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@article{ficarelli_targeted_2021,
title = {Targeted Restriction of Viral Gene Expression and Replication by the {ZAP} Antiviral System},
volume = {8},
url = {https://doi.org/10.1146/annurev-virology-091919-104213},
doi = {10.1146/annurev-virology-091919-104213},
abstract = {The zinc finger antiviral protein ({ZAP}) restricts the replication of a broad range of {RNA} and {DNA} viruses. {ZAP} directly binds viral {RNA}, targeting it for degradation and inhibiting its translation. While the full scope of {RNA} determinants involved in mediating selective {ZAP} activity is unclear, {ZAP} binds {CpG} dinucleotides, dictating at least part of its target specificity. {ZAP} interacts with many cellular proteins, although only a few have been demonstrated to be essential for its antiviral activity, including the 3′–5′ exoribonuclease exosome complex, {TRIM}25, and {KHNYN}. In addition to inhibiting viral gene expression, {ZAP} also directly and indirectly targets a subset of cellular messenger {RNAs} to regulate the innate immune response. Overall, {ZAP} protects a cell from viral infection by restricting viral replication and regulating cellular gene expression. Further understanding of the {ZAP} antiviral system may allow for novel viral vaccine and anticancer therapy development.},
pages = {265--283},
number = {1},
journaltitle = {Annual Review of Virology},
author = {Ficarelli, Mattia and Neil, Stuart J.D. and Swanson, Chad M.},
urldate = {2023-04-16},
date = {2021},
pmid = {34129371},
note = {\_eprint: https://doi.org/10.1146/annurev-virology-091919-104213},
keywords = {{CpG} dinucleotide, interferon-stimulated gene, zinc finger antiviral protein, {PARP}13, virus, {ZAP}, {ZC}3HAV1},
}
@article{simmonds_sse_2012,
title = {{SSE}: a nucleotide and amino acid sequence analysis platform},
volume = {5},
rights = {2012 Simmonds; licensee {BioMed} Central Ltd.},
issn = {1756-0500},
url = {https://bmcresnotes.biomedcentral.com/articles/10.1186/1756-0500-5-50},
doi = {10.1186/1756-0500-5-50},
shorttitle = {{SSE}},
abstract = {There is an increasing need to develop bioinformatic tools to organise and analyse the rapidly growing amount of nucleotide and amino acid sequence data in organisms ranging from viruses to eukaryotes. A simple sequence editor ({SSE}) was developed to create an integrated environment where sequences can be aligned, annotated, classified and directly analysed by a number of built-in bioinformatic programs. {SSE} incorporates a sequence editor for the creation of sequence alignments, a process assisted by integrated {CLUSTAL}/{MUSCLE} alignment programs and automated removal of indels. Sequences can be fully annotated and classified into groups and annotated of sequences and sequence groups and access to analytical programs that analyse diversity, recombination and {RNA} secondary structure. Methods for analysing sequence diversity include measures of divergence and evolutionary distances, identity plots to detect regions of nucleotide or amino acid homology, reconstruction of sequence changes, mono-, di- and higher order nucleotide compositional biases and codon usage. Association Index calculations, {GroupScans}, Bootscanning and {TreeOrder} scans perform phylogenetic analyses that reconcile group membership with tree branching orders and provide powerful methods for examining segregation of alleles and detection of recombination events. Phylogeny changes across alignments and scoring of branching order differences between trees using the Robinson-Fould algorithm allow effective visualisation of the sites of recombination events. {RNA} secondary and tertiary structures play important roles in gene expression and {RNA} virus replication. For the latter, persistence of infection is additionally associated with pervasive {RNA} secondary structure throughout viral genomic {RNA} that modulates interactions with innate cell defences. {SSE} provides several programs to scan alignments for {RNA} secondary structure through folding energy thermodynamic calculations and phylogenetic methods (detection of co-variant changes, and structure conservation between divergent sequences). These analyses complement methods based on detection of sequence constraints, such as suppression of synonymous site variability. For each program, results can be plotted in real time during analysis through an integrated graphics package, providing publication quality graphs. Results can be also directed to tabulated datafiles for import into spreadsheet or database programs for further analysis. {SSE} combines sequence editor functions with analytical tools in a comprehensive and user-friendly package that assists considerably in bioinformatic and evolution research.},
pages = {1--10},
number = {1},
journaltitle = {{BMC} Research Notes},
shortjournal = {{BMC} Res Notes},
author = {Simmonds, Peter},
urldate = {2023-08-20},
date = {2012-12},
langid = {english},
note = {Number: 1
Publisher: {BioMed} Central},
}
@software{gu_synmut_2023,
title = {{SynMut}: Designing Synonymously Mutated Sequences with Different Genomic Signatures},
rights = {{GPL}-2},
url = {https://bioconductor.org/packages/SynMut/},
shorttitle = {{SynMut}},
abstract = {There are increasing demands on designing virus mutants with specific dinucleotide or codon composition. This tool can take both dinucleotide preference and/or codon usage bias into account while designing mutants. It is a powerful tool for in silico designs of {DNA} sequence mutants.},
version = {1.16.0},
publisher = {Bioconductor version: Release (3.17)},
author = {Gu, Haogao and Poon, Leo L. M.},
urldate = {2023-08-20},
date = {2023},
doi = {10.18129/B9.bioc.SynMut},
keywords = {Software, {ExperimentalDesign}, Preprocessing, {SequenceMatching}},
}
@article{greenbaum_patterns_2008,
title = {Patterns of Evolution and Host Gene Mimicry in Influenza and Other {RNA} Viruses},
volume = {4},
issn = {1553-7374},
url = {https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1000079},
doi = {10.1371/journal.ppat.1000079},
abstract = {It is well known that the dinucleotide {CpG} is under-represented in the genomic {DNA} of many vertebrates. This is commonly thought to be due to the methylation of cytosine residues in this dinucleotide and the corresponding high rate of deamination of 5-methycytosine, which lowers the frequency of this dinucleotide in {DNA}. Surprisingly, many single-stranded {RNA} viruses that replicate in these vertebrate hosts also have a very low presence of {CpG} dinucleotides in their genomes. Viruses are obligate intracellular parasites and the evolution of a virus is inexorably linked to the nature and fate of its host. One therefore expects that virus and host genomes should have common features. In this work, we compare evolutionary patterns in the genomes of {ssRNA} viruses and their hosts. In particular, we have analyzed dinucleotide patterns and found that the same patterns are pervasively over- or under-represented in many {RNA} viruses and their hosts suggesting that many {RNA} viruses evolve by mimicking some of the features of their host's genes ({DNA}) and likely also their corresponding {mRNAs}. When a virus crosses a species barrier into a different host, the pressure to replicate, survive and adapt, leaves a footprint in dinucleotide frequencies. For instance, since human genes seem to be under higher pressure to eliminate {CpG} dinucleotide motifs than avian genes, this pressure might be reflected in the genomes of human viruses ({DNA} and {RNA} viruses) when compared to those of the same viruses replicating in avian hosts. To test this idea we have analyzed the evolution of the influenza virus since 1918. We find that the influenza A virus, which originated from an avian reservoir and has been replicating in humans over many generations, evolves in a direction strongly selected to reduce the frequency of {CpG} dinucleotides in its genome. Consistent with this observation, we find that the influenza B virus, which has spent much more time in the human population, has adapted to its human host and exhibits an extremely low {CpG} dinucleotide content. We believe that these observations directly show that the evolution of {RNA} viral genomes can be shaped by pressures observed in the host genome. As a possible explanation, we suggest that the strong selection pressures acting on these {RNA} viruses are most likely related to the innate immune response and to nucleotide motifs in the host {DNA} and {RNAs}.},
pages = {e1000079},
number = {6},
journaltitle = {{PLOS} Pathogens},
shortjournal = {{PLOS} Pathogens},
author = {Greenbaum, Benjamin D. and Levine, Arnold J. and Bhanot, Gyan and Rabadan, Raul},
urldate = {2023-08-20},
date = {2008-06-06},
langid = {english},
note = {Publisher: Public Library of Science},
keywords = {{RNA} viruses, Influenza A virus, Bird genomics, {DNA} methylation, Viral evolution, {dsRNA} viruses, {ssRNA} viruses, Viral genomics},
}
@article{le_nouen_attenuation_2019,
title = {Attenuation of Human Respiratory Viruses by Synonymous Genome Recoding},
volume = {10},
issn = {1664-3224},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2019.01250},
doi = {10.3389/fimmu.2019.01250},
abstract = {Using computer algorithms and commercial {DNA} synthesis, one or more {ORFs} of a microbial pathogen such as a virus can be recoded and deoptimized by several strategies that may involve the introduction of up to thousands of nucleotide (nt) changes without affecting amino acid (aa) coding. The synonymous recoding strategies that have been applied to {RNA} viruses include: deoptimization of codon or codon-pair usage, which may reduce protein expression among other effects; increased content of immunomodulatory {CpG} and {UpA} {RNA}, which increase immune responses and thereby restrict viral replication; and substitution of serine and leucine codons with synonymous codons for which single-nt substitutions can yield nonsense codons, thus limiting evolutionary potential. This can reduce pathogen fitness and create potential live-attenuated vaccines that may have improved properties. The combined approach of genome recoding, synthetic biology, and reverse genetics offers several advantages for the generation of attenuated {RNA} viruses. First, synonymous recoding involves many mutations, which should reduce the rate and magnitude of de-attenuation. Second, increasing the amount of recoding can provide increased attenuation. Third, because there are no changes at the aa level, all of the relevant epitopes should be expressed. Fourth, attenuation frequently does not compromise immunogenicity, suggesting that the recoded viruses have increased immunogenicity per infectious particle. Synonymous deoptimization approaches have been applied to two important human viral pathogens, namely respiratory syncytial virus ({RSV}) and influenza A virus ({IAV}). This manuscript will briefly review the use of these different methods of synonymous recoding to generate attenuated {RSV} and {IAV} strains. It also will review the characterization of these vaccine candidates in vitro and in animal models, and describe several surprising findings with respect to phenotypic and genetic instability of some of these candidates.},
journaltitle = {Frontiers in Immunology},
author = {Le Nouën, Cyril and Collins, Peter L. and Buchholz, Ursula J.},
urldate = {2023-08-20},
date = {2019},
}
@article{angeloni_sequence_2021,
title = {Sequence determinants, function, and evolution of {CpG} islands},
volume = {49},
issn = {1470-8752},
doi = {10.1042/BST20200695},
abstract = {In vertebrates, cytosine-guanine ({CpG}) dinucleotides are predominantly methylated, with ∼80\% of all {CpG} sites containing 5-methylcytosine (5mC), a repressive mark associated with long-term gene silencing. The exceptions to such a globally hypermethylated state are {CpG}-rich {DNA} sequences called {CpG} islands ({CGIs}), which are mostly hypomethylated relative to the bulk genome. {CGIs} overlap promoters from the earliest vertebrates to humans, indicating a concerted evolutionary drive compatible with {CGI} retention. {CGIs} are characterised by {DNA} sequence features that include {DNA} hypomethylation, elevated {CpG} and {GC} content and the presence of transcription factor binding sites. These sequence characteristics are congruous with the recruitment of transcription factors and chromatin modifying enzymes, and transcriptional activation in general. {CGIs} colocalize with sites of transcriptional initiation in hypermethylated vertebrate genomes, however, a growing body of evidence indicates that {CGIs} might exert their gene regulatory function in other genomic contexts. In this review, we discuss the diverse regulatory features of {CGIs}, their functional readout, and the evolutionary implications associated with {CGI} retention in vertebrates and possibly in invertebrates.},
pages = {1109--1119},
number = {3},
journaltitle = {Biochemical Society Transactions},
shortjournal = {Biochem Soc Trans},
author = {Angeloni, Allegra and Bogdanovic, Ozren},
date = {2021-06-30},
pmid = {34156435},
pmcid = {PMC8286816},
keywords = {Humans, Animals, Gene Expression Regulation, Binding Sites, {DNA} methylation, {CpG} Islands, Transcription Factors, chromatin, Chromatin, {CpG} islands, {DNA} Methylation, Genome, orphan {CpG} islands, Promoter Regions, Genetic},
}
@article{forni_dinucleotide_2023,
title = {Dinucleotide biases in {RNA} viruses that infect vertebrates or invertebrates},
volume = {0},
url = {https://journals.asm.org/doi/full/10.1128/spectrum.02529-23},
doi = {10.1128/spectrum.02529-23},
pages = {e02529--23},
number = {0},
journaltitle = {Microbiology Spectrum},
author = {Forni, Diego and Pozzoli, Uberto and Cagliani, Rachele and Clerici, Mario and Sironi, Manuela},
urldate = {2023-10-17},
date = {2023-10-06},
note = {Publisher: American Society for Microbiology},
}
@article{sharp_cpg_2023,
title = {{CpG} dinucleotide enrichment in the influenza A virus genome as a live attenuated vaccine development strategy},
volume = {19},
issn = {1553-7374},
url = {https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1011357},
doi = {10.1371/journal.ppat.1011357},
abstract = {Synonymous recoding of {RNA} virus genomes is a promising approach for generating attenuated viruses to use as vaccines. Problematically, recoding typically hinders virus growth, but this may be rectified using {CpG} dinucleotide enrichment. {CpGs} are recognised by cellular zinc-finger antiviral protein ({ZAP}), and so in principle, removing {ZAP} sensing from a virus propagation system will reverse attenuation of a {CpG}-enriched virus, enabling high titre yield of a vaccine virus. We tested this using a vaccine strain of influenza A virus ({IAV}) engineered for increased {CpG} content in genome segment 1. Virus attenuation was mediated by the short isoform of {ZAP}, correlated with the number of {CpGs} added, and was enacted via turnover of viral transcripts. The {CpG}-enriched virus was strongly attenuated in mice, yet conveyed protection from a potentially lethal challenge dose of wildtype virus. Importantly for vaccine development, {CpG}-enriched viruses were genetically stable during serial passage. Unexpectedly, in both {MDCK} cells and embryonated hens’ eggs that are used to propagate live attenuated influenza vaccines, the {ZAP}-sensitive virus was fully replication competent. Thus, {ZAP}-sensitive {CpG} enriched viruses that are defective in human systems can yield high titre in vaccine propagation systems, providing a realistic, economically viable platform to augment existing live attenuated vaccines.},
pages = {e1011357},
number = {5},
journaltitle = {{PLOS} Pathogens},
shortjournal = {{PLOS} Pathogens},
author = {Sharp, Colin P. and Thompson, Beth H. and Nash, Tessa J. and Diebold, Ola and Pinto, Rute M. and Thorley, Luke and Lin, Yao-Tang and Sives, Samantha and Wise, Helen and Hendry, Sara Clohisey and Grey, Finn and Vervelde, Lonneke and Simmonds, Peter and Digard, Paul and Gaunt, Eleanor R.},
urldate = {2023-10-17},
date = {2023-05-05},
langid = {english},
note = {Publisher: Public Library of Science},
keywords = {Microbial mutation, Viral vaccines, Influenza A virus, Chickens, {DNA} methylation, Viral genomics, Viral replication, {RNA} sequencing},
}
@article{gaunt_elevation_2016,
title = {Elevation of {CpG} frequencies in influenza A genome attenuates pathogenicity but enhances host response to infection},
volume = {5},
issn = {2050-084X},
url = {https://doi.org/10.7554/eLife.12735},
doi = {10.7554/eLife.12735},
abstract = {Previously, we demonstrated that frequencies of {CpG} and {UpA} dinucleotides profoundly influence the replication ability of echovirus 7 (Tulloch et al., 2014). Here, we show that that influenza A virus ({IAV}) with maximised frequencies of these dinucleotides in segment 5 showed comparable attenuation in cell culture compared to unmodified virus and a permuted control ({CDLR}). Attenuation was also manifested in vivo, with 10-100 fold reduced viral loads in lungs of mice infected with 200PFU of {CpG}-high and {UpA}-high mutants. However, both induced powerful inflammatory cytokine and adaptive (T cell and neutralising antibody) responses disproportionate to their replication. {CpG}-high infected mice also showed markedly reduced clinical severity, minimal weight loss and reduced immmunopathology in lung, yet sterilising immunity to lethal dose {WT} challenge was achieved after low dose (20PFU) pre-immunisation with this mutant. Increasing {CpG} dinucleotide frequencies represents a generic and potentially highly effective method for generating safe, highly immunoreactive vaccines.},
pages = {e12735},
journaltitle = {{eLife}},
author = {Gaunt, Eleanor and Wise, Helen M and Zhang, Huayu and Lee, Lian N and Atkinson, Nicky J and Nicol, Marlynne Quigg and Highton, Andrew J and Klenerman, Paul and Beard, Philippa M and Dutia, Bernadette M and Digard, Paul and Simmonds, Peter},
editor = {Lipsitch, Marc},
urldate = {2023-10-17},
date = {2016-02-16},
note = {Publisher: {eLife} Sciences Publications, Ltd},
keywords = {{CpG} dinucleotide, immunization, Influenza A virus, {UpA} dinucleotide, vaccine},
}
@article{goncalves-carneiro_rational_2022,
title = {Rational attenuation of {RNA} viruses with zinc finger antiviral protein},
volume = {7},
rights = {2022 The Author(s)},
issn = {2058-5276},
url = {https://www.nature.com/articles/s41564-022-01223-8},
doi = {10.1038/s41564-022-01223-8},
abstract = {Attenuation of a virulent virus is a proven approach for generating vaccines but can be unpredictable. For example, synonymous recoding of viral genomes can attenuate replication but sometimes results in pleiotropic effects that confound rational vaccine design. To enable specific, conditional attenuation of viruses, we examined target {RNA} features that enable zinc finger antiviral protein ({ZAP}) function. {ZAP} recognized {CpG} dinucleotides and targeted {CpG}-rich {RNAs} for depletion, but {RNA} features such as {CpG} numbers, spacing and surrounding nucleotide composition that enable specific modulation by {ZAP} were undefined. Using synonymously mutated {HIV}-1 genomes, we defined several sequence features that govern {ZAP} sensitivity and enable stable attenuation. We applied rules derived from experiments with {HIV}-1 to engineer a mutant enterovirus A71 genome whose attenuation was stable and strictly {ZAP}-dependent, both in cell culture and in mice. The conditionally attenuated enterovirus A71 mutant elicited neutralizing antibodies that were protective against wild-type enterovirus A71 infection and disease in mice. {ZAP} sensitivity can thus be readily applied for the rational design of conditionally attenuated viral vaccines.},
pages = {1558--1567},
number = {10},
journaltitle = {Nature Microbiology},
shortjournal = {Nat Microbiol},
author = {Gonçalves-Carneiro, Daniel and Mastrocola, Emily and Lei, Xiao and {DaSilva}, Justin and Chan, Yoke Fun and Bieniasz, Paul D.},
urldate = {2023-10-17},
date = {2022-10},
langid = {english},
note = {Number: 10
Publisher: Nature Publishing Group},
keywords = {Live attenuated vaccines, Restriction factors},
}
@software{bokeh_development_team_bokeh_2024,
title = {Bokeh: Python library for interactive visualization},
url = {https://docs.bokeh.org/en/3.3.4/},
shorttitle = {Bokeh},
abstract = {Interactive Data Visualization in the browser, from Python - bokeh/bokeh},
version = {3.3.4},
author = {{Bokeh Development Team}},
urldate = {2024-03-28},
date = {2024-01},
}
@article{cock_biopython_2009,
title = {Biopython: freely available Python tools for computational molecular biology and bioinformatics},
volume = {25},
issn = {1367-4803},
url = {https://doi.org/10.1093/bioinformatics/btp163},
doi = {10.1093/bioinformatics/btp163},
shorttitle = {Biopython},
abstract = {Summary: The Biopython project is a mature open source international collaboration of volunteer developers, providing Python libraries for a wide range of bioinformatics problems. Biopython includes modules for reading and writing different sequence file formats and multiple sequence alignments, dealing with 3D macro molecular structures, interacting with common tools such as {BLAST}, {ClustalW} and {EMBOSS}, accessing key online databases, as well as providing numerical methods for statistical learning.Availability: Biopython is freely available, with documentation and source code at www.biopython.org under the Biopython license.Contact: All queries should be directed to the Biopython mailing lists, see www.biopython.org/wiki/\_Mailing\_listspeter.cock@scri.ac.uk.},
pages = {1422--1423},
number = {11},
journaltitle = {Bioinformatics},
shortjournal = {Bioinformatics},
author = {Cock, Peter J. A. and Antao, Tiago and Chang, Jeffrey T. and Chapman, Brad A. and Cox, Cymon J. and Dalke, Andrew and Friedberg, Iddo and Hamelryck, Thomas and Kauff, Frank and Wilczynski, Bartek and de Hoon, Michiel J. L.},
urldate = {2024-03-25},
date = {2009-06-01},
}
@online{mdn_web_docs_progressive_2023,
title = {Progressive web apps},
url = {https://developer.mozilla.org/en-US/docs/Web/Progressive_web_apps},
abstract = {A progressive web app ({PWA}) is an app that's built using web platform technologies, but that provides a user experience like that of a platform-specific app.},
author = {{MDN Web Docs}},
urldate = {2024-03-25},
date = {2023-10-25},
langid = {american},
}
@software{the_pyodide_development_team_pyodidepyodide_2023,
title = {pyodide/pyodide: a Python distribution for the browser and Node.js based on WebAssembly},
url = {https://zenodo.org/records/8378122},
shorttitle = {pyodide/pyodide},
abstract = {Pyodide is a Python distribution for the browser and Node.js based on {WebAssembly}},
version = {0.24.1},
publisher = {Zenodo},
author = {{The Pyodide development team}},
urldate = {2024-03-25},
date = {2023-09-25},
doi = {10.5281/zenodo.8378122},
}
@software{panel_development_team_holovizpanel_2024,
title = {holoviz/panel: The powerful data exploration & web app framework for Python},
url = {https://zenodo.org/records/10563859},
shorttitle = {holoviz/panel},
version = {v1.3.8},
publisher = {Zenodo},
author = {{Panel Development Team}},
urldate = {2024-03-25},
date = {2024-01-24},
doi = {10.5281/zenodo.10563859},
}