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dc.contributor.authorSadykov, Mukhtar
dc.contributor.authorMourier, Tobias
dc.contributor.authorGuan, Qingtian
dc.contributor.authorPain, Arnab
dc.date.accessioned2020-06-22T12:48:48Z
dc.date.available2020-06-22T12:48:48Z
dc.date.issued2020-06-20
dc.identifier.citationSadykov, M., Mourier, T., Guan, Q., & Pain, A. (2020). Cytosine deamination in SARS-CoV-2 leads to progressive CpG depletion. doi:10.1101/2020.06.19.161687
dc.identifier.doi10.1101/2020.06.19.161687
dc.identifier.urihttp://hdl.handle.net/10754/663776
dc.description.abstractRNA viruses use CpG reduction to evade the host cell defense, but the driving mechanism is still largely unknown. To address this, we used rapidly growing genomic dataset of SARS-CoV-2 with relevant metadata information. SARS-CoV-2 genomes show a progressive increase of C-to-U substitutions resulting in CpG loss over just a few months. This is consistent with APOBEC-mediated RNA editing resulting in CpG reduction, thus allowing the virus to escape ZAP-mediated RNA degradation. Our results thus link the dynamics of target sequences in viral genome for two known host molecular defense mechanisms, the APOBEC and ZAP proteins.
dc.description.sponsorshipWe thank all laboratories which have contributed sequences to the GISAID database and Zhadyra Yerkesh for giving her comments and helpful discussions. This work was supported by funding from King Abdullah University of Science and Technology (KAUST), Office of Sponsored Research (OSR). Work in AP’s laboratory is supported by the KAUST faculty baseline fund (BAS/1/1020-01-01).
dc.publisherCold Spring Harbor Laboratory
dc.relation.urlhttp://biorxiv.org/lookup/doi/10.1101/2020.06.19.161687
dc.relation.urlhttps://www.biorxiv.org/content/biorxiv/early/2020/06/19/2020.06.19.161687.full.pdf
dc.rightsArchived with thanks to Cold Spring Harbor Laboratory
dc.titleCytosine deamination in SARS-CoV-2 leads to progressive CpG depletion.
dc.typePreprint
dc.contributor.departmentBiological and Environmental Sciences and Engineering (BESE) Division
dc.contributor.departmentBioscience
dc.contributor.departmentBioscience Program
dc.contributor.departmentEnvironmental Science and Engineering Program
dc.contributor.departmentKing Abdullah University of Science and Technology (KAUST), Pathogen Genomics Laboratory, Biological and Environmental Science and Engineering (BESE), Thuwal8 Jeddah, 23955-6900, Saudi Arabia.
dc.contributor.departmentPathogen Genomics Laboratory
dc.eprint.versionPre-print
dc.contributor.institutionResearch Center for Zoonosis Control, Global Institution for Collaborative Research and Education (GI-CoRE); Hokkaido University, N20 W10 Kita-ku, Sapporo, 001-0020 Japan.
dc.contributor.institutionNuffield Division of Clinical Laboratory Sciences (NDCLS), University of Oxford, Headington, Oxford, OX3 9DU, United Kingdom
kaust.personSadykov, Mukhtar
kaust.personMourier, Tobias
kaust.personGuan, Qingtian
kaust.personPain, Arnab
kaust.grant.numberBAS/1/1020-01-01
refterms.dateFOA2020-06-22T12:49:42Z
kaust.acknowledged.supportUnitOffice of Sponsored Research (OSR)


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