Authors

Rebecca Earnest, Yale School of Public Health
Rockib Uddin, Massachusetts General Hospital
Nicholas Matluk, Maine Center for Disease Control and Prevention
Nicholas Renzette, The Jackson Laboratory for Genomic Medicine
Katherine J. Siddle, Broad Institute of MIT and Harvard
Christine Loreth, Broad Institute of MIT and Harvard
Gordon Adams, Broad Institute of MIT and Harvard
Christopher H. Tomkins-Tinch, Broad Institute of MIT and Harvard
Mary E. Petrone, Yale School of Public Health
Jessica E. Rothman, Yale School of Public Health
Mallery I. Breban, Yale School of Public Health
Robert Tobias Koch, Yale School of Public Health
Kendall Billig, Yale School of Public Health
Joseph R. Fauver, University of Nebraska Medical CenterFollow
Chantal B.F. Vogels, Yale School of Public Health
Sarah Turbett, Massachusetts General Hospital
Kaya Bilguvar, Yale University
Bony De Kumar, Yale University
Marie L. Landry, Yale University School of Medicine
David R. Peaper, Yale University School of Medicine
Kevin Kelly, The Jackson Laboratory for Genomic Medicine
Greg Omerza, The Jackson Laboratory for Genomic Medicine
Heather Grieser, Maine Center for Disease Control and Prevention
Sim Meak, Maine Center for Disease Control and Prevention
John Martha, Maine Center for Disease Control and Prevention
Hannah H. Dewey, The Jackson Laboratory
Susan Kales, The Jackson Laboratory
Daniel Berenzy, The Jackson Laboratory
Kristin Carpenter-Azevedo, State Health Laboratories
Ewa King, State Health Laboratories
Richard C. Huard, State Health Laboratories
Sandra C. Smole, Massachusetts Department of Public Health
Catherine M. Brown, Massachusetts Department of Public Health
Timelia Fink, Massachusetts Department of Public Health
Andrew S. Lang, Massachusetts Department of Public Health
Glen R. Gallagher, Massachusetts Department of Public Health
Pardis C. Sabeti, Broad Institute of MIT and Harvard
Stacey Gabriel, Broad Institute of MIT and Harvard
Bronwyn L. MacInnis, Broad Institute of MIT and Harvard
New England Variant Investigation Team
Ryan Tewhey, Acibadem University School of Medicine
Mark D. Adams, The Jackson Laboratory for Genomic Medicine
Daniel J. Park, Broad Institute of MIT and Harvard
Jacob E. Lemieux, Massachusetts General Hospita
Nathan D. Grubaugh, Yale School of Public Health

Document Type

Article

Journal Title

Cell Reports Medicine

Publication Date

2022

Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Delta variant quickly rose to dominance in mid-2021, displacing other variants, including Alpha. Studies using data from the United Kingdom and India estimated that Delta was 40-80% more transmissible than Alpha, allowing Delta to become the globally dominant variant. However, it was unclear if the ostensible difference in relative transmissibility was due mostly to innate properties of Delta's infectiousness or differences in the study populations. To investigate, we formed a partnership with SARS-CoV-2 genomic surveillance programs from all six New England US states. By comparing logistic growth rates, we found that Delta emerged 37-163% faster than Alpha in early 2021 (37% Massachusetts, 75% New Hampshire, 95% Maine, 98% Rhode Island, 151% Connecticut, and 163% Vermont). We next computed variant-specific effective reproductive numbers and estimated that Delta was 58-120% more transmissible than Alpha across New England (58% New Hampshire, 68% Massachusetts, 76% Connecticut, 85% Rhode Island, 98% Maine, and 120% Vermont). Finally, using RT-PCR data, we estimated that Delta infections generate on average ∼6 times more viral RNA copies per mL than Alpha infections. Overall, our evidence indicates that Delta's enhanced transmissibility could be attributed to its innate ability to increase infectiousness, but its epidemiological dynamics may vary depending on the underlying immunity and behavior of distinct populations.

ISSN

2666-3791

Included in

Epidemiology Commons

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