Abstract
Like all obligate intracellular pathogens, influenza A virus (IAV) reprograms host cell’s glucose and lipid metabolism to promote its own replication. However, the impact of influenza infection on white adipose tissue (WAT), a key tissue in the control of systemic energy homeostasis, has not been yet characterized. Here, we show that influenza infection induces alterations in whole-body glucose metabolism that persist long after the virus has been cleared. We report depot-specific changes in the WAT of IAV-infected mice, notably characterized by the appearance of thermogenic brown-like adipocytes within the subcutaneous fat depot. Importantly, viral RNA- and viral antigen-harboring cells are detected in the WAT of infected mice. Using in vitro approaches, we find that IAV infection enhances the expression of brown-adipogenesis-related genes in preadipocytes. Overall, our findings shed light on the role that the white adipose tissue, which lies at the crossroads of nutrition, metabolism and immunity, may play in influenza infection.
Highlights
Like all obligate intracellular pathogens, influenza A virus (IAV) reprograms host cell’s glucose and lipid metabolism to promote its own replication
It is noteworthy that the mass of subcutaneous adipose tissue (SCAT) was positively correlated with the mass of EWAT in both mock-treated and IAV-infected animals (Supplementary Fig. 1); this indicates that influenza infection did not lead to major changes in body fat distribution
Infection was associated with decreased expression of lipogenic genes, such as those encoding glucose transporter 4 (Glut4), malic enzyme 2 (Me2), and fatty acid synthase (Fasn) (Fig. 1c)
Summary
Like all obligate intracellular pathogens, influenza A virus (IAV) reprograms host cell’s glucose and lipid metabolism to promote its own replication. The impact of influenza infection on white adipose tissue (WAT), a key tissue in the control of systemic energy homeostasis, has not been yet characterized. We show that influenza infection induces alterations in whole-body glucose metabolism that persist long after the virus has been cleared. We report depot-specific changes in the WAT of IAV-infected mice, notably characterized by the appearance of thermogenic brown-like adipocytes within the subcutaneous fat depot. Influenza A viruses (IAVs) are important human respiratory pathogens that lead to substantial morbidity and severe disability during annual epidemics[1]. A few case reports have suggested that influenza infection per se may trigger, unmask or aggravate metabolic disorders[4]
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