Lammi, Vilma and Nakanishi, Tomoko and Jones, Samuel E. and Andrews, Shea J. and Karjalainen, Juha and Cortes, Beatriz and O'Brien, Heath E. and Ochoa-Guzman, Ana and Fulton-Howard, Brian E. and Broberg, Martin and Haapaniemi, Hele H. and Kanai, Masahiro and Pirinen, Matti and Schmidt, Axel and Mitchell, Ruth E. and Mousas, Abdou and Mangino, Massimo and Huerta-Chagoya, Alicia and Sinnott-Armstrong, Nasa and Cirulli, Elizabeth T. and Vaudel, Marc and Kwong, Alex S. F. and Maiti, Amit K. and Marttila, Minttu M. and Posner, Daniel C. and Rodriguez, Alexis A. and Batini, Chiara and Minnai, Francesca and Dearman, Anna R. and Warmerdam, C. A. Robert and Sequeros, Celia B. and Winkler, Thomas W. and Jordan, Daniel M. and Rescenko, Raimonds and Miano, Lorenzo and Lane, Jacqueline M. and Chung, Ryan K. and Guillen-Guio, Beatriz and Leavy, Olivia C. and Carvajal-Silva, Laura and Aguilar-Valdes, Kevin and Frangione, Erika and Guare, Lindsay and Vergasova, Ekaterina and Marouli, Eirini and Striano, Pasquale and Zainulabid, Ummu Afeera and Kumar, Ashutosh and Ahmad, Hajar Fauzan and Edahiro, Ryuya and Azekawa, Shuhei and Luoh, Shiuh-Wen and Erikstrup, Christian and Pedersen, Ole B. V. and Lerner-Ellis, Jordan and Colombo, Alicia and Grzymski, Joseph J. and Ishii, Makoto and Okada, Yukinori and Beckmann, Noam D. and Kumari, Meena and Wagner, Ralf and Heid, Iris M. and John, Catherine and Short, Patrick J. and Magnus, Per and Ansone, Laura and Valenti, Luca V. C. and Lee, Sulggi A. and Wain, Louise V. and Verdugo, Ricardo A. and Banasik, Karina and Geller, Frank and Franke, Lude H. and Rakitko, Alexander and Duncan, Emma L. and Renieri, Alessandra and Tsilidis, Konstantinos K. and de Cida, Rafael and Niavarani, Ahmadreza and Abner, Erik and Tusie-Luna, Teresa and Verma, Shefali S. and Smith, George Davey and Timpson, Nicholas J. and Madduri, Ravi K. and Choa, Kelly and Daly, Mark J. and Ganna, Andrea and Schulte, Eva C. and Richards, J. Brent and Ludwig, Kerstin U. and Marks-Hultstroem, Michael and Zeberg, Hugo and Ollila, Hanna M. (2025) Genome-wide association study of long COVID. NATURE GENETICS, 57 (6). ISSN 1061-4036, 1546-1718
Full text not available from this repository. (Request a copy)Abstract
Infections can lead to persistent symptoms and diseases such as shingles after varicella zoster or rheumatic fever after streptococcal infections. Similarly, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can result in long coronavirus disease (COVID), typically manifesting as fatigue, pulmonary symptoms and cognitive dysfunction. The biological mechanisms behind long COVID remain unclear. We performed a genome-wide association study for long COVID including up to 6,450 long COVID cases and 1,093,995 population controls from 24 studies across 16 countries. We discovered an association of FOXP4 with long COVID, independent of its previously identified association with severe COVID-19. The signal was replicated in 9,500 long COVID cases and 798,835 population controls. Given the transcription factor FOXP4's role in lung physiology and pathology, our findings highlight the importance of lung function in the pathophysiology of long COVID.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | EXPRESSION; FOXP4; METAANALYSIS; PULMONARY; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Medizinische Mikrobiologie und Hygiene Medicine > Institut für Epidemiologie und Präventivmedizin > Lehrstuhl für Genetische Epidemiologie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 24 Mar 2026 07:53 |
| Last Modified: | 24 Mar 2026 07:53 |
| URI: | https://pred.uni-regensburg.de/id/eprint/68074 |
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