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10.1038/s41467-020-19818-2 http://scihub22266oqcxt.onion/10.1038/s41467-020-19818-2 33239633!7688939!33239633     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2020 ; 11 (1): 5986 Nephropedia Template TP {{tp|p=33239633|t=2020. No evidence for increased transmissibility from recurrent mutations in SARS-CoV-2 |pdf=|usr=}}{{33239633}} gab.com Text No evidence for increased transmissibility from recurrent mutations in SARS-CoV-2 JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=33239633 #FOAvip 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. Twit Text FOAVip No evidence for increased transmissibility from recurrent mutations in SARS-CoV-2 ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=33239633 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33239633 #FOAvip English Wikipedia <ref>{{Cite pmid|33239633}}</ref> No evidence for increased transmissibility from recurrent mutations in SARS-CoV-2 #MMPMID33239633 van Dorp L; Richard D; Tan CCS; Shaw LP; Acman M; Balloux F Nat Commun 2020[Nov]; 11 (1): 5986 PMID33239633show ga 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. |*Genetic Fitness[MESH] |*Mutation Rate[MESH] |Alleles[MESH] |Animals[MESH] |COVID-19/epidemiology/*transmission/virology[MESH] |Genome, Viral/genetics[MESH] |Host-Pathogen Interactions/*genetics[MESH] |Humans[MESH] |Pandemics[MESH] |Phylogeny[MESH] |RNA Editing[MESH] |RNA, Viral/genetics[MESH] |SARS-CoV-2/*genetics/pathogenicity[MESH]No evidence for increased transmissibility from recurrent mutations in(epmc).pdf DeepDyve Pubget Overpricing