A High-Fat Diet Increases Influenza A Virus-Associated Cardiovascular Damage.
Animals
Body Mass Index
Body Weight
Cytokines
/ blood
Diet, High-Fat
Echocardiography
Female
Gene Expression Profiling
Heart
/ virology
Heart Diseases
/ pathology
Heart Ventricles
/ diagnostic imaging
Humans
Hypoxia-Inducible Factor 1, alpha Subunit
/ metabolism
Inflammation
/ genetics
Influenza A Virus, H1N1 Subtype
Influenza, Human
/ complications
Interferon Regulatory Factor-7
/ genetics
Interleukin-1beta
/ genetics
Lung
/ metabolism
Male
Mice
Mice, Inbred C57BL
Myocardium
/ metabolism
Orthomyxoviridae Infections
/ blood
RNA, Viral
/ metabolism
Risk Factors
Signal Transduction
/ genetics
Ubiquitins
/ genetics
body mass index
cardiac disease
extrarespiratory complications
high-fat diet
influenza
obesity
overweight
Journal
The Journal of infectious diseases
ISSN: 1537-6613
Titre abrégé: J Infect Dis
Pays: United States
ID NLM: 0413675
Informations de publication
Date de publication:
04 08 2020
04 08 2020
Historique:
received:
07
02
2020
accepted:
02
04
2020
pubmed:
5
4
2020
medline:
3
3
2021
entrez:
5
4
2020
Statut:
ppublish
Résumé
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. 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. 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. 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.
Sections du résumé
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.
Identifiants
pubmed: 32246148
pii: 5815741
doi: 10.1093/infdis/jiaa159
doi:
Substances chimiques
Cytokines
0
G1p2 protein, mouse
0
Hif1a protein, mouse
0
Hypoxia-Inducible Factor 1, alpha Subunit
0
IL1B protein, mouse
0
Interferon Regulatory Factor-7
0
Interleukin-1beta
0
Irf7 protein, mouse
0
RNA, Viral
0
Ubiquitins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
820-831Subventions
Organisme : Medical Research Council
ID : MC_G1001212
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/R005982/1
Pays : United Kingdom
Informations de copyright
© The Author(s) 2020. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.