University of New South Wales, Australia - Study uncovers how bacteria use ancient mechanisms to self-repair [Phys.org, November 2022]

Title:

Study uncovers how bacteria use ancient mechanisms to self-repair

 

By:

University of New South Wales, Australia

 

Published:

Phys.org, 23 November 2022

https://phys.org/news/2022-11-uncovers-bacteria-ancient-mechanisms-self-repair.html

 

From the article:

A new study led by UNSW Sydney scientists unveils how nature's oldest wheel, found within bacteria, can fix itself when times get tough.  

 

The findings, published today in Science Advances, show how the flagellar—the ancient motor that powers the swimming ability of bacteria—can also help these tiny organisms adjust to conditions where their motility is impaired.

 

Emergence of genomic diversity and recurrent mutations in SARS-CoV-2 [Scholarly Article - Infection, Genetics and Evolution, 2020]

Title:

Emergence of genomic diversity and recurrent mutations in SARS-CoV-2

 

Authors:

Lucy van Dorp, Mislav Acman, Damien Richard [et al.]

 

Published:

Infection, Genetics and Evolution, Volume 83, 2020

https://www.sciencedirect.com/science/article/abs/pii/S1567134820301829

Abstract:

SARS-CoV-2 is a SARS-like coronavirus of likely zoonotic origin first identified in December 2019 in Wuhan, the capital of China's Hubei province. The virus has since spread globally, resulting in the currently ongoing COVID-19 pandemic. The first whole genome sequence was published on January 5 2020, and thousands of genomes have been sequenced since this date. This resource allows unprecedented insights into the past demography of SARS-CoV-2 but also monitoring of how the virus is adapting to its novel human host, providing information to direct drug and vaccine design. We curated a dataset of 7666 public genome assemblies and analysed the emergence of genomic diversity over time. Our results are in line with previous estimates and point to all sequences sharing a common ancestor towards the end of 2019, supporting this as the period when SARS-CoV-2 jumped into its human host. Due to extensive transmission, the genetic diversity of the virus in several countries recapitulates a large fraction of its worldwide genetic diversity. We identify regions of the SARS-CoV-2 genome that have remained largely invariant to date, and others that have already accumulated diversity. By focusing on mutations which have emerged independently multiple times (homoplasies), we identify 198 filtered recurrent mutations in the SARS-CoV-2 genome. Nearly 80% of the recurrent mutations produced non-synonymous changes at the protein level, suggesting possible ongoing adaptation of SARS-CoV-2. Three sites in Orf1ab in the regions encoding Nsp6, Nsp11, Nsp13, and one in the Spike protein are characterised by a particularly large number of recurrent mutations (>15 events) which may signpost convergent evolution and are of particular interest in the context of adaptation of SARS-CoV-2 to the human host. We additionally provide an interactive user-friendly web-application to query the alignment of the 7666 SARS-CoV-2 genomes.

No evidence for increased transmissibility from recurrent mutations in SARS-CoV-2 [Scholarly Article - Nature Communications, 25 November 2020]

Title:

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

 

Authors:

Lucy van Dorp, Damien Richard, Cedric C. S. Tan, Liam P. Shaw, Mislav Acman & François Balloux 

Published:

Nature Communications, Volume 11, Article number: 5986 (25 November 2020)

https://www.nature.com/articles/s41467-020-19818-2

 

Abstract:

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.