Michael Worobey

Michael Worobey


Research Focus & Metrics

Academic Career Length

23Years (2004-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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2 October 2008 in Nature
Verified
Journal Article
Closed access
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MWMichael Worobey
Michael Worobey
MGMarlea Gemmel
Marlea Gemmel
DTDirk E. Teuwen
Dirk E. Teuwen
THTamara Haselkorn
Tamara Haselkorn
KKKevin Kunstman
Kevin Kunstman
SWSteven M. Wolinsky
Steven M. Wolinsky

11 November 2016 in Science
Verified
Journal Article
Closed access
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KGKatelyn M. Gostic
Katelyn M. Gostic
MAMonique Ambrose
Monique Ambrose
MWMichael Worobey
Michael Worobey
JLJames O. Lloyd-Smith
James O. Lloyd-Smith
Lifelong protection against severe influenza: The first influenza attack that a child suffers can affect the way that their lifelong immunity to the virus builds up. A wide range of influenza A virus subtypes infect humans. Subtype H5 belongs to HA group 1 (which also includes H1 and H2 subtypes), and subtype H7 belongs to HA group 2 (which also includes the H3 subtype). Gostic et al. found that birth-year cohorts that experienced first infections with seasonal H3 subtype viruses were less susceptible to the potentially fatal avian influenza H7N9 virus (see the Perspective by Viboud and Epstein). Conversely, older individuals who were exposed to H1 or H2 subtype viruses as youngsters were less susceptible to avian H5N1-bearing viruses. A mathematical model of the protective effect of this imprinting could potentially prove useful to predict the age distribution and severity of future pandemics. Science , this issue p. 722 ; see also p. 706

26 August 2022 in Science
Verified
Journal Article
Open access
MWMichael Worobey
Michael Worobey
JLJoshua I. Levy
Joshua I. Levy
LSLorena Malpica Serrano
Lorena Malpica Serrano
ACAlexander Crits-Christoph
Alexander Crits-Christoph
JPJonathan E. Pekar
Jonathan E. Pekar
KAKristian G. Andersen
Kristian G. Andersen
Understanding how severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged in 2019 is critical to preventing future zoonotic outbreaks before they become the next pandemic. The Huanan Seafood Wholesale Market in Wuhan, China, was identified as a likely source of cases in early reports, but later this conclusion became controversial. We show here that the earliest known COVID-19 cases from December 2019, including those without reported direct links, were geographically centered on this market. We report that live SARS-CoV-2–susceptible mammals were sold at the market in late 2019 and that within the market, SARS-CoV-2–positive environmental samples were spatially associated with vendors selling live mammals. Although there is insufficient evidence to define upstream events, and exact circumstances remain obscure, our analyses indicate that the emergence of SARS-CoV-2 occurred through the live wildlife trade in China and show that the Huanan market was the epicenter of the COVID-19 pandemic.

30 October 2020 in Science
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Journal Article
Open access
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MWMichael Worobey
Michael Worobey
JPJonathan Pekar
Jonathan Pekar
BLBrendan B. Larsen
Brendan B. Larsen
MNMartha I. Nelson
Martha I. Nelson
VHVerity Hill
Verity Hill
PLPhilippe Lemey
Philippe Lemey
A series of unfortunate events: The history of how severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spread around the planet has been far from clear. Several narratives have been propagated by social media and, in some cases, national policies were forged in response. Now that many thousands of virus sequences are available, two studies analyzed some of the key early events in the spread of SARS-CoV-2. Bedford et al. found that the virus arrived in Washington state in late January or early February. The viral genome from the first case detected had mutations similar to those found in Chinese samples and rapidly spread and dominated subsequent undetected community transmission. The other viruses detected had origins in Europe. Worobey et al. found that early introductions into Germany and the west coast of the United States were extinguished by vigorous public health efforts, but these successes were largely unrecognized. Unfortunately, several major travel events occurred in February, including repatriations from China, with lax public health follow-up. Serial, independent introductions triggered the major outbreaks in the United States and Europe that still hold us in the grip of control measures. Science , this issue p. 571 , p. 564

20 November 2007 in Proceedings of the National Academy of Sciences
Verified
Journal Article
Closed access
MGM. Thomas P. Gilbert
M. Thomas P. Gilbert
ARAndrew Rambaut
Andrew Rambaut
GWGabriela Wlasiuk
Gabriela Wlasiuk
TSThomas J. Spira
Thomas J. Spira
APArthur E. Pitchenik
Arthur E. Pitchenik
MWMichael Worobey
Michael Worobey
HIV-1 group M subtype B was the first HIV discovered and is the predominant variant of AIDS virus in most countries outside of sub-Saharan Africa. However, the circumstances of its origin and emergence remain unresolved. Here we propose a geographic sequence and time line for the origin of subtype B and the emergence of pandemic HIV/AIDS out of Africa. Using HIV-1 gene sequences recovered from archival samples from some of the earliest known Haitian AIDS patients, we find that subtype B likely moved from Africa to Haiti in or around 1966 (1962–1970) and then spread there for some years before successfully dispersing elsewhere. A “pandemic” clade, encompassing the vast majority of non-Haitian subtype B infections in the United States and elsewhere around the world, subsequently emerged after a single migration of the virus out of Haiti in or around 1969 (1966–1972). Haiti appears to have the oldest HIV/AIDS epidemic outside sub-Saharan Africa and the most genetically diverse subtype B epidemic, which might present challenges for HIV-1 vaccine design and testing. The emergence of the pandemic variant of subtype B was an important turning point in the history of AIDS, but its spread was likely driven by ecological rather than evolutionary factors. Our results suggest that HIV-1 circulated cryptically in the United States for ≈12 years before the recognition of AIDS in 1981.

28 April 2014 in Proceedings of the National Academy of Sciences
Verified
Journal Article
Closed access
PDF file
MWMichael Worobey
Michael Worobey
GHGuan-Zhu Han
Guan-Zhu Han
ARAndrew Rambaut
Andrew Rambaut
Significance: The origin of the 1918 pandemic influenza A virus (IAV) and the reasons for its unusual severity are two of the foremost biomedical mysteries of the past century. We infer that the virus arose via reassortment between a preexisting human H1 IAV lineage and an avian virus. Phylogenetic, seroarcheological, and epidemiological evidence indicates those born earlier or later than ∼1880–1900 would have had some protection against the 1918 H1N1 virus, whereas many young adults born from ∼1880–1900 may have lacked such protection because of childhood exposure to an antigenically distinct H3N8 virus. Our findings suggest that better understanding of how initial exposure shapes lifetime immunity may enhance the prediction and control of future IAV pandemics and seasonal epidemics.