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•Phylogenetic estimates support that the COVID-2 pandemic started sometimes around 6 October 2019–11 December 2019, which corresponds to the time of the host-jump into humans.
•The diversity of SARS-CoV-2 strains in many countries recapitulates its full global diversity, consistent with multiple introductions of the virus to regions throughout the world seeding local transmission events.
•198 sites in the SARS-CoV-2 genome appear to have already undergone recurrent, independent mutations based on a large-scale analysis of public genome assemblies.
•Detected recurrent mutations may indicate ongoing adaptation of SARS-CoV-2 to its novel human host.
•Monitoring the build-up and patterns of genetic diversity in SARS-CoV-2 has potential to inform targets for drug and vaccine development.
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 52,020, 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.
Mutations in SARS-CoV-2 offer insights into virus evolution
By analysing virus genomes from over 7,500 people infected with Covid-19, a UCL-led research team has characterised patterns of diversity of SARS-CoV-2 virus genome, offering clues to direct drugs and vaccine targets.
The study, led by the UCL Genetics Institute, identified close to 200 recurrent genetic mutations in the virus, highlighting how it may be adapting and evolving to its human hosts.
Researchers found that a large proportion of the global genetic diversity of SARS-CoV-2 is found in all hardest-hit countries, suggesting extensive global transmission from early on in the epidemic and the absence of single 'Patient Zeroes' in most countries.
The findings, published today in Infection, Genetics and Evolution, also further establish the virus only emerged recently in late 2019, before quickly spreading across the globe.Scientists analysed the emergence of genomic diversity in SARS-CoV-2, the new coronavirus causing Covid-19, by screening the genomes of over 7,500 viruses from infected patients around the globe. They identified 198 mutations that appear to have independently occurred more than once, which may hold clues to how the virus is adapting.
Co-lead author Professor Francois Balloux (UCL Genetics Institute) said: "All viruses naturally mutate. Mutations in themselves are not a bad thing and there is nothing to suggest SARS-CoV-2 is mutating faster or slower than expected. So far we cannot say whether SARS-CoV-2 is becoming more or less lethal and contagious."
The small genetic changes, or mutations, identified were not evenly distributed across the virus genome. As some parts of the genome had very few mutations, the researchers say those invariant parts of the virus could be better targets for drug and vaccine development.
"A major challenge to defeating viruses is that a vaccine or drug might no longer be effective if the virus has mutated. If we focus our efforts on parts of the virus that are less likely to mutate, we have a better chance of developing drugs that will be effective in the long run," Professor Balloux explained.
"We need to develop drugs and vaccines that cannot be easily evaded by the virus."
Co-lead author Dr. Lucy van Dorp (UCL Genetics Institute) added: "There are still very few genetic differences or mutations between viruses. We found that some of these differences have occurred multiple times, independently of one another during the course of the pandemic—we need to continue to monitor these as more genomes become available and conduct research to understand exactly what they do."
The results add to a growing body of evidence that SARS-CoV-2 viruses share a common ancestor from late 2019, suggesting that this was when the virus jumped from a previous animal host, into people. This means it is most unlikely the virus causing Covid-19 was in human circulation for long before it was first detected.
In many countries including the UK, the diversity of viruses sampled was almost as much as that seen across the whole world, meaning the virus entered the UK numerous times independently, rather than via any one index case.
The research team have developed a new interactive, open-source online application so that researchers across the globe can also review the virus genomes and apply similar approaches to better understand its evolution.
Dr. van Dorp said: "Being able to analyse such an extraordinary number of virus genomes within the first few months of the pandemic could be invaluable to drug development efforts, and showcases how far genomic research has come even within the last decade. We are all benefiting from a tremendous effort by hundreds of researchers globally who have been sequencing virus genomes and making them available online."
Coronavirus quickly spread around the world starting late last year, new genetic analysis shows
Maggie Fox
May 6, 2020
A new genetic analysis of the virus that causes Covid-19 taken from more than 7,600 patients around the world shows it has been circulating in people since late last year, and must have spread extremely quickly after the first infection.
Researchers in Britain looked at mutations in the virus and found evidence of quick spread, but no evidence the virus is becoming more easily transmitted or more likely to cause serious disease.
"The virus is changing, but this in itself does not mean it's getting worse," genetics researcher Francois Balloux of the University College London Genetics Institute told CNN.Balloux and colleagues pulled viral sequences from a giant global database that scientists around the world are using to share data. They looked at samples taken at different times and from different places, and said they indicate that the virus first started infecting people at the end of last year.
"This rules out any scenario that assumes SARSCoV-2 may have been in circulation long before it was identified, and hence have already infected large proportions of the population," Balloux's team wrote in their report, published in the journal Infection, Genetics and Evolution.
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
date of writing (April 23 2020).
Mutations in SARS-CoV-2 offer insights into virus evolution
By analysing virus genomes from over 7,500 people infected with Covid-19, a UCL-led research team has characterised patterns of diversity of SARS-CoV-2 virus genome, offering clues to direct drugs and vaccine targets.
The study, led by the UCL Genetics Institute, identified close to 200 recurrent genetic mutations in the virus, highlighting how it may be adapting and evolving to its human hosts.
Researchers found that a large proportion of the global genetic diversity of SARS-CoV-2 is found in all hardest-hit countries, suggesting extensive global transmission from early on in the epidemic and the absence of single 'Patient Zeroes' in most countries.
The findings, published today in Infection, Genetics and Evolution, also further establish the virus only emerged recently in late 2019, before quickly spreading across the globe.Scientists analysed the emergence of genomic diversity in SARS-CoV-2, the new coronavirus causing Covid-19, by screening the genomes of over 7,500 viruses from infected patients around the globe. They identified 198 mutations that appear to have independently occurred more than once, which may hold clues to how the virus is adapting.
Co-lead author Professor Francois Balloux (UCL Genetics Institute) said: "All viruses naturally mutate. Mutations in themselves are not a bad thing and there is nothing to suggest SARS-CoV-2 is mutating faster or slower than expected. So far we cannot say whether SARS-CoV-2 is becoming more or less lethal and contagious."
The small genetic changes, or mutations, identified were not evenly distributed across the virus genome. As some parts of the genome had very few mutations, the researchers say those invariant parts of the virus could be better targets for drug and vaccine development.
"A major challenge to defeating viruses is that a vaccine or drug might no longer be effective if the virus has mutated. If we focus our efforts on parts of the virus that are less likely to mutate, we have a better chance of developing drugs that will be effective in the long run," Professor Balloux explained.
"We need to develop drugs and vaccines that cannot be easily evaded by the virus."
Co-lead author Dr. Lucy van Dorp (UCL Genetics Institute) added: "There are still very few genetic differences or mutations between viruses. We found that some of these differences have occurred multiple times, independently of one another during the course of the pandemic—we need to continue to monitor these as more genomes become available and conduct research to understand exactly what they do."
The results add to a growing body of evidence that SARS-CoV-2 viruses share a common ancestor from late 2019, suggesting that this was when the virus jumped from a previous animal host, into people. This means it is most unlikely the virus causing Covid-19 was in human circulation for long before it was first detected.
In many countries including the UK, the diversity of viruses sampled was almost as much as that seen across the whole world, meaning the virus entered the UK numerous times independently, rather than via any one index case.
The research team have developed a new interactive, open-source online application so that researchers across the globe can also review the virus genomes and apply similar approaches to better understand its evolution.
Dr. van Dorp said: "Being able to analyse such an extraordinary number of virus genomes within the first few months of the pandemic could be invaluable to drug development efforts, and showcases how far genomic research has come even within the last decade. We are all benefiting from a tremendous effort by hundreds of researchers globally who have been sequencing virus genomes and making them available online."
I think we need more information about the genetics developed. It may be possible that SARS-Cov-2 "jumped" into humans early in 2019 but lacked all of the genetic code to transmit efficiently. After several thousand passages through humans it could have gradually obtained the necessary genetic changes to enable it to be more efficient. I think this is the likely scenario. In the end science will tell us. I think we should keep open minds.
