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A novel influenza A virus mitochondrial protein that induces cell death
TLDR
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
TLDR
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
TLDR
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
TLDR
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.
TLDR
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
TLDR
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
TLDR
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
TLDR
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.
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