@article{Schuermans_A-2024_220016,
title = {Human genetics implicate thromboembolism in the pathogenesis of long COVID in individuals of European ancestry},
author = {Schuermans, A. and Verstraete, A. and Lammi, V. and Nakanishi, T. and Ardissino, M. and Van den Eynde, J. and Sun, B. and Georgakis, M. and Guillen-Guio, B. and Wain, L. and Brightling, C. and van Weyenbergh, J. and Lewandowski, A. and Raman, B. and Zeberg, H. and Ollila, H. and Burgess, S. and Natarajan, P. and Honigberg, M. and Freson, K. and Vanassche, T. and Verhamme, P. and The PHOSP-COVID Collaborative Group},
month = {dec},
year = {2024},
abstract = {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. Here, we tested the association of thromboembolism-related genetic variants with long COVID in the Long COVID Host Genetics Initiative ( n cases =3,018; n controls =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%CI: 1.08-1.35; P =1.2×10 -3 ). This association was independent of acute COVID-19 severity, robust across genetic instruments and methods, and replicated in external datasets for both venous thromboembolism and long COVID. 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 thromboembolism in long COVID pathogenesis.},
journal = {MedRXiv},
publisher = {MedRxiv},
url = {https://doi.org/10.1101/2024.05.17.24307553},
}
