scholarly journals Molecular Characterization of Human Papillomavirus Type 159 (HPV159)

Viruses ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1668
Author(s):  
Iva Marković ◽  
Lea Hošnjak ◽  
Katja Seme ◽  
Mario Poljak

Human papillomavirus type 159 (HPV159) was identified in an anal swab sample and preliminarily genetically characterized by our group in 2012. Here we present a detailed molecular in silico analysis that showed that the HPV159 viral genome is 7443 bp in length and divided into five early and two late genes, with conserved functional domains and motifs, and a non-coding long control region (LCR) with significant regulatory sequences that allow the virus to complete its life cycle and infect novel host cells. HPV159, clustering into the cutaneotropic Betapapillomavirus (Beta-PV) genus, is phylogenetically most similar to HPV9, forming an individual phylogenetic group in the viral species Beta-2. After testing a large representative collection of clinical samples with HPV159 type-specific RT-PCR, in addition to the anal canal from which the first HPV159 isolate was obtained, HPV159 was further detected in other muco-cutaneous (4/181, 2.2%), mucosal (22/764, 2.9%), and cutaneous (14/554, 2.5%) clinical samples, suggesting its extensive tissue tropism. However, because very low HPV159 viral loads were estimated in the majority of positive samples, it seemed that HPV159 mainly caused clinically insignificant infections of the skin and mucosa. Using newly developed, highly sensitive HPV159-specific nested PCRs, two additional HPV159 LCR viral variants were identified. Nevertheless, all HPV159 mutations were demonstrated outside important functional domains of the LCR, suggesting that the HPV159 viral variants were most probably not pathogenically different. This complete molecular characterization of HPV159 enhances our knowledge of the genome characteristics, tissue tropism, and phylogenetic diversity of Beta-PVs that infect humans.

2010 ◽  
Vol 7 (1) ◽  
pp. 189 ◽  
Author(s):  
Kudukkil P Niyas ◽  
Rachy Abraham ◽  
Ramakrishnan Unnikrishnan ◽  
Thomas Mathew ◽  
Sajith Nair ◽  
...  

2011 ◽  
Vol 28 (6) ◽  
pp. 1124-1128 ◽  
Author(s):  
Tatsuya Akiyama ◽  
Ashraf A. Khan ◽  
Chorng-Ming Cheng ◽  
Rossina Stefanova

PLoS ONE ◽  
2017 ◽  
Vol 12 (8) ◽  
pp. e0183607 ◽  
Author(s):  
Marjan Shekarabi ◽  
Bahareh Hajikhani ◽  
Alireza Salimi Chirani ◽  
Maryam Fazeli ◽  
Mehdi Goudarzi

2004 ◽  
Vol 78 (23) ◽  
pp. 12762-12772 ◽  
Author(s):  
Mina Kalantari ◽  
Itzel E. Calleja-Macias ◽  
Devansu Tewari ◽  
Bjørn Hagmar ◽  
Kathrine Lie ◽  
...  

ABSTRACT DNA methylation contributes to the chromatin conformation that represses transcription of human papillomavirus type16 (HPV-16), which is prevalent in the etiology of cervical carcinoma. In an effort to clarify the role of this phenomenon in the regulation and carcinogenicity of HPV-16, 115 clinical samples were studied to establish the methylation patterns of the 19 CpG dinucleotides within the long control region and part of the L1 gene by bisulfite modification, PCR amplification, DNA cloning, and sequencing. We observed major heterogeneities between clones from different samples as well as between clones from individual samples. The methylation frequency of CpGs was measured at 14.5%. In addition, 0.21 and 0.23%, respectively, of the CpA and CpT sites, indicators of de novo methylation, were methylated. Methylation frequencies exceeded 30% in the CpGs overlapping with the L1 gene and were about 10% for most other positions. A CpG site located in the linker between two nucleosomes positioned over the enhancer and promoter of HPV-16 had minimal methylation. This region forms part of the HPV replication origin and is close to binding sites of master-regulators of transcription during epithelial differentiation. Methylation of most sites was highest in carcinomas, possibly due to tandem repetition and chromosomal integration of HPV-16 DNA. Methylation was lowest in dysplasia, likely reflecting the transcriptional activity in these infections. Our data document the efficient targeting of HPV genomes by the epithelial methylation machinery, possibly as a cellular defense mechanism, and suggest involvement of methylation in HPV oncogene expression and the early-late switch.


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