作者: Amber M. Smith , Frederick R. Adler , Julie L. McAuley , Ryan N. Gutenkunst , Ruy M. Ribeiro
DOI: 10.1371/JOURNAL.PCBI.1001081
关键词: Influenza A virus 、 Virology 、 Virus 、 Virulence 、 Viral replication 、 Viral load 、 In vivo 、 Apoptosis 、 Programmed cell death 、 Microbiology 、 Biology 、 Ecology (disciplines) 、 Modelling and Simulation 、 Computational Theory and Mathematics 、 Genetics 、 Ecology, Evolution, Behavior and Systematics 、 Molecular biology 、 Cellular and Molecular Neuroscience
摘要: Relatively little is known about the viral factors contributing to lethality of 1918 pandemic, although its unparalleled virulence was likely due in part newly discovered PB1-F2 protein. This protein, while unnecessary for replication, increases apoptosis monocytes, alters polymerase activity vitro, enhances inflammation and secondary pneumonia vivo. However, effects protein have vivo remain unclear. To address mechanisms involved, we intranasally infected groups mice with either influenza A virus PR8 or a genetically engineered that expresses on background, PR8-PB1-F2(1918). Mice inoculated had concentrations peaking at 72 hours, those PR8-PB1-F2(1918) reached peak earlier, 48 hours. given also showed faster decline loads. We fit mathematical model these data estimate parameter values. The supports higher production rate per cell death virus. discuss implications during an infection expressing virulent possibility pandemic importance antiviral treatments.