Transcriptional Regulation of BK Virus by Nuclear Factor of Activated T Cells

Jordan, Joslynn A.; Manley, Kate; Dugan, Aisling S.; O’Hara, Bethany A.; Atwood, Walter J.

doi:10.1128/jvi.01918-09

Cited by 21 publications

(23 citation statements)

References 55 publications

(64 reference statements)

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“…Pretreatment of cells with HD5 modestly neutralized infection, suggesting that HD5 also has potential indirect effects on the target cell promoting an antiviral response. Nuclear factor of activated T cells (NFAT) and NF-B are transcription factors that are known to coordinate immune responses and are vital for JCPyV infection (57)(58)(59). Alpha defensin genes have NFAT and NF-B binding sites, so the modest reduction in infection could be attributed to the beginning of a cellular response initiated by these factors due to exogenous HD5 addition.…”

Section: Discussionmentioning

confidence: 99%

The Human Alpha Defensin HD5 Neutralizes JC Polyomavirus Infection by Reducing Endoplasmic Reticulum Traffic and Stabilizing the Viral Capsid

Zins

Nelson

Maginnis

et al. 2014

J Virol

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Section: Discussionmentioning

confidence: 99%

The Human Alpha Defensin HD5 Neutralizes JC Polyomavirus Infection by Reducing Endoplasmic Reticulum Traffic and Stabilizing the Viral Capsid

Zins

Nelson

Maginnis

et al. 2014

J Virol

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“…While the presence of these receptors is essential for infection, cellular factors that bind the HPyV promoter or HPyV regulatory proteins will affect viral transcription and replication and effect viral production (e.g. Gorrill & Khalili, 2005;Feng et al, 2011;Ferenczy et al, 2013;Jordan et al, 2010;Liang et al, 2012;Marshall et al, 2012;Ravichandran & Major, 2006;Romagnoli et al, 2009;Safak & Khalili, 2001;Wang et al, 2012;White et al, 2014;Wollebo et al, 2012). Hence, these interactions will determine the cell tropism of the HPyV.…”

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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“…Binding sites for numerous cellular transcription factors, including nuclear factor I (NFI) (14-16, 22, 47), Sp1 (14,22,47), NFAT (40), AP1 (15,22,47), Smad3 (1), ERE and GRE/PRE (53), p53 (80), NF-B (28), and C/EBP (28), have been identified in the archetype BKV enhancer and rearranged BKV variants, with experimental evidence supporting the importance of some of these sites for viral transcription and replication. Also, putative binding sites for Ets1, PEA3, AP-2, CREB, and granulocyte-macrophage colony-stimulating factor (GM-CSF) have been predicted by sequence homology (52,75), but their functional importance is unproven.…”

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confidence: 99%

Stimulation of BK Virus DNA Replication by NFI Family Transcription Factors

Liang

Tikhanovich

Nasheuer

et al. 2012

J Virol

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b BK polyomavirus (BKV) establishes persistent, low-level, and asymptomatic infections in most humans and causes polyomavirus-associated nephropathy (PVAN) and other pathologies in some individuals. The activation of BKV replication following kidney transplantation, leading to viruria, viremia, and, ultimately, PVAN, is associated with immune suppression as well as inflammation and stress from ischemia-reperfusion injury of the allograft, but the stimuli and molecular mechanisms leading to these pathologies are not well defined. The replication of BKV DNA in cell cultures is regulated by the viral noncoding control region (NCCR) comprising the core origin and flanking sequences, to which BKV T antigen (Tag), cellular proteins, and small regulatory RNAs bind. Six nuclear factor I (NFI) binding sites occur in sequences flanking the late side of the core origin (the enhancer) of the archetype virus, and their mutation, either individually or in toto, reduces BKV DNA replication when placed in competition with templates containing intact BKV NCCRs. NFI family members interacted with the helicase domain of BKV Tag in pulldown assays, suggesting that NFI helps recruit Tag to the viral core origin and may modulate its function. However, Tag may not be the sole target of the replication-modulatory activities of NFI: the NFIC/CTF1 isotype stimulates BKV template replication in vitro at low concentrations of DNA polymerase-␣ primase (Pol-primase), and the p58 subunit of Polprimase associates with NFIC/CTF1, suggesting that NFI also recruits Pol-primase to the NCCR. These results suggest that NFI proteins (and the signaling pathways that target them) activate BKV replication and contribute to the consequent pathologies caused by acute infection.

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Transcriptional Regulation of BK Virus by Nuclear Factor of Activated T Cells

Cited by 21 publications

References 55 publications

The Human Alpha Defensin HD5 Neutralizes JC Polyomavirus Infection by Reducing Endoplasmic Reticulum Traffic and Stabilizing the Viral Capsid

The Human Alpha Defensin HD5 Neutralizes JC Polyomavirus Infection by Reducing Endoplasmic Reticulum Traffic and Stabilizing the Viral Capsid

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

Stimulation of BK Virus DNA Replication by NFI Family Transcription Factors

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