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A High-Fat Diet Increases Influenza A Virus-Associated Cardiovascular Damage

Authors :
Günter Weiss
Mellissa E Reichelt
Rebecca M. Koch
Brian W.C. Tse
Conor J. Bloxham
Boris Novakovic
Debby van Riel
Timothy J. C. Bruxner
Francesco Robert Burkert
Rosa Bellmann-Weiler
Kamil A. Sokolowski
Erich Pawelka
Katina D. Hulme
Peter J. M. Openshaw
Rebecca J. Marshall
Romit J Samanta
Lonneke M. Leijten
Keng Yih Chew
Walter G. Thomas
Mario Karolyi
Angelika N. Christ
Jurre Y. Siegers
Kirsty R. Short
Helle Bielefeldt-Ohmann
Peter van Run
Greg Howe
Karen Knox
Virology
National Institute for Health Research
Wellcome Trust
Asthma UK
Medical Research Council (MRC)
GlaxoSmithKline Biologicals
Source :
The Journal of Infectious Diseases, 222, 5, pp. 820-831, The Journal of Infectious Diseases, 222, 820-831, The Journal of infectious diseases, 222(5), 820-831. Oxford University Press
Publication Year :
2020

Abstract

BackgroundInfluenza 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.MethodsHere, we sought to use transcriptional profiling, virology, histology, and echocardiograms to investigate the role of a high-fat diet in IAV-associated cardiac damage.ResultsTranscriptional 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.ConclusionsTogether, 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.

Details

ISSN :
00221899
Database :
OpenAIRE
Journal :
The Journal of Infectious Diseases, 222, 5, pp. 820-831, The Journal of Infectious Diseases, 222, 820-831, The Journal of infectious diseases, 222(5), 820-831. Oxford University Press
Accession number :
edsair.doi.dedup.....a0eb13d5feeea556f84a06e796b5783e