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Molecular Underpinnings of Severe Coronavirus Disease 2019

Educational Objective
To understand the molecular underpinnings of severe COVID-19
1 Credit CME

The molecular underpinnings of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and the disease it causes, coronavirus disease 2019 (COVID-19), are poorly understood. Inherited genetic variation is an important tool to disentangle cause and consequence, which in turn can generate insights to guide therapeutic interventions to prevent or treat disease. To date, little is known about genetic susceptibility to SARS-CoV-2 infection and severe forms of COVID-19.1,2

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Article Information

Corresponding Author: Robert M. Plenge, MD, PhD, Research & Early Development, Bristol Myers Squibb, 200 Cambridgepark Dr, Cambridge, MA 02140 (robert.plenge@gmail.com).

Published Online: July 24, 2020. doi:10.1001/jama.2020.14015

Conflict of Interest Disclosures: Dr Plenge is an employee of Bristol Myers Squibb (BMS). None of the therapies mentioned in this article is a BMS product.

References
1.
Ellinghaus  D , Degenhardt  F , Bujanda  L ,  et al; Severe Covid-19 GWAS Group.  Genomewide association study of severe Covid-19 with respiratory failure.   N Engl J Med. Published online June 17, 2020. doi:10.1056/NEJMoa2020283PubMedGoogle Scholar
2.
The COVID-19 Host Genetics Initiative. Accessed July 22, 2020. www.covid19hg.org/
3.
van der Made  CI , Simons  A , Schuurs-Hoeijmakers  J ,  et al.  Presence of genetic variants among young men with severe COVID-19.   JAMA. Published online July 24, 2020. doi:10.1001.jama.2020.13719Google Scholar
4.
Vabret  N , Britton  GJ , Gruber  C ,  et al; Sinai Immunology Review Project.  Immunology of COVID-19: current state of the science.   Immunity. 2020;52(6):910-941. doi:10.1016/j.immuni.2020.05.002 PubMedGoogle ScholarCrossref
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Park  A , Iwasaki  A .  Type I and type III interferons: induction, signaling, evasion, and application to combat COVID-19.   Cell Host Microbe. 2020;27(6):870-878. doi:10.1016/j.chom.2020.05.008PubMedGoogle ScholarCrossref
6.
Hung  IF-N , Lung  K-C , Tso  EY-K ,  et al.  Triple combination of interferon beta-1b, lopinavir-ritonavir, and ribavirin in the treatment of patients admitted to hospital with COVID-19: an open-label, randomised, phase 2 trial.   Lancet. 2020;395(10238):1695-1704. doi:10.1016/S0140-6736(20)31042-4PubMedGoogle ScholarCrossref
7.
The RECOVERY Collaborative Group.  Dexamethasone in hospitalized patients with Covid-19: preliminary report.   N Engl J Med. Published online July 17, 2020. doi:10.1056/NEJMoa2021436Google Scholar
8.
Broad Institute. Genome Aggregation Database. Accessed July 22, 2020. https://gnomad.broadinstitute.org/
9.
Beigel  JH , Tomashek  KM , Dodd  LE ,  et al; ACTT-1 Study Group Members.  Remdesivir for the treatment of Covid-19: preliminary report.   N Engl J Med. Published online May 22, 2020. doi:10.1056/NEJMoa2007764PubMedGoogle Scholar
10.
Grein  J , Ohmagari  N , Shin  D ,  et al.  Compassionate use of remdesivir for patients with severe Covid-19.   N Engl J Med. 2020;382(24):2327-2336. doi:10.1056/NEJMoa2007016PubMedGoogle ScholarCrossref
11.
Sempowski  GD , Saunders  KO , Acharya  P , Wiehe  KJ , Haynes  BF .  Pandemic preparedness: developing vaccines and therapeutic.   Cell. 2020;181(7):1458-1463. doi:10.1016/j.cell.2020.05.041PubMedGoogle ScholarCrossref
12.
Sanders  JM , Monogue  ML , Jodlowski  TZ , Cutrell  JB .  Pharmacologic treatments for coronavirus disease 2019 (COVID-19): a review.   JAMA. 2020;323(18):1824-1836. doi:10.1001/jama.2020.6019PubMedGoogle Scholar
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