作者: Amber M. Smith , Frederick R. Adler , Ruy M. Ribeiro , Ryan N. Gutenkunst , Julie L. McAuley
DOI: 10.1371/JOURNAL.PPAT.1003238
关键词:
摘要: Secondary bacterial infections are a leading cause of illness and death during epidemic pandemic influenza. Experimental studies suggest lethal synergism between influenza certain bacteria, particularly Streptococcus pneumoniae, but the precise processes involved unclear. To address mechanisms determine influences pathogen dose strain on disease, we infected groups mice with either H1N1 subtype A virus A/Puerto Rico/8/34 (PR8) or version expressing 1918 PB1-F2 protein (PR8-PB1-F2(1918)), followed seven days later one two S. pneumoniae strains, type 2 D39 3 A66.1. We determined that, following infection, viral titers initially rebound then decline slowly. Bacterial rapidly rise to high levels remain elevated. used kinetic model explore coupled interactions study dominant controlling mechanisms. hypothesize that in presence bacteria due enhanced release from cells, increase alveolar macrophage impairment. Dynamics affected by initial not expression protein. Our provides framework investigate interaction coinfections uncover dynamical differences based inoculum size strain.