Department of Economics and Business Economics

Proteome-wide Mendelian randomization identifies causal links between blood proteins and severe COVID-19

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Proteome-wide Mendelian randomization identifies causal links between blood proteins and severe COVID-19. / Palmos, Alish B; Millischer, Vincent; Menon, David K et al.

In: PLOS Genetics, Vol. 18, No. 3, e1010042, 03.2022.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Harvard

Palmos, AB, Millischer, V, Menon, DK, Nicholson, TR, Taams, LS, Michael, B, Sunderland, G, Griffiths, MJ, Hübel, C, Breen, G & COVID Clinical Neuroscience Study Consortium 2022, 'Proteome-wide Mendelian randomization identifies causal links between blood proteins and severe COVID-19', PLOS Genetics, vol. 18, no. 3, e1010042. https://doi.org/10.1371/journal.pgen.1010042

APA

Palmos, A. B., Millischer, V., Menon, D. K., Nicholson, T. R., Taams, L. S., Michael, B., Sunderland, G., Griffiths, M. J., Hübel, C., Breen, G., & COVID Clinical Neuroscience Study Consortium (2022). Proteome-wide Mendelian randomization identifies causal links between blood proteins and severe COVID-19. PLOS Genetics, 18(3), [e1010042]. https://doi.org/10.1371/journal.pgen.1010042

CBE

Palmos AB, Millischer V, Menon DK, Nicholson TR, Taams LS, Michael B, Sunderland G, Griffiths MJ, Hübel C, Breen G, et al. 2022. Proteome-wide Mendelian randomization identifies causal links between blood proteins and severe COVID-19. PLOS Genetics. 18(3):Article e1010042. https://doi.org/10.1371/journal.pgen.1010042

MLA

Vancouver

Palmos AB, Millischer V, Menon DK, Nicholson TR, Taams LS, Michael B et al. Proteome-wide Mendelian randomization identifies causal links between blood proteins and severe COVID-19. PLOS Genetics. 2022 Mar;18(3):e1010042. doi: 10.1371/journal.pgen.1010042

Author

Palmos, Alish B ; Millischer, Vincent ; Menon, David K et al. / Proteome-wide Mendelian randomization identifies causal links between blood proteins and severe COVID-19. In: PLOS Genetics. 2022 ; Vol. 18, No. 3.

Bibtex

@article{803780afc6d24a4fb00a44f7fe1c1acc,
title = "Proteome-wide Mendelian randomization identifies causal links between blood proteins and severe COVID-19",
abstract = "In November 2021, the COVID-19 pandemic death toll surpassed five million individuals. We applied Mendelian randomization including >3,000 blood proteins as exposures to identify potential biomarkers that may indicate risk for hospitalization or need for respiratory support or death due to COVID-19, respectively. After multiple testing correction, using genetic instruments and under the assumptions of Mendelian Randomization, our results were consistent with higher blood levels of five proteins GCNT4, CD207, RAB14, C1GALT1C1, and ABO being causally associated with an increased risk of hospitalization or respiratory support/death due to COVID-19 (ORs = 1.12-1.35). Higher levels of FAAH2 were solely associated with an increased risk of hospitalization (OR = 1.19). On the contrary, higher levels of SELL, SELE, and PECAM-1 decrease risk of hospitalization or need for respiratory support/death (ORs = 0.80-0.91). Higher levels of LCTL, SFTPD, KEL, and ATP2A3 were solely associated with a decreased risk of hospitalization (ORs = 0.86-0.93), whilst higher levels of ICAM-1 were solely associated with a decreased risk of respiratory support/death of COVID-19 (OR = 0.84). Our findings implicate blood group markers and binding proteins in both hospitalization and need for respiratory support/death. They, additionally, suggest that higher levels of endocannabinoid enzymes may increase the risk of hospitalization. Our research replicates findings of blood markers previously associated with COVID-19 and prioritises additional blood markers for risk prediction of severe forms of COVID-19. Furthermore, we pinpoint druggable targets potentially implicated in disease pathology.",
author = "Palmos, {Alish B} and Vincent Millischer and Menon, {David K} and Nicholson, {Timothy R} and Taams, {Leonie S} and Benedict Michael and Geraint Sunderland and Griffiths, {Michael J} and Christopher H{\"u}bel and Gerome Breen and {COVID Clinical Neuroscience Study Consortium}",
year = "2022",
month = mar,
doi = "10.1371/journal.pgen.1010042",
language = "English",
volume = "18",
journal = "P L o S Genetics",
issn = "1553-7390",
publisher = "public library of science",
number = "3",

}

RIS

TY - JOUR

T1 - Proteome-wide Mendelian randomization identifies causal links between blood proteins and severe COVID-19

AU - Palmos, Alish B

AU - Millischer, Vincent

AU - Menon, David K

AU - Nicholson, Timothy R

AU - Taams, Leonie S

AU - Michael, Benedict

AU - Sunderland, Geraint

AU - Griffiths, Michael J

AU - Hübel, Christopher

AU - Breen, Gerome

AU - COVID Clinical Neuroscience Study Consortium

PY - 2022/3

Y1 - 2022/3

N2 - In November 2021, the COVID-19 pandemic death toll surpassed five million individuals. We applied Mendelian randomization including >3,000 blood proteins as exposures to identify potential biomarkers that may indicate risk for hospitalization or need for respiratory support or death due to COVID-19, respectively. After multiple testing correction, using genetic instruments and under the assumptions of Mendelian Randomization, our results were consistent with higher blood levels of five proteins GCNT4, CD207, RAB14, C1GALT1C1, and ABO being causally associated with an increased risk of hospitalization or respiratory support/death due to COVID-19 (ORs = 1.12-1.35). Higher levels of FAAH2 were solely associated with an increased risk of hospitalization (OR = 1.19). On the contrary, higher levels of SELL, SELE, and PECAM-1 decrease risk of hospitalization or need for respiratory support/death (ORs = 0.80-0.91). Higher levels of LCTL, SFTPD, KEL, and ATP2A3 were solely associated with a decreased risk of hospitalization (ORs = 0.86-0.93), whilst higher levels of ICAM-1 were solely associated with a decreased risk of respiratory support/death of COVID-19 (OR = 0.84). Our findings implicate blood group markers and binding proteins in both hospitalization and need for respiratory support/death. They, additionally, suggest that higher levels of endocannabinoid enzymes may increase the risk of hospitalization. Our research replicates findings of blood markers previously associated with COVID-19 and prioritises additional blood markers for risk prediction of severe forms of COVID-19. Furthermore, we pinpoint druggable targets potentially implicated in disease pathology.

AB - In November 2021, the COVID-19 pandemic death toll surpassed five million individuals. We applied Mendelian randomization including >3,000 blood proteins as exposures to identify potential biomarkers that may indicate risk for hospitalization or need for respiratory support or death due to COVID-19, respectively. After multiple testing correction, using genetic instruments and under the assumptions of Mendelian Randomization, our results were consistent with higher blood levels of five proteins GCNT4, CD207, RAB14, C1GALT1C1, and ABO being causally associated with an increased risk of hospitalization or respiratory support/death due to COVID-19 (ORs = 1.12-1.35). Higher levels of FAAH2 were solely associated with an increased risk of hospitalization (OR = 1.19). On the contrary, higher levels of SELL, SELE, and PECAM-1 decrease risk of hospitalization or need for respiratory support/death (ORs = 0.80-0.91). Higher levels of LCTL, SFTPD, KEL, and ATP2A3 were solely associated with a decreased risk of hospitalization (ORs = 0.86-0.93), whilst higher levels of ICAM-1 were solely associated with a decreased risk of respiratory support/death of COVID-19 (OR = 0.84). Our findings implicate blood group markers and binding proteins in both hospitalization and need for respiratory support/death. They, additionally, suggest that higher levels of endocannabinoid enzymes may increase the risk of hospitalization. Our research replicates findings of blood markers previously associated with COVID-19 and prioritises additional blood markers for risk prediction of severe forms of COVID-19. Furthermore, we pinpoint druggable targets potentially implicated in disease pathology.

U2 - 10.1371/journal.pgen.1010042

DO - 10.1371/journal.pgen.1010042

M3 - Journal article

C2 - 35239653

VL - 18

JO - P L o S Genetics

JF - P L o S Genetics

SN - 1553-7390

IS - 3

M1 - e1010042

ER -