摘要：AbstractThe influenza A virus (IAV) infections provide a susceptibility to a secondary bacterial infection mainly driven byStreptococcus pneumoniae (S. pneumoniae).This lethal synergy is one of the main causative agents for severe respiratory diseases provoking high rates of hospitalization and death. Although significant improvements have been made in our knowledge of IAV infections, holistic understanding of the interactions between IAV, bacteria and immune modulation remains largely fragmented. Our steady-state analysis suggests that influenza increases substrates as nutrients for bacterial growth affecting only the steady-state that the bacteria would reach, but more nutrients would not contribute directly to the bacterial decision to colonize. Furthermore, using a Markov branching process, the hypothesis of cell to cell heterogeneity in single bacterial infection is supported, however, this plays a minimal role in the case of coinfection.
关键词：KeywordsModelingVirusBacteriaInfectionsInfluenzaMarkov Branching Process
