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CpG and UpA dinucleotides in both coding and non-coding regions of echovirus 7 inhibit replication initiation post-entry

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CpG and UpA dinucleotides in both coding and non-coding regions of echovirus 7 inhibit replication initiation post-entry. / Fros, Jelke J.; Dietrich, Isabelle; Alshaikhahmed, Kinda; Passchier, Tim C.; Evans, David John; Simmonds, Peter.

In: eLife, Vol. 6, e29112, 29.09.2017.

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Fros, JJ, Dietrich, I, Alshaikhahmed, K, Passchier, TC, Evans, DJ & Simmonds, P 2017, 'CpG and UpA dinucleotides in both coding and non-coding regions of echovirus 7 inhibit replication initiation post-entry' eLife, vol. 6, e29112. https://doi.org/10.7554/eLife.29112

APA

Fros, J. J., Dietrich, I., Alshaikhahmed, K., Passchier, T. C., Evans, D. J., & Simmonds, P. (2017). CpG and UpA dinucleotides in both coding and non-coding regions of echovirus 7 inhibit replication initiation post-entry. eLife, 6, [e29112]. https://doi.org/10.7554/eLife.29112

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Fros JJ, Dietrich I, Alshaikhahmed K, Passchier TC, Evans DJ, Simmonds P. CpG and UpA dinucleotides in both coding and non-coding regions of echovirus 7 inhibit replication initiation post-entry. eLife. 2017 Sep 29;6. e29112. https://doi.org/10.7554/eLife.29112

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Fros, Jelke J. ; Dietrich, Isabelle ; Alshaikhahmed, Kinda ; Passchier, Tim C. ; Evans, David John ; Simmonds, Peter. / CpG and UpA dinucleotides in both coding and non-coding regions of echovirus 7 inhibit replication initiation post-entry. In: eLife. 2017 ; Vol. 6.

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@article{59389387ad454b2c9e0d6be5999e36de,
title = "CpG and UpA dinucleotides in both coding and non-coding regions of echovirus 7 inhibit replication initiation post-entry",
abstract = "Most vertebrate and plant RNA and small DNA viruses suppress genomic CpG and UpA dinucleotide frequencies, apparently mimicking host mRNA composition. Artificially increasing CpG/UpA dinucleotides attenuates viruses through an entirely unknown mechanism. Using the echovirus 7 (E7) model in several cell types, we show that the restriction in E7 replication in mutants with increased CpG/UpA dinucleotides occurred immediately after viral entry, with incoming virions failing to form replication complexes. Sequences of CpG/UpA-high virus stocks showed no evidence of increased mutational errors that would render them replication defective, these viral RNAs were not differentially sequestered in cytoplasmic stress granules nor did they induce a systemic antiviral state. Importantly, restriction was not mediated through effects on translation efficiency since replicons with high CpG/UpA sequences inserted into a non-coding region were similarly replication defective. Host-cells thus possess intrinsic defence pathways that prevent replication of viruses with increased CpG/UpA frequencies independently of codon usage.",
author = "Fros, {Jelke J.} and Isabelle Dietrich and Kinda Alshaikhahmed and Passchier, {Tim C.} and Evans, {David John} and Peter Simmonds",
note = "Funding: Wellcome (WT103767MA) Peter Simmonds.",
year = "2017",
month = "9",
day = "29",
doi = "10.7554/eLife.29112",
language = "English",
volume = "6",
journal = "eLife",
issn = "2050-084X",
publisher = "eLife Sciences Publications, Ltd",

}

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TY - JOUR

T1 - CpG and UpA dinucleotides in both coding and non-coding regions of echovirus 7 inhibit replication initiation post-entry

AU - Fros, Jelke J.

AU - Dietrich, Isabelle

AU - Alshaikhahmed, Kinda

AU - Passchier, Tim C.

AU - Evans, David John

AU - Simmonds, Peter

N1 - Funding: Wellcome (WT103767MA) Peter Simmonds.

PY - 2017/9/29

Y1 - 2017/9/29

N2 - Most vertebrate and plant RNA and small DNA viruses suppress genomic CpG and UpA dinucleotide frequencies, apparently mimicking host mRNA composition. Artificially increasing CpG/UpA dinucleotides attenuates viruses through an entirely unknown mechanism. Using the echovirus 7 (E7) model in several cell types, we show that the restriction in E7 replication in mutants with increased CpG/UpA dinucleotides occurred immediately after viral entry, with incoming virions failing to form replication complexes. Sequences of CpG/UpA-high virus stocks showed no evidence of increased mutational errors that would render them replication defective, these viral RNAs were not differentially sequestered in cytoplasmic stress granules nor did they induce a systemic antiviral state. Importantly, restriction was not mediated through effects on translation efficiency since replicons with high CpG/UpA sequences inserted into a non-coding region were similarly replication defective. Host-cells thus possess intrinsic defence pathways that prevent replication of viruses with increased CpG/UpA frequencies independently of codon usage.

AB - Most vertebrate and plant RNA and small DNA viruses suppress genomic CpG and UpA dinucleotide frequencies, apparently mimicking host mRNA composition. Artificially increasing CpG/UpA dinucleotides attenuates viruses through an entirely unknown mechanism. Using the echovirus 7 (E7) model in several cell types, we show that the restriction in E7 replication in mutants with increased CpG/UpA dinucleotides occurred immediately after viral entry, with incoming virions failing to form replication complexes. Sequences of CpG/UpA-high virus stocks showed no evidence of increased mutational errors that would render them replication defective, these viral RNAs were not differentially sequestered in cytoplasmic stress granules nor did they induce a systemic antiviral state. Importantly, restriction was not mediated through effects on translation efficiency since replicons with high CpG/UpA sequences inserted into a non-coding region were similarly replication defective. Host-cells thus possess intrinsic defence pathways that prevent replication of viruses with increased CpG/UpA frequencies independently of codon usage.

U2 - 10.7554/eLife.29112

DO - 10.7554/eLife.29112

M3 - Article

VL - 6

JO - eLife

T2 - eLife

JF - eLife

SN - 2050-084X

M1 - e29112

ER -

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ID: 251245103