An unusually high substitution rate in transplant-associated BK polyomavirus in vivo is further concentrated in HLA-C-bound viral peptides

Domingo‐Calap, Pilar; Schubert, Benjamin; Joly, Mélanie; Solis, Morgane; Untrau, Meiggie; Carapito, Raphaël; Georgel, Philippe; Caillard, Sophie; Fafi‐Kremer, Samira; Paul, Nicodéme; Kohlbacher, Oliver; Gónzález-Candelas, Fernando; Bahram, Seiamak

doi:10.1371/journal.ppat.1007368

Cited by 24 publications

(17 citation statements)

References 89 publications

(87 reference statements)

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“…S1 and S2). This rate also falls in line with those observed in other coronaviruses 25,26 and is fairly unremarkable relative to other positive single-stranded RNA viruses, which do not have a viral proof-reading mechanism 27,28 .…”

Section: Resultssupporting

confidence: 84%

No evidence for increased transmissibility from recurrent mutations in SARS-CoV-2

et al. 2020

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COVID-19 is caused by the coronavirus SARS-CoV-2, which jumped into the human population in late 2019 from a currently uncharacterised animal reservoir. Due to this recent association with humans, SARS-CoV-2 may not yet be fully adapted to its human host. This has led to speculations that SARS-CoV-2 may be evolving towards higher transmissibility. The most plausible mutations under putative natural selection are those which have emerged repeatedly and independently (homoplasies). Here, we formally test whether any homoplasies observed in SARS-CoV-2 to date are significantly associated with increased viral transmission. To do so, we develop a phylogenetic index to quantify the relative number of descendants in sister clades with and without a specific allele. We apply this index to a curated set of recurrent mutations identified within a dataset of 46,723 SARS-CoV-2 genomes isolated from patients worldwide. We do not identify a single recurrent mutation in this set convincingly associated with increased viral transmission. Instead, recurrent mutations currently in circulation appear to be evolutionary neutral and primarily induced by the human immune system via RNA editing, rather than being signatures of adaptation. At this stage we find no evidence for significantly more transmissible lineages of SARS-CoV-2 due to recurrent mutations.

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Section: Resultssupporting

confidence: 84%

No evidence for increased transmissibility from recurrent mutations in SARS-CoV-2

et al. 2020

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“…We informally estimate the mutation rate over our alignment to 9.6 x 10 -4 substitutions per site per year, which is consistent with previous rates estimated for SARS-CoV-2 [1-4] ( Figure S1-S2). This rate also falls in line with those observed in other coronaviruses [24,25], and is fairly unremarkable relative to other positive single-stranded RNA viruses, which do not have a viral proof-reading mechanism [26,27]. Table S1.…”

Section: Global Diversity Of Sars-cov-2supporting

confidence: 83%

No evidence for increased transmissibility from recurrent mutations in SARS-CoV-2

Dorp

Richard

Tan

et al. 2020

Preprint

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AbstractThe COVID-19 pandemic is caused by the coronavirus SARS-CoV-2, which jumped into the human population in late 2019 from a currently uncharacterised reservoir. Due to this extremely recent association with humans, SARS-CoV-2 may not yet be fully adapted to its human host. This has led to speculations that some lineages of SARS-CoV-2 may be evolving towards higher transmissibility. The most plausible candidate mutations under putative natural selection are those which have emerged repeatedly and independently (homoplasies). Here, we formally test whether any of the recurrent mutations that have been observed in SARS-CoV-2 to date are significantly associated with increased viral transmission. To do so, we developed a phylogenetic index to quantify the relative number of descendants in sister clades with and without a specific allele. We apply this index to a carefully curated set of recurrent mutations identified within a dataset of over 23,000 SARS-CoV-2 genomes isolated from patients worldwide. We do not identify a single recurrent mutation in this set convincingly associated with increased viral transmission. Instead, recurrent SARS-CoV-2 mutations currently in circulation appear to be evolutionary neutral. Recurrent mutations also seem primarily induced by the human immune system via host RNA editing, rather than being signatures of adaption to the novel human host. We find no evidence at this stage for the emergence of more transmissible lineages of SARS-CoV-2 due to recurrent mutations.

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“…Among the proteins described in the present study, some contain domains typical for bacteriophages, but no direct homology was found. This is probably due to the fast evolutions of viral genomes [ 69 , 70 ] which can mask the similarity of related proteins [ 71 ]. Nevertheless, cysteine-rich repeats can serve as an instrument to find new cases of prokaryote to eukaryote HGT.…”

Section: Discussionmentioning

confidence: 99%

Amino acid sequence associated with bacteriophage recombination site helps to reveal genes potentially acquired through horizontal gene transfer

2020

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Background Horizontal gene transfer, i.e. the acquisition of genetic material from nonparent organism, is considered an important force driving species evolution. Many cases of horizontal gene transfer from prokaryotes to eukaryotes have been registered, but no transfer mechanism has been deciphered so far, although viruses were proposed as possible vectors in several studies. In agreement with this idea, in our previous study we discovered that in two eukaryotic proteins bacteriophage recombination site (AttP) was adjacent to the regions originating via horizontal gene transfer. In one of those cases AttP site was present inside the introns of cysteine-rich repeats. In the present study we aimed to apply computational tools for finding multiple horizontal gene transfer events in large genome databases. For that purpose we used a sequence of cysteine-rich repeats to identify genes potentially acquired through horizontal transfer. Results HMMER remote similarity search significantly detected 382 proteins containing cysteine-rich repeats. All of them, except 8 sequences, belong to eukaryotes. In 124 proteins the presence of conserved structural domains was predicted. In spite of the fact that cysteine-rich repeats are found almost exclusively in eukaryotic proteins, many predicted domains are most common for prokaryotes or bacteriophages. Ninety-eight proteins out of 124 contain typical prokaryotic domains. In those cases proteins were considered as potentially originating via horizontal transfer. In addition, HHblits search revealed that two domains of the same fungal protein, Glycoside hydrolase and Peptidase M15, have high similarity with proteins of two different prokaryotic species, hinting at independent horizontal gene transfer events. Conclusions Cysteine-rich repeats in eukaryotic proteins are usually accompanied by conserved domains typical for prokaryotes or bacteriophages. These proteins, containing both cysteine-rich repeats, and characteristic prokaryotic domains, might represent multiple independent horizontal gene transfer events from prokaryotes to eukaryotes. We believe that the presence of bacteriophage recombination site inside cysteine-rich repeat coding sequence may facilitate horizontal genes transfer. Thus computational approach, described in the present study, can help finding multiple sequences originated from horizontal transfer in eukaryotic genomes.

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An unusually high substitution rate in transplant-associated BK polyomavirus in vivo is further concentrated in HLA-C-bound viral peptides

Cited by 24 publications

References 89 publications

No evidence for increased transmissibility from recurrent mutations in SARS-CoV-2

No evidence for increased transmissibility from recurrent mutations in SARS-CoV-2

No evidence for increased transmissibility from recurrent mutations in SARS-CoV-2

Amino acid sequence associated with bacteriophage recombination site helps to reveal genes potentially acquired through horizontal gene transfer

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