Resumen:
he virus-bacterial synergism implicated in secondary bacterial infections caused by Streptococcuspneumoniae following infection with epidemic or pandemic influenza A virus (IAV)is well documented. However, the molecular mechanisms behind such synergism remainlargely ill-defined. In pneumocytes infected with influenza A virus, subsequent infection withS. pneumoniae leads to enhanced pneumococcal intracellular survival. The pneumococcaltwo-component system SirRH appears essential for such enhanced survival. Through comparativetranscriptomic analysis between the ΔsirR and wt strains, a list of 179 differentiallyexpressed genes was defined. Among those, the clpL protein chaperone gene and the psaBMn+2 transporter gene, which are involved in the stress response, are important in enhancingS. pneumoniae survival in influenza-infected cells. The ΔsirR, ΔclpL and ΔpsaB deletionmutants display increased susceptibility to acidic and oxidative stress and no enhancementof intra