A global effort to dissect the human genetic basis of resistance to SARS-CoV-2 infection

COVID Human Genetic Effort

doi:10.1038/s41590-021-01030-z

A global effort to dissect the human genetic basis of resistance to SARS-CoV-2 infection

COVID Human Genetic Effort

University of Sharjah

Academy of Athens
Rockefeller University
Université Paris Cité
McGill University
MNM Diagnostics Inc.
University of Wisconsin-Madison
Trinity College Dublin
University of Rome Tor Vergata
Hospital de Gran Canaria Dr. Negrin
University Fernando Pessoa Canarias
Ghent University
Faculdades Pequeno Príncipe
Bellvitge Biomedical Research Institute
ICREA
Centro de Investigación Biomédica en Red de Enfermedades Raras
University of British Columbia
Helix OpCo LLC
Shupyk National Healthcare University of Ukraine
Karolinska Institutet
Emory University
Department of Paediatrics
Universidade de São Paulo
Université catholique de Louvain
Tel Aviv University
Swiss Federal Institute of Technology Lausanne
University of Lausanne
Hospital Universitario Nuestra Senora de Candelaria
Centro de Investigacion Biomedica en Red Enfermedades Respiratorias (CIBERES)
Institute of Technology and Renewable Energies
The University of Hong Kong
KU Leuven
Aarhus University
Hiroshima University
Tokyo Institute of Technology
Bilkent University
Universidad Autónoma de Madrid
Interdepartmental Group of Immunodeficiencies
August Pi i Sunyer Biomedical Research Institute
Institut Pasteur Paris
Collège de France
Agency for Science, Technology and Research, Singapore
Nanyang Technological University
University Hospital St. Marina
Charles University
Dmitry Rogachev National Research Center of Pediatric Hematology, Oncology and Immunology
Masaryk University
Innsbruck Medical University
NeuroGen
Amsterdam UMC
Adam Mickiewicz University in Poznań
National Institutes of Health
Howard Hughes Medical Institute
Utrecht University

Research output: Contribution to journal › Review article › peer-review

56 Scopus citations

Abstract

SARS-CoV-2 infections display tremendous interindividual variability, ranging from asymptomatic infections to life-threatening disease. Inborn errors of, and autoantibodies directed against, type I interferons (IFNs) account for about 20% of critical COVID-19 cases among SARS-CoV-2-infected individuals. By contrast, the genetic and immunological determinants of resistance to infection per se remain unknown. Following the discovery that autosomal recessive deficiency in the DARC chemokine receptor confers resistance to Plasmodium vivax, autosomal recessive deficiencies of chemokine receptor 5 (CCR5) and the enzyme FUT2 were shown to underlie resistance to HIV-1 and noroviruses, respectively. Along the same lines, we propose a strategy for identifying, recruiting, and genetically analyzing individuals who are naturally resistant to SARS-CoV-2 infection.

Original language	English
Pages (from-to)	159-164
Number of pages	6
Journal	Nature Immunology
Volume	23
Issue number	2
DOIs	https://doi.org/10.1038/s41590-021-01030-z
State	Published - Feb 2022

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SDG 3 Good Health and Well-being

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10.1038/s41590-021-01030-z

Cite this

@article{6c0b8d57c7304336840f012003a858a5,

title = "A global effort to dissect the human genetic basis of resistance to SARS-CoV-2 infection",

abstract = "SARS-CoV-2 infections display tremendous interindividual variability, ranging from asymptomatic infections to life-threatening disease. Inborn errors of, and autoantibodies directed against, type I interferons (IFNs) account for about 20\% of critical COVID-19 cases among SARS-CoV-2-infected individuals. By contrast, the genetic and immunological determinants of resistance to infection per se remain unknown. Following the discovery that autosomal recessive deficiency in the DARC chemokine receptor confers resistance to Plasmodium vivax, autosomal recessive deficiencies of chemokine receptor 5 (CCR5) and the enzyme FUT2 were shown to underlie resistance to HIV-1 and noroviruses, respectively. Along the same lines, we propose a strategy for identifying, recruiting, and genetically analyzing individuals who are naturally resistant to SARS-CoV-2 infection.",

author = "\{COVID Human Genetic Effort\} and Evangelos Andreakos and Laurent Abel and Vinh, \{Donald C.\} and El{\.z}bieta Kaja and Drolet, \{Beth A.\} and Qian Zhang and Cliona O{\textquoteright}Farrelly and Giuseppe Novelli and Carlos Rodr{\'i}guez-Gallego and Filomeen Haerynck and Carolina Prando and Aurora Pujol and Paul Bastard and Biggs, \{Catherine M.\} and Benedetta Bigio and Bertrand Boisson and Alexandre Bolze and Anastasiia Bondarenko and Petter Brodin and Samya Chakravorty and John Christodoulou and Aureli{\'e} Cobat and Antonio Condino-Neto and Constantinescu, \{Stefan N.\} and Feldman, \{Hagit Baris\} and Jacques Fellay and Carlos Flores and Rabih Halwani and Emmanuelle Jouanguy and Lau, \{Yu Lung\} and Isabelle Meyts and Mogensen, \{Trine H.\} and Satoshi Okada and Keisuke Okamoto and Tayfun Ozcelik and Qiang Pan-Hammarstr{\"o}m and Diego, \{Rebeca P{\'e}rez de\} and Planas, \{Anna M.\} and Anne Puel and Lluis Quintana-Murci and Laurent Renia and Igor Resnick and Anna Sediva and Anna Shcherbina and Ondrej Slaby and Ivan Tancevski and Turvey, \{Stuart E.\} and Uddin, \{K. M.Furkan\} and \{van de Beek\}, Diederik and Mayana Zatz",

note = "Publisher Copyright: {\textcopyright} 2021, Springer Nature America, Inc.",

year = "2022",

month = feb,

doi = "10.1038/s41590-021-01030-z",

language = "English",

volume = "23",

pages = "159--164",

journal = "Nature Immunology",

issn = "1529-2908",

publisher = "Nature Research",

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T1 - A global effort to dissect the human genetic basis of resistance to SARS-CoV-2 infection

AU - COVID Human Genetic Effort

AU - Andreakos, Evangelos

AU - Abel, Laurent

AU - Vinh, Donald C.

AU - Kaja, Elżbieta

AU - Drolet, Beth A.

AU - Zhang, Qian

AU - O’Farrelly, Cliona

AU - Novelli, Giuseppe

AU - Rodríguez-Gallego, Carlos

AU - Haerynck, Filomeen

AU - Prando, Carolina

AU - Pujol, Aurora

AU - Bastard, Paul

AU - Biggs, Catherine M.

AU - Bigio, Benedetta

AU - Boisson, Bertrand

AU - Bolze, Alexandre

AU - Bondarenko, Anastasiia

AU - Brodin, Petter

AU - Chakravorty, Samya

AU - Christodoulou, John

AU - Cobat, Aurelié

AU - Condino-Neto, Antonio

AU - Constantinescu, Stefan N.

AU - Feldman, Hagit Baris

AU - Fellay, Jacques

AU - Flores, Carlos

AU - Halwani, Rabih

AU - Jouanguy, Emmanuelle

AU - Lau, Yu Lung

AU - Meyts, Isabelle

AU - Mogensen, Trine H.

AU - Okada, Satoshi

AU - Okamoto, Keisuke

AU - Ozcelik, Tayfun

AU - Pan-Hammarström, Qiang

AU - Diego, Rebeca Pérez de

AU - Planas, Anna M.

AU - Puel, Anne

AU - Quintana-Murci, Lluis

AU - Renia, Laurent

AU - Resnick, Igor

AU - Sediva, Anna

AU - Shcherbina, Anna

AU - Slaby, Ondrej

AU - Tancevski, Ivan

AU - Turvey, Stuart E.

AU - Uddin, K. M.Furkan

AU - van de Beek, Diederik

AU - Zatz, Mayana

PY - 2022/2

Y1 - 2022/2

N2 - SARS-CoV-2 infections display tremendous interindividual variability, ranging from asymptomatic infections to life-threatening disease. Inborn errors of, and autoantibodies directed against, type I interferons (IFNs) account for about 20% of critical COVID-19 cases among SARS-CoV-2-infected individuals. By contrast, the genetic and immunological determinants of resistance to infection per se remain unknown. Following the discovery that autosomal recessive deficiency in the DARC chemokine receptor confers resistance to Plasmodium vivax, autosomal recessive deficiencies of chemokine receptor 5 (CCR5) and the enzyme FUT2 were shown to underlie resistance to HIV-1 and noroviruses, respectively. Along the same lines, we propose a strategy for identifying, recruiting, and genetically analyzing individuals who are naturally resistant to SARS-CoV-2 infection.

AB - SARS-CoV-2 infections display tremendous interindividual variability, ranging from asymptomatic infections to life-threatening disease. Inborn errors of, and autoantibodies directed against, type I interferons (IFNs) account for about 20% of critical COVID-19 cases among SARS-CoV-2-infected individuals. By contrast, the genetic and immunological determinants of resistance to infection per se remain unknown. Following the discovery that autosomal recessive deficiency in the DARC chemokine receptor confers resistance to Plasmodium vivax, autosomal recessive deficiencies of chemokine receptor 5 (CCR5) and the enzyme FUT2 were shown to underlie resistance to HIV-1 and noroviruses, respectively. Along the same lines, we propose a strategy for identifying, recruiting, and genetically analyzing individuals who are naturally resistant to SARS-CoV-2 infection.

UR - https://www.scopus.com/pages/publications/85117437869

U2 - 10.1038/s41590-021-01030-z

DO - 10.1038/s41590-021-01030-z

M3 - Review article

C2 - 34667308

AN - SCOPUS:85117437869

SN - 1529-2908

VL - 23

SP - 159

EP - 164

JO - Nature Immunology

JF - Nature Immunology

IS - 2

ER -

A global effort to dissect the human genetic basis of resistance to SARS-CoV-2 infection

Abstract

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