Jurre Y Siegers1, Boris Novakovic2, Katina D Hulme3, Rebecca J Marshall3, Conor J Bloxham4, Walter G Thomas4, Mellissa E Reichelt4, Lonneke Leijten1, Peter van Run1, Karen Knox5, Kamil A Sokolowski5, Brian W C Tse5, Keng Yih Chew3, Angelika N Christ6, Greg Howe6, Timothy J C Bruxner6, Mario Karolyi7, Erich Pawelka7, Rebecca M Koch8, Rosa Bellmann-Weiler9, Francesco Burkert9, Günter Weiss9, Romit J Samanta10, Peter J M Openshaw11, Helle Bielefeldt-Ohmann3,12, Debby van Riel1, Kirsty R Short3,12. 1. Department of Viroscience, Erasmus Medical Center, Rotterdam, the Netherlands. 2. Epigenetics Research, Murdoch Children's Research Institute and Department of Paediatrics, University of Melbourne, Parkville, Australia. 3. School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, Australia. 4. School of Biomedical Science, The University of Queensland, Brisbane, Australia. 5. Preclinical Imaging Facility, Translational Research Institute Australia, Brisbane, Australia. 6. Institute for Molecular Bioscience, The University of Queensland, Brisbane, Australia. 7. Department for Infectious Diseases, Kaiser Franz Josef Hospital, Vienna, Austria. 8. Radboud University Medical Center, Department of Intensive Care Medicine, Nijmegen, the Netherlands. 9. Department of Internal Medicine II, Medical University of Innsbruck, Innsbruck, Austria. 10. Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge, United Kingdom. 11. Respiratory Infection Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom. 12. Australian Infectious Diseases Research Centre, The University of Queensland, Brisbane, Australia.
Abstract
BACKGROUND: Influenza A virus (IAV) causes a wide range of extrarespiratory complications. However, the role of host factors in these complications of influenza virus infection remains to be defined. METHODS: Here, we sought to use transcriptional profiling, virology, histology, and echocardiograms to investigate the role of a high-fat diet in IAV-associated cardiac damage. RESULTS: Transcriptional profiling showed that, compared to their low-fat counterparts (LF mice), mice fed a high-fat diet (HF mice) had impairments in inflammatory signaling in the lung and heart after IAV infection. This was associated with increased viral titers in the heart, increased left ventricular mass, and thickening of the left ventricular wall in IAV-infected HF mice compared to both IAV-infected LF mice and uninfected HF mice. Retrospective analysis of clinical data revealed that cardiac complications were more common in patients with excess weight, an association which was significant in 2 out of 4 studies. CONCLUSIONS: Together, these data provide the first evidence that a high-fat diet may be a risk factor for the development of IAV-associated cardiovascular damage and emphasizes the need for further clinical research in this area.
BACKGROUND:Influenza A virus (IAV) causes a wide range of extrarespiratory complications. However, the role of host factors in these complications of influenza virus infection remains to be defined. METHODS: Here, we sought to use transcriptional profiling, virology, histology, and echocardiograms to investigate the role of a high-fat diet in IAV-associated cardiac damage. RESULTS: Transcriptional profiling showed that, compared to their low-fat counterparts (LF mice), mice fed a high-fat diet (HF mice) had impairments in inflammatory signaling in the lung and heart after IAV infection. This was associated with increased viral titers in the heart, increased left ventricular mass, and thickening of the left ventricular wall in IAV-infected HF mice compared to both IAV-infected LF mice and uninfected HF mice. Retrospective analysis of clinical data revealed that cardiac complications were more common in patients with excess weight, an association which was significant in 2 out of 4 studies. CONCLUSIONS: Together, these data provide the first evidence that a high-fat diet may be a risk factor for the development of IAV-associated cardiovascular damage and emphasizes the need for further clinical research in this area.
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