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Mendelian randomisation analysis reveals the possible causal relationship between infections, microbiota and clinical disease
  1. Shifang Li,
  2. Meijiao Gong
  1. Laboratory of Immunology and Vaccinology, FARAH, University of Liege, Liege, Belgium
  1. Correspondence to Dr Shifang Li, University of Liege, Liege 4000, Belgium; fruceslee{at}

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We read with interest the recent report by Nashed et al that described changes in the microbiota caused by viral infections, which in turn affected the severity of the clinical disease.1–4 Interactions between viral infections and microbiota complicate their relationship with host immunity and clinical diseases. However, it is unclear whether those associations are causal. Furthermore, the interactions between the microbiota and infections, as well as the outcomes of those interactions, have only been studied to a limited extent.5–8 We conducted an in-depth statistical analysis based on two-sample bidirectional Mendelian randomisation (MR) to broaden our understanding and provide a comprehensive assessment of the causal relationship between 9 common infections, 140 microbes and 38 clinical diseases.

As instrumental variables for MR analysis, independent genetic variants with genome-wide suggestive significance (p<5e-06) in each exposed dataset from public genome-wide association studies were chosen (online supplemental table 1). The MR causality test was primarily performed with the inverse variance weighted method (figure 1A). Pleiotropy was assessed using the MR Egger regression, and heterogeneity was examined using Cochran’s Q-test. Subsequently, a rigorous filtering procedure was performed, specifically removing MR results based on fewer than three single-nucleotide polymorphisms (SNPs) and MR results that …

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  • Contributors SF and MJ were the doctoral fellow of the Chinese Scholarship Council (number: 201803250062 and 201908620093).

  • Funding SF and MJ were the fellow of the Chinese Scholarship Council.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.