Influenza A virus (IAV), the causative agent of influenza, is a negative strand virus causing acute respiratory infections in humans. Secondary bacterial infections are the leading cause of morbidity and mortality in influenza. It is indicated that commensal microbiota provide a shield against invading bacterial pathogens. However, there is little information on the impact of acute viral infection, i.e. IAV infections, on composition, kinetics and quantity of commensal microbiota in a given host site. In this thesis, we report qualitative and quantitative alterations of local and systemic microbiota following IAV infection in mice. We further evaluated these alterations in context of IAV induced predisposition of lung and small intestine to bacterial super-infections. Our findings suggests that qualitative and quantitative changes in microbiota in the course of an IAV infection could increase the risk of bacterial super-infection, by reducing the threshold this natural shield of commensals poses to invading bacterial pathogens.