Abstract
Influenza virus is a well-known respiratory pathogen, which still leads to many severe pulmonary infections in the human population every year. Morbidity and mortality rates are further increased if virus infection coincides with co-infections or superinfections caused by bacteria such as Streptococcus pneumoniae (S. pneumoniae) and Staphylococcus aureus (S. aureus). This enhanced pathogenicity is due to complex interactions between the different pathogens and the host and its immune system and is mainly governed by altered intracellular signaling processes. In this review, we summarize the recent findings regarding the innate and adaptive immune responses during co-infection with influenza virus and S. pneumoniae or S. aureus, describing the signaling pathways involved and how these interactions influence disease outcomes.
Highlights
Influenza viruses cause highly infectious lung diseases and infect hundreds of thousands of people every year worldwide
CoEnvcleunstihoonusgh co-infections with influenza viruses and S. pneumoniae or S. aureus have beenEkvneonwthnotuogehxcisot-ifnofredcteicoandsews,itthheinyfslutiellnpzarevsiernutseascahnadlleSn. gpneeiunmcolinniaiceso. rTSh.earuerfeourse,hiatvies boefemnakjonrowimnptooretaxnisctefotor dobectaaidnesa, btheettyerstuilnl dperressteanntdainchgaollfetnhgeecionmclpinleixcsi.nTtehrearcetfioornes, iotfisthoef pathogens with the host and with each other, in order to potentially identify new targets for therapeutic interventions to mitigate or even impede secondary bacterial infections in the future
In comparison to single infections, the presence of both pathogens results in dysregulated cytokine and chemokine production after pathogen sensing via typical pattern recognition receptors (PRRs), leading to dynamic changes in immune cell recruitment and activation
Summary
Influenza viruses cause highly infectious lung diseases and infect hundreds of thousands of people every year worldwide. Secondary pulmonary infections caused by influenza viruses in combination with bacteria lead to challenging problems in clinics, including increased numbers of fatal cases It has been known for a long time that influenza viruses pave the way for secondary bacterial infections, e.g., by increasing the exposure of surface receptors on epithelial cells to facilitate bacterial adherence or damaging the epithelial barrier to enable bacterial invasion into deeper tissues [3,4]. In these cases, clinicians are confronted with severe lung damage induced by a dysregulated immune response, which is caused by misdirected signal transduction [5,6]. We summarize the latest scientific results regarding co-infections with influenza viruses and S. pneumoniae or S. aureus, including essential changes in the innate and adaptive immune responses, mediated by the mutual impact of the pathogens on molecular signal transduction pathways
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