tetano
Editor, Senior Moderator
J Med Virol
. 2022 Jun 8.
doi: 10.1002/jmv.27920. Online ahead of print.
COVID-19 and Platelet Traits: A Bi-directional Mendelian Randomization Study
Ching-Lung Cheung[SUP] 1 2 [/SUP], Shun-Cheung Ho[SUP] 1 [/SUP], Suhas Krishnamoorthy[SUP] 1 [/SUP], Gloria Hoi-Yee Li[SUP] 3 [/SUP]
Affiliations
Abstract
Objective: This study aimed to evaluate the host genetic liability of covid-19 with platelet traits using the Mendelian Randomization (MR) approach.
Method: We conducted a bi-directional two-sample MR using summary statistics from the largest genome-wide association study (GWAS) of three covid-19 severity (SARS-CoV-2 infection, covid-19 hospitalization and severe covid, N~1,059,456 to 1,557,411) and four platelet traits (mean platelet volume [MPV], plateletcrit, platelet distribution width, and platelet count; N=408,112). Inverse variance weighted (IVW), median weighted, MR-Egger, and contamination mixture methods were used to estimate the causal association.
Result: Null and inconsistent association in the IVW and sensitivity analyses were observed for SARS-CoV-2 infection and covid-19 hospitalization with platelet traits. For severe covid-19, significant associations with MPV and platelet count were observed in the IVW and sensitivity analyses, with the beta[SUB]IVW[/SUB] of 0.01 (95% CI: 0.005 to 0.016, p-value=3.51x10[SUP]-4[/SUP] ) and -0.009 (95% CI: -0.015 to -0.002, p-value=0.008) per doubling in odds of severe covid-19, respectively. Conversely, null associations were observed for platelet traits with covid-19 traits.
Conclusion: Host genetic liability to severe covid-19 was causally associated with increased MPV and reduced platelet count, which may provide insight in evaluating hypercoagulability and thromboembolic events in covid-19 patients. This article is protected by copyright. All rights reserved.
Keywords: Blood; Epidemiology; Genetic variation; Genetics; SARS coronavirus; Virus classification.
. 2022 Jun 8.
doi: 10.1002/jmv.27920. Online ahead of print.
COVID-19 and Platelet Traits: A Bi-directional Mendelian Randomization Study
Ching-Lung Cheung[SUP] 1 2 [/SUP], Shun-Cheung Ho[SUP] 1 [/SUP], Suhas Krishnamoorthy[SUP] 1 [/SUP], Gloria Hoi-Yee Li[SUP] 3 [/SUP]
Affiliations
- PMID: 35676178
- DOI: 10.1002/jmv.27920
Abstract
Objective: This study aimed to evaluate the host genetic liability of covid-19 with platelet traits using the Mendelian Randomization (MR) approach.
Method: We conducted a bi-directional two-sample MR using summary statistics from the largest genome-wide association study (GWAS) of three covid-19 severity (SARS-CoV-2 infection, covid-19 hospitalization and severe covid, N~1,059,456 to 1,557,411) and four platelet traits (mean platelet volume [MPV], plateletcrit, platelet distribution width, and platelet count; N=408,112). Inverse variance weighted (IVW), median weighted, MR-Egger, and contamination mixture methods were used to estimate the causal association.
Result: Null and inconsistent association in the IVW and sensitivity analyses were observed for SARS-CoV-2 infection and covid-19 hospitalization with platelet traits. For severe covid-19, significant associations with MPV and platelet count were observed in the IVW and sensitivity analyses, with the beta[SUB]IVW[/SUB] of 0.01 (95% CI: 0.005 to 0.016, p-value=3.51x10[SUP]-4[/SUP] ) and -0.009 (95% CI: -0.015 to -0.002, p-value=0.008) per doubling in odds of severe covid-19, respectively. Conversely, null associations were observed for platelet traits with covid-19 traits.
Conclusion: Host genetic liability to severe covid-19 was causally associated with increased MPV and reduced platelet count, which may provide insight in evaluating hypercoagulability and thromboembolic events in covid-19 patients. This article is protected by copyright. All rights reserved.
Keywords: Blood; Epidemiology; Genetic variation; Genetics; SARS coronavirus; Virus classification.