Identification of the novel KI Polyomavirus in paranasal and lung tissues

Babakir‐Mina, Muhammed; Ciccozzi, Massimo; Campitelli, Laura; Aquaro, Stefano; Coco, Achille Lo; Perno, Carlo Federico; Ciotti, Marco

doi:10.1002/jmv.21417

Cited by 35 publications

(42 citation statements)

References 23 publications

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“…Following this finding, other body compartments and specimen types have been screened: stool (6,17,23,(46)(47)(48), whole blood (45,48), plasma (18,49,50), serum (49), cerebrospinal fluid (51), lymphoid tissue (16,40,47), urine (6,7,48), and lung tissue (24,52). Detection rates of KIPyV and WUPyV in biological specimens are reported in Tables 1 and 2.…”

Section: Specimens Collectionmentioning

confidence: 99%

The human polyomaviruses KI and WU: virological background and clinical implications

Babakir‐Mina

Ciccozzi²,

Perno

et al. 2013

APMIS

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Babakir-Mina M, Ciccozzi M, Perno CF, Ciotti M. The human polyomaviruses KI and WU: virological background and clinical implications. APMIS 2013; 121: 746-54. In 2007, two novel polyomaviruses KI and WU were uncovered in the respiratory secretions of children with acute respiratory symptoms. Seroepidemiological studies showed that infection by these viruses is widespread in the human population. Following these findings, different biological specimens and body compartments have been screened by real-time PCR in the attempt to establish a pathogenetic role for KI polyomavirus (KIPyV) and WU polyomavirus (WUPyV) in human diseases. Although both viruses have been found mainly in respiratory tract samples of immunocompromised patients, a clear causative link with the respiratory disease has not been established. Indeed, the lack of specific clinical or radiological findings, the frequent co-detection with other respiratory pathogens, the detection in subjects without signs or symptoms of respiratory disease, and the variability of the viral loads measured did not allow drawing a definitive conclusion. Prospective studies carried out on a large sample size including both immunocompromised and immunocompetent patients with and without respiratory symptoms are needed. Standardized quantitative real-time PCR methods, definition of a clear clinical cutoff value, timing in the collection of respiratory samples, are also crucial to understand the pathogenic role, if any, of KIPyV and WUPyV in human pathology.

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Section: Specimens Collectionmentioning

confidence: 99%

The human polyomaviruses KI and WU: virological background and clinical implications

Babakir‐Mina

Ciccozzi²,

Perno

et al. 2013

APMIS

Self Cite

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“…Little is known about the cell tropism of this virus, but viral sequences are predominantly found in respiratory tract secretions, with prevalence ranging between 0.5 and 6.5 % (Babakir-Mina et al, 2013). KIPyV DNA has occasionally been amplified from paranasal tissue (Babakir-Mina et al, 2009b), tonsil (Babakir-Mina et al, 2009b;Astegiano et al, 2010), lymphoid tissue (Sharp et al, 2009), lung tissue (Babakir-Mina et al, 2009c;Teramoto et al, 2011), stool (Allander et al, 2007;Babakir-Mina et al, 2009a;Bialasiewicz et al, 2009;Kantola et al, 2009;Mourez et al, 2009;Li et al, 2013), brain (Barzon et al, 2009b), eyebrow hair (Hampras et al, 2015), normal skin (Hampras et al, 2015) and blood and plasma (Barzon et al, 2009a;Babakir-Mina et al, 2010;Csoma et al, 2012;Touinssi et al, 2013). Immunohistochemical assay of spleen tissue from a 42-year-old human immunodeficiency virus (HIV)-positive male with a monoclonal antibody against the capsid protein VP1 of KIPyV stained positive, but the identity of the KIPyV VP1-positive cell type could not be determined (Siebrasse et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Characterization of the non-coding control region of polyomavirus KI isolated from nasopharyngeal samples from patients with respiratory symptoms or infection and from blood from healthy blood donors in Norway

Song

Ghelue

Ludvigsen

et al. 2016

Journal of General Virology

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Seroepidemiological studies showed that the human polyomavirus KI (KIPyV) is common in the human population, with age-specific seroprevalence ranging from 40-90 %. Genome epidemiological analyses demonstrated that KIPyV DNA is predominantly found in respiratory tract samples of immunocompromised individuals and children suffering from respiratory diseases, but viral sequences have also been detected in brain, tonsil, lymphoid tissue studies, plasma, blood and faeces. Little is known about the sequence variation in the non-coding control region of KIPyV variants residing in different sites of the human body and whether specific strains dominate in certain parts of the world. In this study, we sequenced the non-coding control region (NCCR) of naturally occurring KIPyV variants in nasopharyngeal samples from patients with respiratory symptoms or infection and in blood from healthy donors in Norway. In total 86 sequences were obtained, 44 of which were identical to the original isolated Stockholm 60 variant. The remaining NCCRs contained one or several mutations, none of them previously reported. The same mutations were detected in NCCRs amplified from blood and nasopharyngeal samples. Some patients had different variants in their specimens. Transient transfection studies in HEK293 cells with a luciferase reporter plasmid demonstrated that some single mutations had a significant effect on the relative early and late promoter strength compared with the Stockholm 60 promoter. The effect of the NCCR mutations on viral replication and possible virulence properties remains to be established. INTRODUCTIONPolyomaviruses are non-enveloped viruses with a circular dsDNA genome of approximately 5000 bp. These viruses are common in birds and mammals, and recently the first complete fish polyomavirus genome has been published (Johne et al., 2011;Peretti et al., 2015). Their genome can †These authors contributed equally to this work.The GenBank/EMBL/DDBJ accession numbers for the sequences of the mutant NCCRs are KU564911-564952. ã 2016 The Authors Printed in Great Britain 1647Journal of General Virology (2016), 97, 1647-1657 DOI 10.1099 be divided into three functional regions: the early region, encoding regulatory proteins required for transcription and viral DNA replication; the late region, encoding the capsid proteins; and interspersed between these the non-coding control region (NCCR), encompassing the origin of replication and the promoters controlling transcription of the early and late genes, respectively (DeCaprio & Garcea, 2013). The first human polyomaviruses, BK and JC, were detected using histology or cytology followed by electron microscopy, and their existence was reported in 1971 (Gardner et al., 1971; Padgett et al., 1971). The development of new techniques such as high-throughput sequencing, rolling circle amplification and polymerase chain reaction with degenerate primers has led in recent years to the discovery of new polyomaviruses that can infect humans. KI polyomavirus, named after the researchers' instit...

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“…WUPyV DNA was also detected in cerebral spinal fluid (CSF) of one patient (Barzon et al, 2009b). KIPyV DNA or VP1 protein was found in lung cancer tissue and in alveolar macrophages and spleen (Babakir-Mina et al, 2009;Siebrasse et al, 2014). MCPyV seems to be a common skin commensal (Bellaud et al, 2014;Hampras et al, 2015;Mertz et al, 2013;Schowalter et al, 2010), but DNA is also found in blood, eyebrow hairs, tonsils, gall bladder, intestine, appendix, liver, lung, lymphoid tissue, saliva and oral samples, and urine (reviewed by Baez et al, 2013;Hampras et al, 2015;Signorini et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Early and late promoters of BK polyomavirus, Merkel cell polyomavirus, Trichodysplasia spinulosa-associated polyomavirus and human polyomavirus 12 are among the strongest of all known human polyomaviruses in 10 different cell lines

Moens

Ghelue

Ludvigsen

et al. 2015

Journal of General Virology

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Early and late promoters of BK polyomavirus, Merkel cell polyomavirus, Trichodysplasia spinulosa-associated polyomavirus and human polyomavirus 12 are among the strongest of all known human polyomaviruses in 10 different cell lines Little is known about cell tropism of the novel HPyVs, and cell cultures allowing virus propagation are lacking. Because viral tropism partially depends on the interaction of cellular transcription factors with the viral promoter, we monitored the promoter activity of all known HPyVs. Therefore, we compared the relative early and late promoter activity of the BK polyomavirus (BKPyV) (WW strain) with the corresponding activities of the other HPyVs in 10 different cell lines derived from brain, colon, kidney, liver, lung, the oral cavity and skin. Our results show that the BKPyV, MCPyV, TSPyV and HPyV12 early promoters displayed the strongest activity in most cell lines tested, while the remaining HPyV had relative low early promoter activity. HPyV12 showed the highest late promoter activity of all HPyVs in most cell lines, but also the BKPyV, MCPyV and TSPyV late promoters belonged to the stronger ones among HPyVs. The HPyVs with weak early promoter activity had in general also weak late promoter activity, except for HPyV10 whose late promoter was relatively strong in six of the 10 cell lines. A 20 bp deletion in the promoter of an HPyV12 variant significantly affected both early and late promoter activity in most cell lines. In conclusion, our findings suggest which cell lines may be suitable for virus propagation and may give an indication of the cell tropism of the HPyVs.

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Identification of the novel KI Polyomavirus in paranasal and lung tissues

Cited by 35 publications

References 23 publications

The human polyomaviruses KI and WU: virological background and clinical implications

The human polyomaviruses KI and WU: virological background and clinical implications

Characterization of the non-coding control region of polyomavirus KI isolated from nasopharyngeal samples from patients with respiratory symptoms or infection and from blood from healthy blood donors in Norway

Early and late promoters of BK polyomavirus, Merkel cell polyomavirus, Trichodysplasia spinulosa-associated polyomavirus and human polyomavirus 12 are among the strongest of all known human polyomaviruses in 10 different cell lines

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