Publications scientifiques

Publications de la BQC19


The Biobanque québécoise de la COVID-19 (BQC19)—A cohort to prospectively study the clinical and biological determinants of COVID-19 clinical trajectories

Karine Tremblay , Simon Rousseau , Ma’n H. Zawati , Daniel Auld, Michaël Chassé, Daniel Coderre, Emilia Liana Falcone, Nicolas Gauthier, Nathalie Grandvaux, François Gros-Louis, Carole Jabet, Yann Joly, Daniel E. Kaufmann, Catherine Laprise, Catherine Larochelle, François Maltais, Anne-Marie Mes-Masson, Alexandre Montpetit, Alain Piché, J. Brent Richards, Sze Man Tse, Alexis F. Turgeon, Gustavo Turecki, Donald C. Vinh, Han Ting Wang, Vincent Mooser, on behalf of BQC19


SARS-CoV-2 infection causing the novel coronavirus disease 2019 (COVID–19) has been responsible for more than 2.8 million deaths and nearly 125 million infections worldwide as of March 2021. In March 2020, the World Health Organization determined that the COVID–19 outbreak is a global pandemic. The urgency and magnitude of this pandemic demanded immediate action and coordination between local, regional, national, and international actors. In that mission, researchers require access to high-quality biological materials and data from SARS-CoV-2 infected and uninfected patients, covering the spectrum of disease manifestations. The “Biobanque québécoise de la COVID-19” (BQC19) is a pan–provincial initiative undertaken in Québec, Canada to enable the collection, storage and sharing of samples and data related to the COVID-19 crisis. As a disease-oriented biobank based on high-quality biosamples and clinical data of hospitalized and non-hospitalized SARS-CoV-2 PCR positive and negative individuals. The BQC19 follows a legal and ethical management framework approved by local health authorities. The biosamples include plasma, serum, peripheral blood mononuclear cells and DNA and RNA isolated from whole blood. In addition to the clinical variables, BQC19 will provide in-depth analytical data derived from the biosamples including whole genome and transcriptome sequencing, proteome and metabolome analyses, multiplex measurements of key circulating markers as well as anti-SARS-CoV-2 antibody responses. BQC19 will provide the scientific and medical communities access to data and samples to better understand, manage and ultimately limit, the impact of COVID-19. In this paper we present BQC19, describe the process according to which it is governed and organized, and address opportunities for future research collaborations. BQC19 aims to be a part of a global communal effort addressing the challenges of COVID–19.

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Publications des collaborateurs de la BQC19

Nature Medecine

A Neanderthal OAS1 isoform protects individuals of European ancestry against COVID-19 susceptibility and severity, Sirui Zhou et coll., Nature Medicine

Sirui Zhou, Guillaume Butler-Laporte, Tomoko Nakanishi, David R. Morrison, Jonathan Afilalo, Marc Afilalo, Laetitia Laurent, Maik Pietzner, Nicola Kerrison, Kaiqiong Zhao, Elsa Brunet-Ratnasingham, Danielle Henry, Nofar Kimchi, Zaman Afrasiabi, Nardin Rezk, Meriem Bouab, Louis Petitjean, Charlotte Guzman, Xiaoqing Xue, Chris Tselios, Branka Vulesevic, Olumide Adeleye, Tala Abdullah, Noor Almamlouk, Yiheng Chen, Michaël Chassé, Madeleine Durand, Clare Paterson, Johan Normark, Robert Frithiof, Miklós Lipcsey, Michael Hultström, Celia M. T. Greenwood, Hugo Zeberg, Claudia Langenberg, Elin Thysell, Michael Pollak, Vincent Mooser, Vincenzo Forgetta, Daniel E. Kaufmann & J. Brent Richards


To identify circulating proteins influencing Coronavirus Disease 2019 (COVID-19) susceptibility and severity, we undertook a two-sample Mendelian randomization (MR) study, rapidly scanning hundreds of circulating proteins while reducing bias due to reverse causation and confounding. In up to 14,134 cases and 1.2 million controls, we found that an s.d. increase in OAS1 levels was associated with reduced COVID-19 death or ventilation (odds ratio (OR) = 0.54, P = 7 × 10-8), hospitalization (OR = 0.61, P = 8 × 10-8) and susceptibility (OR = 0.78, P = 8 × 10-6). Measuring OAS1 levels in 504 individuals, we found that higher plasma OAS1 levels in a non-infectious state were associated with reduced COVID-19 susceptibility and severity. Further analyses suggested that a Neanderthal isoform of OAS1 in individuals of European ancestry affords this protection. Thus, evidence from MR and a case–control study support a protective role for OAS1 in COVID-19 adverse outcomes. Available pharmacological agents that increase OAS1 levels could be prioritized for drug development.

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The Journal of Clinical Investigation

Identification of SARS-CoV-2–specific immune alterations in acutely ill patients

Rose-Marie Rébillard, Marc Charabati, Camille Grasmuck, Abdelali Filali-Mouhim,2 Olivier Tastet, Nathalie Brassard, Audrey Daigneault, Lyne Bourbonnière, Sai Priya Anand, Renaud Balthazard, Guillaume Beaudoin-Bussières, Romain Gasser, Mehdi Benlarbi, Ana Carmena Moratalla, Yves Carpentier Solorio, Marianne Boutin, Negar Farzam-kia, Jade Descôteaux-Dinelle, Antoine Philippe Fournier, Elizabeth Gowing, Annemarie Laumaea, Hélène Jamann, Boaz Lahav, Guillaume Goyette, Florent Lemaître, Victoria Hannah Mamane, Jérémie Prévost, Jonathan Richard, Karine Thai, Jean-François Cailhier, Nicolas Chomont, Andrés Finzi, Michaël Chassé, Madeleine Durand, Nathalie Arbour, Daniel E. Kaufmann, Alexandre Prat, and Catherine Larochelle


Dysregulated immune profiles have been described in symptomatic patients infected with SARS-CoV-2. Whether the reported immune alterations are specific to SARS-CoV-2 infection or also triggered by other acute illnesses remains unclear. We performed flow cytometry analysis on fresh peripheral blood from a consecutive cohort of (a) patients hospitalized with acute SARS-CoV-2 infection, (b) patients of comparable age and sex hospitalized for another acute disease (SARS-CoV-2 negative), and (c) healthy controls. Using both data-driven and hypothesis-driven analyses, we found several dysregulations in immune cell subsets (e.g., decreased proportion of T cells) that were similarly associated with acute SARS-CoV-2 infection and non–COVID-19-related acute illnesses. In contrast, we identified specific differences in myeloid and lymphocyte subsets that were associated with SARS-CoV-2 status (e.g., elevated proportion of ICAM-1+ mature/activated neutrophils, ALCAM+ monocytes, and CD38+CD8+ T cells). A subset of SARS-CoV-2–specific immune alterations correlated with disease severity, disease outcome at 30 days, and mortality. Our data provide an understanding of the immune dysregulation specifically associated with SARS-CoV-2 infection among acute care hospitalized patients. Our study lays the foundation for the development of specific biomarkers to stratify SARS-CoV-2–positive patients at risk of unfavorable outcomes and to uncover candidate molecules to investigate from a therapeutic perspective.

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