McAuley JL, Hornung F, Boyd KL, Smith AM, McKeon R. Expression of the 1918 Influenza A Virus PB1-F2 Enhances the Pathogenesis of Viral and Secondary Bacterial Pneumonia. Cell Host Microbe. 2007 Oct 11;2(4):240-249
Secondary bacterial pneumonia frequently claimed the lives of victims during the devastating 1918 influenza A virus pandemic. Little is known about the viral factors contributing to the lethality of the 1918 pandemic. Here we show that expression of the viral accessory protein PB1-F2 enhances inflammation during primary viral infection of mice and increases both the frequency and severity of secondary bacterial pneumonia. The priming effect of PB1-F2 on bacterial pneumonia could be recapitulated in mice by intranasal delivery of a synthetic peptide derived from the C-terminal portion of the PB1-F2. Relative to its isogenic parent, an influenza virus engineered to express a PB1-F2 with coding changes matching the 1918 pandemic strain was more virulent in mice, induced more pulmonary immunopathology, and led to more severe secondary bacterial pneumonia. These findings help explain both the unparalleled virulence of the 1918 strain and the high incidence of fatal pneumonia during the pandemic.
See Also:
Latest articles in those days:
- Outbreak of Highly Pathogenic Avian Influenza A(H5N1) Virus in Seals, St. Lawrence Estuary, Quebec, Canada 2 days ago
- Molecular characterization of influenza virus circulating in Nepal in the year 2019 2 days ago
- Seasonal antigenic prediction of influenza A H3N2 using machine learning 2 days ago
- Probable extinction of influenza B/Yamagata and its public health implications: a systematic literature review and assessment of global surveillance databases 2 days ago
- Code to reproduce analysis in Nguyen et al, Emergence and interstate spread of highly pathogenic avian influenza A (H5N1) in dairy cattle. 2 days ago
[Go Top] [Close Window]