillomavirus type‐16 mrnas in pre‐cancerous lesions and carcinomas of the cervix, in human keratinocytes immortalized by HPV 16, and in cell lines established from cervical cancersInternational Journal of Cancer, 1992