A common variant close to the “tripwire” linker region of NLRP1 contributes to severe COVID-19

Objective and design The heterogeneity of response to SARS-CoV-2 infection is directly linked to the individual genetic background. Genetic variants of inflammasome-related genes have been pointed as risk factors for several inflammatory sterile and infectious disease. In the group of inflammasome r...

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Published in:Inflammation research Vol. 72; no. 10-11; pp. 1933 - 1940
Main Authors: Leal, Vinicius N. C., Paulino, Leandro M., Cambui, Raylane A. G., Zupelli, Thiago G., Yamada, Suemy M., Oliveira, Leonardo A. T., Dutra, Valéria de F., Bub, Carolina B., Sakashita, Araci M., Yokoyama, Ana Paula H., Kutner, José M., Vieira, Camila A., Santiago, Wellyngton M. de S., Andrade, Milena M. S., Teixeira, Franciane M. E., Alberca, Ricardo W., Gozzi-Silva, Sarah C., Yendo, Tatiana M., Netto, Lucas C., Duarte, Alberto J. S., Sato, Maria N., Venturini, James, Pontillo, Alessandra
Format: Journal Article
Language:English
Published: Cham Springer International Publishing 01-11-2023
Springer Nature B.V
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Summary:Objective and design The heterogeneity of response to SARS-CoV-2 infection is directly linked to the individual genetic background. Genetic variants of inflammasome-related genes have been pointed as risk factors for several inflammatory sterile and infectious disease. In the group of inflammasome receptors, NLRP1 stands out as a good novel candidate as severity factor for COVID-19 disease. Methods To address this question, we performed an association study of NLRP1 , DPP9 , CARD8 , IL1B , and IL18 single nucleotide variants (SNVs) in a cohort of 945 COVID-19 patients. Results The NLRP1 p.Leu155His in the linker region, target of viral protease, was significantly associated to COVID-19 severity, which could contribute to the excessive cytokine release reported in severe cases. Conclusion Inflammasome genetic background contributes to individual response to SARS-CoV-2.
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Responsible Editor: John Di Battista.
ISSN:1023-3830
1420-908X
DOI:10.1007/s00011-022-01670-3