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<p>SARS-CoV-2 infection can result in long COVID, characterized by post-acute symptoms from multiple organs. Current hypotheses on mechanisms underlying long COVID include persistent inflammation and thromboembolism; however, compelling evidence from humans is limited and causal associations remain unclear. In this study, we tested the association of thromboembolism-related genetic variants with long COVID in the Long COVID Host Genetics Initiative (<i>n</i><sub>cases</sub> = 3,018; <i>n</i><sub>controls</sub> = 994,582). Primary analyses revealed that each unit increase in the log odds of genetically predicted venous thromboembolism risk was associated with 1.21-fold odds of long COVID (95% confidence interval (CI): 1.08−1.35; <i>P</i> = 1.2 × 10<sup>−3</sup>). This association was independent of acute COVID-19 severity, was robust across various sensitivity analyses and was replicated in external datasets. Downstream analyses using gene-specific instruments, along with protein and gene expression data, suggested the protease-activated receptor 1 (PAR-1) as a potential molecular contributor to long COVID. These findings provide human genetic evidence implicating shared pathogenetic pathways in thromboembolism and long COVID.</p>

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Human genetics implicate thromboembolism in the pathogenesis of long COVID in individuals of European ancestry

  • 期刊论文

  • 发表日期：

    2025年12月16日

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  • Art Schuermans,
  • Andreas Verstraete,
  • Vilma Lammi,
  • Tomoko Nakanishi,
  • Maddalena Ardissino,
  • Jef Van den Eynde,
  • Benjamin B. Sun,
  • Marios K. Georgakis,
  • Beatriz Guillen-Guio,
  • Louise V. Wain,
  • Christopher E. Brightling,
  • Johan Van Weyenbergh,
  • Adam J. Lewandowski,
  • Betty Raman,
  • Hugo Zeberg,
  • Hanna M. Ollila,
  • Stephen Burgess,
  • Pradeep Natarajan,
  • Michael C. Honigberg,
  • Kathleen Freson,
  • Thomas Vanassche,
  • Peter Verhamme

摘要

SARS-CoV-2 infection can result in long COVID, characterized by post-acute symptoms from multiple organs. Current hypotheses on mechanisms underlying long COVID include persistent inflammation and thromboembolism; however, compelling evidence from humans is limited and causal associations remain unclear. In this study, we tested the association of thromboembolism-related genetic variants with long COVID in the Long COVID Host Genetics Initiative (ncases = 3,018; ncontrols = 994,582). Primary analyses revealed that each unit increase in the log odds of genetically predicted venous thromboembolism risk was associated with 1.21-fold odds of long COVID (95% confidence interval (CI): 1.08−1.35; P = 1.2 × 10−3). This association was independent of acute COVID-19 severity, was robust across various sensitivity analyses and was replicated in external datasets. Downstream analyses using gene-specific instruments, along with protein and gene expression data, suggested the protease-activated receptor 1 (PAR-1) as a potential molecular contributor to long COVID. These findings provide human genetic evidence implicating shared pathogenetic pathways in thromboembolism and long COVID.