Let’s chew the fat about influenza A virus and adipose tissue

Our paper, published on May 14 in Communications Biology, shows that influenza A virus infection durably impacts on the host’s systemic energy metabolism, and promotes depot-specific metabolic reprogramming of fat tissues, in mice. Blog posted by J. Barthelemy (PhD student) and I. Wolowczuk.
Published in Microbiology

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Adipose (fat) tissues are specialized connective tissues that contribute to many of an organism’s essential needs such as energy metabolism and immune defense, notably against infection by parasites (Trypanosoma spp., Plasmodium spp.), bacteria (Mycobacterium spp.), and viruses (lymphocytic choriomeningitis virus, human and simian immunodeficiency viruses, adenovirus, vaccinia virus).

We studied the metabolic consequences of influenza A virus (IAV) infection in mice, and the impact of infection on the major fat depots (subcutaneous and visceral). We show that infected cells can be detected in both fat depots, where they initiate an antiviral innate immune response. Metabolic rewiring, characterized by repression of glycolysis, OXPHOS and TCA cycle, activation of sirtuin signaling pathways, and induction of UCP1-expressing thermogenic brown-like/beige adipocytes, occurred only in the subcutaneous depot (Figure).


Legend to Figure: Graphical representation summarizing the main findings of the study. Influenza A virus (IAV)-infected mice present alterations in whole-body energy metabolism that persist long after the virus has been cleared (green box). Albeit at lower levels than in the lungs, viral RNA is detected in both the subcutaneous and the visceral fat depots. Viral-antigen-harboring immune cells are found in the fat tissues (mostly the subcutaneous depot), and this associates with the concomitant activation of type I IFN signaling pathways and inhibition of cholesterol biosynthesis pathways in both fat depots; suggesting activation of antiviral innate immune response (blue boxes). Energy metabolism rewiring only occurs in subcutaneous fat (grey box). How infected cells reach fat tissues still remains to be discovered. IFN: Interferon, UCP1: uncoupling protein 1, OXPHOS: oxidative phosphorylation, TCA cycle: tricarboxylic acid cycle.

We also show that mouse and human adipocytes and adipocyte progenitors (preadipocytes) sustain in vitro IAV infection, yet replication is abortive in these cells (no production of infectious progeny virions). Importantly, in vitro IAV infection of preadipocytes initiates the browning-like/beige adipogenic program, and this was associated with activation of the serine-one-carbon-glycine (SOG) metabolic pathway (off-shoot of glycolysis).

At this stage, there remain more questions than answers and we are currently addressing them. How do infected cells reach fat tissues? Are adipocytes and preadipocytes of fat tissues infected (in vivo)? What is the phenotype of the infected immune cells that were found in fat tissues, and do they participate to the host’s defense against infection? What is the mechanism of IAV-infection-induced browning-like/beiging process?

We believe that the context of this study is important regarding the repeatedly reported associations between viral infections (including IAV) and obesity (a state of excessive (dysfunctional) fat mass).

Influenza infection rewires energy metabolism and induces browning features in adipose cells and tissues “, by AYARI, A. & colleagues. Communications Biology. DOI: 10.1038/s42003-020-0965-6. https://rdcu.be/b4aip

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