Increased virus dissemination leads to enhanced lung injury but not inflammation during influenza-associated secondary bacterial infection.

ABSTRACT: Secondary bacterial infections increase influenza-related morbidity and mortality, particularly if acquired after 5-7 d from the viral onset. Synergistic host responses and direct pathogen-pathogen interactions are thought to lead to a state of hyperinflammation, but the kinetics of the lung pathology have not yet been detailed, and identifying the contribution of different mechanisms to disease is difficult because these may change over time. To address this gap, we examined host-pathogen and lung pathology dynamics following a secondary bacterial infection initiated at different time points after influenza within a murine model. We then used a mathematical approach to quantify the increased virus dissemination in the lung, coinfection time-dependent bacterial kinetics, and virus-mediated

SUBMITTER: Smith AP 

PROVIDER: S-EPMC10117793 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature