OmniVira

Literature detail

The molecular epidemiology of multiple zoonotic origins of SARS-CoV-2.

Jonathan E Pekar1,2 Andrew Magee3 Edyth Parker4 Niema Moshiri5 Katherine Izhikevich5,6 Jennifer L Havens1 Karthik Gangavarapu3 Lorena Mariana Malpica Serrano7 Alexander Crits-Christoph8 Nathaniel L Matteson4 Mark Zeller4 Joshua I Levy4 Jade C Wang9 Scott Hughes9 Jungmin Lee10 Heedo Park10,11 Man-Seong Park10,11 Katherine Ching Zi Yan12 Raymond Tzer Pin Lin12 Mohd Noor Mat Isa13 Yusuf Muhammad Noor13 Tetyana I Vasylyeva14 Robert F Garry15,16,17 Edward C Holmes18 Andrew Rambaut19 Marc A Suchard3,20,21 Kristian G Andersen4,22 Michael Worobey7 Joel O Wertheim14
Affiliations 22 institutions
  1. Bioinformatics and Systems Biology Graduate Program, University of California, San Diego, La Jolla, CA 92093, USA.
  2. Department of Biomedical Informatics, University of California, San Diego, La Jolla, CA 92093, USA.
  3. Department of Human Genetics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
  4. Department of Immunology and Microbiology, The Scripps Research Institute, La Jolla, CA 92037, USA.
  5. Department of Computer Science and Engineering, University of California, San Diego, La Jolla, CA 92093, USA.
  6. Department of Mathematics, University of California, San Diego, La Jolla, CA 92093, USA.
  7. Department of Ecology and Evolutionary Biology, University of Arizona, Tucson, AZ 85721, USA.
  8. W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA.
  9. New York City Public Health Laboratory, New York City Department of Health and Mental Hygiene, New York, NY 11101, USA.
  10. Department of Microbiology, Institute for Viral Diseases, Biosafety Center, College of Medicine, Korea University, Seoul, South Korea.
  11. BK21 Graduate Program, Department of Biomedical Sciences, Korea University College of Medicine, Seoul 02841, Republic of Korea.
  12. National Public Health Laboratory, National Centre for Infectious Diseases, Singapore.
  13. Malaysia Genome and Vaccine Institute, Jalan Bangi, 43000 Kajang, Selangor, Malaysia.
  14. Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
  15. Department of Microbiology and Immunology, School of Medicine, Tulane University, New Orleans, LA 70112, USA.
  16. Zalgen Labs, Frederick, MD 21703, USA.
  17. Global Virus Network (GVN), Baltimore, MD 21201, USA.
  18. Sydney Institute for Infectious Diseases, School of Life and Environmental Sciences and School of Medical Sciences, The University of Sydney, Sydney, NSW 2006, Australia.
  19. Institute of Evolutionary Biology, University of Edinburgh, King's Buildings, Edinburgh EH9 3FL, UK.
  20. Department of Biomathematics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
  21. Department of Biostatistics, Fielding School of Public Health, University of California, Los Angeles, Los Angeles, CA 90095, USA.
  22. Scripps Research Translational Institute, La Jolla, CA 92037, USA.
PMID 35881005 2022 Science eng ppublish
PubMed DOI Browse context

Article

Publication summary

Understanding the circumstances that lead to pandemics is important for their prevention. We analyzed the genomic diversity of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) early in the coronavirus disease 2019 (COVID-19) pandemic. We show that SARS-CoV-2 genomic diversity before February 2020 likely comprised only two distinct viral lineages, denoted "A" and "B." Phylodynamic rooting methods, coupled with epidemic simulations, reveal that these lineages were the result of at least two separate cross-species transmission events into humans. The first zoonotic transmission likely involved lineage B viruses around 18 November 2019 (23 October to 8 December), and the separate introduction of lineage A likely occurred within weeks of this event. These findings indicate that it is unlikely that SARS-CoV-2 circulated widely in humans before November 2019 and define the narrow window between when SARS-CoV-2 first jumped into humans and when the first cases of COVID-19 were reported. As with other coronaviruses, SARS-CoV-2 emergence likely resulted from multiple zoonotic events.

COVID-19 Pandemics SARS-CoV-2 Viral Zoonoses Animals Computer Simulation Genetic Variation Genomics Humans Molecular Epidemiology Phylogeny

Structured evidence records

Evidence records

2 total
Genomic Evolution 1 records
Genomic Evolution Extraction confidence 0.93
Key finding

Genomic and phylodynamic analyses indicate that SARS-CoV-2 lineages A and B originated from two separate zoonotic transmissions into humans.

Virus
SARS-CoV-2
Location
Not specified
Supporting text

We analyzed the genomic diversity of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) early in the coronavirus disease 2019 (COVID-19) pandemic. Phylodynamic rooting methods, coupled with epidemic simulations, reveal that these lineages were the result of at least two separate cross-species transmission events into humans.

Analysis methods
genomic analysis; phylodynamic analysis
Spillover Event 1 records
Spillover Event Extraction confidence 0.97
Key finding

Two distinct cross-species transmission events introduced SARS-CoV-2 lineages A and B from an animal source into humans in late 2019.

Virus
SARS-CoV-2
Location
Not specified
Supporting text

Phylodynamic rooting methods, coupled with epidemic simulations, reveal that these lineages were the result of at least two separate cross-species transmission events into humans.

Method
phylodynamic rooting; epidemic simulations; genomic analysis
Study design
phylogenetic analysis
Transmission direction
animal-to-human