Identification of a Novel Polyomavirus in a Pancreatic Transplant Recipient With Retinal Blindness and Vasculitic Myopathy

Mishra, Nischay; Pereira, Marcus R.; Rhodes, Roy H.; An, Ping; Pipas, James M.; Jain, Komal; Kapoor, Amit; Briese, Thomas; Faust, Phyllis L.; Lipkin, W. Ian

doi:10.1093/infdis/jiu250

Cited by 133 publications

(112 citation statements)

References 13 publications

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“…Thirteen human polyomaviruses (HPyVs) have been described so far: BKPyV, JCPyV, KIPyV, WUPyV, Merkel cell PyV (MCPyV), HPyV6, HPyV7, Trichodysplasia spinulosa-associated polyomavirus (TSPyV), HPyV9, HPyV10 and the isolates MW and MX, STLPyV, HPyV12 and NJPyV-2013 (Allander et al, 2007;Buck et al, 2012;Feng et al, 2008;Gardner et al, 1971;Gaynor et al, 2007;Korup et al, 2013;Lim et al, 2013;Mishra et al, 2014;Padgett et al, 1971;Schowalter et al, 2010;Scuda et al, 2011;Siebrasse et al, 2012a;van der Meijden et al, 2010;Yu et al, 2012). Seropositivity for most HPyVs is w50 %, implying that individuals are co-infected with several different HPyVs.…”

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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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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“…HPyV12 was detected in the liver as well as colon, rectum, and feces of a single individual, but its relation to the disease in humans remains to be investigated (Korup et al 2013). The most recently discovered species, NJPyV, was isolated from the muscle biopsy of a 33-year-old pancreatic transplant recipient (Mishra et al 2014). The name New Jersey polyomavirus was after the place from where the patient belonged.…”

Section: Stlpyv Hpyv12 and Njpyvmentioning

confidence: 99%

“…Malawi polyomavirus (MWPyV) (Siebrasse et al 2012), also known as HPyV10 or Mexico polyomavirus (Yu et al 2012), was detected in stool and skin samples roughly simultaneous. Saint Louis polyomavirus (STLPyV) was detected in a clinical stool specimen (Lim et al 2013), HPyV12 in human liver tissue (Korup et al 2013), and New Jersey polyomavirus (NJPyV) in endothelium of a muscle biopsy from a pancreatic transplant recipient (Mishra et al 2014).…”

Section: Introductionmentioning

confidence: 99%

Entry, infection, replication, and egress of human polyomaviruses: an update

Bhattacharjee

Chattaraj

2017

Can. J. Microbiol.

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Polyomaviruses (PyVs), belonging to the family Polyomaviridae, are a group of small, nonenveloped, double-stranded, circular DNA viruses widely distributed in the vertebrates. PyVs cause no apparent disease in adult laboratory mice but cause a wide variety of tumors when artificially inoculated into neonates or semipermissive animals. A few human PyVs, such as BK, JC, and Merkel cell PyVs, have been unequivocally linked to pathogenesis under conditions of immunosuppression. Infection is thought to occur early in life and persists for the lifespan of the host. Over evolutionary time scales, it appears that PyVs have slowly co-evolved with specific host animal lineages. Host cell surface glycoproteins and glycolipids seem to play a decisive role in the entry stage of viral infection and in channeling the virions to specific intracellular membrane-bound compartments and ultimately to the nucleus, where the genomes are replicated and packaged for release. Therefore the transport of the infecting virion or viral genome to this site of multiplication is an essential process in productive viral infection as well as in latent infection and transformation. This review summarizes the major findings related to the characterization of the nature of the interactions between PyV and host protein and their impact in host cell invasion.

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“…Seven of 13 described human polyomaviruses have been associated with disease in immunocompromised individuals, i.e., JC polyomavirus (JCPyV) (7), BK polyomavirus (BKPyV) (8), Merkel cell polyomavirus (MCPyV) (9), trichodysplasia spinulosa-associated polyomavirus (TSPyV) (10,11), human polyomavirus 6 (HPyV6) (12), human polyomavirus 7 (HPyV7) (13), and New Jersey polyomavirus (NJPyV) (14,15). MCPyV and TSPyV, which belong to orthopolyomavirus lineage I (3,16), are associated with a malignant and a benign hyperproliferative skin disease called Merkel cell carcinoma (MCC) and trichodysplasia spinulosa (TS), respectively.…”

mentioning

confidence: 99%

Characterization of T Antigens, Including Middle T and Alternative T, Expressed by the Human Polyomavirus Associated with Trichodysplasia Spinulosa

Meijden

Kazem

Dargel

et al. 2015

J Virol

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The polyomavirus tumor (T) antigens play crucial roles in viral replication IMPORTANCEThe human trichodysplasia spinulosa-associated polyomavirus (TSPyV) is distinguished among polyomaviruses for combining productive infection with cell-transforming properties. In the research presented here, we further substantiate this unique position by indicating expression of both middle T antigen (MT) and alternative T antigen (ALTO) in TSPyV. So far, none of the human polyomaviruses was shown to express MT, which is considered the most important viral oncoprotein of rodent polyomaviruses. Coexpression of ALTO and MT, which involves a conserved, recently recognized overlapping ORF subject to positive selection, has not been observed before for any polyomavirus. As a result of our findings, this study provides valuable new insights into polyomavirus T gene use and expression. Obviously, these insights will be instrumental in further study and gaining an understanding of TSPyV pathogenicity. More importantly, however, they provide important leads with regard to the interrelationship, functionality, and evolution of polyomaviruses as a whole, indicating that TSPyV is a suitable model virus to study these entities further.H uman polyomaviruses represent a rapidly expanding group of small, circular double-stranded DNA viruses that persistently infect the general population, usually without causing symptoms (1-6). Seven of 13 described human polyomaviruses have been associated with disease in immunocompromised individuals, i.e., JC polyomavirus (JCPyV) (7), BK polyomavirus (BKPyV) (8), Merkel cell polyomavirus (MCPyV) (9), trichodysplasia spinulosa-associated polyomavirus (TSPyV) (10, 11), human polyomavirus 6 (HPyV6) (12), human polyomavirus 7 (HPyV7) (13), and New Jersey polyomavirus (NJPyV) (14, 15). MCPyV and TSPyV, which belong to orthopolyomavirus lineage I (3, 16), are associated with a malignant and a benign hyperproliferative skin disease called Merkel cell carcinoma (MCC) and trichodysplasia spinulosa (TS), respectively. The hyperproliferative phenotype of both diseases indicates involvement of the viral tumor (T) antigens in the patho(onco)genesis.T antigens that play a coordinating role in viral transcription and replication are generally known for their ability to disrupt cellular pathways involved in cell cycle regulation and signaling (17,18). The large T antigen (LT), for example, promotes cell cycle entry through inactivation (hyperphosphorylation) of pRB, as demonstrated, for example, for simian virus 40 (SV40) (18,19).

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Identification of a Novel Polyomavirus in a Pancreatic Transplant Recipient With Retinal Blindness and Vasculitic Myopathy

Abstract: New Jersey polyomavirus (NJPyV-2013) is a novel polyomavirus that may have tropism for vascular endothelial cells.

Cited by 133 publications

References 13 publications

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

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

Entry, infection, replication, and egress of human polyomaviruses: an update

Characterization of T Antigens, Including Middle T and Alternative T, Expressed by the Human Polyomavirus Associated with Trichodysplasia Spinulosa

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