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A novel influenza A virus mitochondrial protein that induces cell death
It is proposed that PB1-F2 functions to kill host immune cells responding to influenza virus infection, and influenza viruses with targeted mutations that interfere with PB1/F2 expression induce less extensive apoptosis in human monocytic cells than those with intact PB1 -F2.
Influenza Virus Transmission Is Dependent on Relative Humidity and Temperature
Direct, experimental evidence is provided to support the role of weather conditions in the dynamics of influenza and thereby address a long-standing question fundamental to the understanding of influenza epidemiology and evolution.
Severe Acute Respiratory Syndrome Coronavirus Open Reading Frame (ORF) 3b, ORF 6, and Nucleocapsid Proteins Function as Interferon Antagonists
- Sarah A. Kopecky-Bromberg, L. Martínez-Sobrido, M. Frieman, Ralph Baric, P. Palese
- BiologyJournal of Virology
- 15 November 2006
It has been determined that SARS-CoV open reading frame (ORF) 3b, ORF 6, and N proteins antagonize interferon, a key component of the innate immune response.
Broadly neutralizing hemagglutinin stalk–specific antibodies require FcγR interactions for protection against influenza virus in vivo
Results suggest that FcγR binding capacity by anti-HA antibodies was dependent on the interaction of the cognate Fab with antigen, a previously uncharacterized property of bNAbs, and guide an approach toward enhancing mAb-mediated antiviral therapeutics.
Influenza A virus lacking the NS1 gene replicates in interferon-deficient systems.
The results indicate that the NS1 of influenza A virus is an auxiliary (virulence) factor which plays a crucial role in inhibiting interferon-mediated antiviral responses of the host.
The influenza virus NEP (NS2 protein) mediates the nuclear export of viral ribonucleoproteins
A model by which NEP acts as a protein adaptor molecule bridging viral ribonucleoproteins and the nuclear pore complex is proposed, suggesting that the Rev‐like NS2 mediates this process.
Activation of Interferon Regulatory Factor 3 Is Inhibited by the Influenza A Virus NS1 Protein
It is proposed that inhibition of IRF-3 activation by a dsRNA binding protein significantly contributes to the virulence of influenza A viruses and possibly to that of other viruses.
Severe Acute Respiratory Syndrome Coronavirus ORF6 Antagonizes STAT1 Function by Sequestering Nuclear Import Factors on the Rough Endoplasmic Reticulum/Golgi Membrane
- M. Frieman, B. Yount, M. Heise, Sarah A. Kopecky-Bromberg, P. Palese, R. Baric
- BiologyJournal of Virology
- 27 June 2007
It is demonstrated that SARS-COV ORF6 protein is localized to the endoplasmic reticulum (ER)/Golgi membrane in infected cells, where it binds to and disrupts nuclear import complex formation by tethering karyopherin alpha 2 and kARYopherin beta 1 to the membrane.
The biology of influenza viruses.