Host succinate inhibits influenza virus infection through succinylation and nuclear retention of the viral nucleoprotein

ABSTRACT: Influenza virus infection causes considerable morbidity and mortality, but current therapies have limited efficacy. We hypothesized that investigating the metabolic signaling during infection may help to design innovative antiviral approaches. Using bronchoalveolar lavages of infected mice, we here demonstrate that influenza virus induces a major reprogramming of lung metabolism. We focused on mitochondria-derived succinate that accumulated both in the respiratory fluids of virus-challenged mice and of patients with influenza pneumonia. Notably, succinate displays a potent antiviral activity in vitro as it inhibits the multiplication of influenza A/H1N1 and A/H3N2 strains and strongly decreases virus-triggered metabolic perturbations and inflammatory responses. Moreover, mice receiving suc

SUBMITTER: Dr. Antoine Guillon 

PROVIDER: S-SCDT-EMBOJ-2021-108306P | biostudies-other |

REPOSITORIES: biostudies-other