A novel influenza A virus mitochondrial protein that induces cell death

2001 ◽  
Vol 7 (12) ◽  
pp. 1306-1312 ◽  
Author(s):  
Weisan Chen ◽  
Paul A. Calvo ◽  
Daniela Malide ◽  
James Gibbs ◽  
Ulrich Schubert ◽  
...  
Keyword(s):  
Cell Death ◽  
Influenza A Virus ◽  
Influenza A ◽  
Mitochondrial Protein ◽  
Novel Influenza A

scholarly journals PB1-F2, an Influenza A Virus-Encoded Proapoptotic Mitochondrial Protein, Creates Variably Sized Pores in Planar Lipid Membranes

2004 ◽  
Vol 78 (12) ◽  
pp. 6304-6312 ◽  
Author(s):  
A. N. Chanturiya ◽  
G. Basañez ◽  
U. Schubert ◽  
P. Henklein ◽  
J. W. Yewdell ◽  
...  
Keyword(s):  
Cell Death ◽  
Influenza A Virus ◽  
Influenza A ◽  
Mitochondrial Protein ◽  
Membrane Conductance ◽  
Rate Of Change ◽  
Phospholipid Bilayer ◽  
Mitochondrial Outer Membrane ◽  
Bathing Solution ◽  
Dependent Manner

ABSTRACT A frameshifted region of the influenza A virus PB1 gene encodes a novel protein, termed PB1-F2, a mitochondrial protein that can induce cell death. Many proapoptotic proteins are believed to act at the mitochondrial outer membrane to form an apoptotic pore with lipids. We studied the interaction of isolated, synthetic PB1-F2 (sPB1-F2) peptide with planar phospholipid bilayer membranes. The presence of nanomolar concentrations of peptide in the bathing solution induced a transmembrane conductance that increased in a potential-dependent manner. Positive potential on the side of protein addition resulted in a severalfold increase in the rate of change of membrane conductance. sPB1-F2-treated membranes became permeable to monovalent cations, chloride, and to a lesser extent, divalent ions. Despite various experimental conditions, we did not detect the distinctive conductance levels typical of large, stable pores, protein channels, or even pores that are partially proteinaceous. Rather, membrane conductance induced by sPB1-F2 fluctuated and visited almost all conductance values. sPB1-F2 also dramatically decreased bilayer stability in an electric field, consistent with a decrease in the line tension of a lipidic pore. Since similar membrane-destabilizing profiles are seen with proapoptotic proteins (e.g., Bax) and the cytoplasmic helix of human immunodeficiency virus gp41, we suggest that the basis for sPB1-F2-induced cell death may be the permeabilization and destabilization of mitochondrial membranes, leading to macromolecular leakage and apoptosis.

scholarly journals Thin-section Computed Tomography Detects Long-term Pulmonary Sequelae 3 Years after Novel Influenza A Virus-associated Pneumonia

2015 ◽  
Vol 128 (7) ◽  
pp. 902-908 ◽  
Author(s):  
Zhi-Heng Xing ◽  
Xin Sun ◽  
Long Xu ◽  
Qi Wu ◽  
Li Li ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Influenza A Virus ◽  
Thin Section ◽  
Influenza A ◽  
Novel Influenza A

scholarly journals Molecular Events Involved in Influenza A Virus-Induced Cell Death

2022 ◽  
Vol 12 ◽  
Author(s):  
Rui Gui ◽  
Quanjiao Chen
Keyword(s):  
Cell Death ◽  
Influenza A Virus ◽  
Influenza A ◽  
Regulatory Networks ◽  
Molecular Mechanisms ◽  
Tissue Destruction ◽  
Inflammatory Reactions ◽  
Molecular Events ◽  
Host Death

Viral infection usually leads to cell death. Moderate cell death is a protective innate immune response. By contrast, excessive, uncontrolled cell death causes tissue destruction, cytokine storm, or even host death. Thus, the struggle between the host and virus determines whether the host survives. Influenza A virus (IAV) infection in humans can lead to unbridled hyper-inflammatory reactions and cause serious illnesses and even death. A full understanding of the molecular mechanisms and regulatory networks through which IAVs induce cell death could facilitate the development of more effective antiviral treatments. In this review, we discuss current progress in research on cell death induced by IAV infection and evaluate the role of cell death in IAV replication and disease prognosis.

Genetic characterization of a novel influenza A virus H5N2 isolated from a dog in China

2012 ◽  
Vol 155 (2-4) ◽  
pp. 409-416 ◽  
Author(s):  
Zhan Guang-jian ◽  
Ling Zong-shuai ◽  
Zhu Yan-li ◽  
Jiang Shi-jin ◽  
Xie Zhi-jing
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
Genetic Characterization ◽  
Novel Influenza A

scholarly journals The Zα2 domain of ZBP1 is a molecular switch regulating influenza-induced PANoptosis and perinatal lethality during development

2020 ◽  
Vol 295 (24) ◽  
pp. 8325-8330 ◽  
Author(s):  
Sannula Kesavardhana ◽  
R. K. Subbarao Malireddi ◽  
Amanda R. Burton ◽  
Shaina N. Porter ◽  
Peter Vogel ◽  
...  
Keyword(s):  
Cell Death ◽  
Nucleic Acids ◽  
Influenza A Virus ◽  
Nlrp3 Inflammasome ◽  
Influenza A ◽  
Defense Responses ◽  
Innate Immune ◽  
Inflammasome Activation ◽  
Perinatal Lethality

Z-DNA-binding protein 1 (ZBP1) is an innate immune sensor of nucleic acids that regulates host defense responses and development. ZBP1 activation triggers inflammation and pyroptosis, necroptosis, and apoptosis (PANoptosis) by activating receptor-interacting Ser/Thr kinase 3 (RIPK3), caspase-8, and the NLRP3 inflammasome. ZBP1 is unique among innate immune sensors because of its N-terminal Zα1 and Zα2 domains, which bind to nucleic acids in the Z-conformation. However, the specific role of these Zα domains in orchestrating ZBP1 activation and subsequent inflammation and cell death is not clear. Here we generated Zbp1ΔZα2/ΔZα2 mice that express ZBP1 lacking the Zα2 domain and demonstrate that this domain is critical for influenza A virus–induced PANoptosis and underlies perinatal lethality in mice in which the RIP homotypic interaction motif domain of RIPK1 has been mutated (Ripk1mRHIM/mRHIM). Deletion of the Zα2 domain in ZBP1 abolished influenza A virus–induced PANoptosis and NLRP3 inflammasome activation. Furthermore, deletion of the Zα2 domain of ZBP1 was sufficient to rescue Ripk1mRHIM/mRHIM mice from perinatal lethality caused by ZBP1-driven cell death and inflammation. Our findings identify the essential role of the Zα2 domain of ZBP1 in several physiological functions and establish a link between Z-RNA sensing via the Zα2 domain and promotion of influenza-induced PANoptosis and perinatal lethality.

scholarly journals The induction and consequences of Influenza A virus-induced cell death

2018 ◽  
Vol 9 (10) ◽  
Author(s):  
Georgia K. Atkin-Smith ◽  
Mubing Duan ◽  
Weisan Chen ◽  
Ivan K. H. Poon
Keyword(s):  
Cell Death ◽  
Influenza A Virus ◽  
Influenza A

scholarly journals Identification of novel influenza A virus exposures by an improved high‐throughput multiplex MAGPIX platform and serum adsorption

2019 ◽  
Vol 14 (2) ◽  
pp. 129-141
Author(s):  
Zhu‐Nan Li ◽  
Emily Cheng ◽  
Eugenie Poirot ◽  
Kimberly M. Weber ◽  
Paul Carney ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
High Throughput ◽  
Influenza A ◽  
Novel Influenza A

scholarly journals Findings in children severely infected with a novel influenza A virus of swine origin: pulmonary imaging

2012 ◽  
Vol 8 (3) ◽  
pp. 240-246 ◽  
Author(s):  
Wei Xu ◽  
Chun-Feng Liu ◽  
Ying Zhao ◽  
Jiu-Jun Li ◽  
Li-Jie Wang ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
Pulmonary Imaging ◽  
Novel Influenza A
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