tetano
Editor, Senior Moderator
Microb Pathog. 2019 Dec 9:103919. doi: 10.1016/j.micpath.2019.103919. [Epub ahead of print] [h=1]Web of interferon stimulated antiviral factors to control the influenza A viruses replication.[/h]
Goraya MU[SUP]1[/SUP], Zaighum F[SUP]2[/SUP], Sajjad N[SUP]3[/SUP], Anjum FR[SUP]4[/SUP], Sakhawat I[SUP]5[/SUP], Rahman SU[SUP]6[/SUP].
[h=3]Author information[/h] 1 Institute of Microbiology, University of Agriculture Faisalabad, 38000, Pakistan. Electronic address: goraya_uaf@yahoo.com. 2 Bahauddin Zakariya University, Multan, Pakistan. 3 College of Life Sciences, Fujian Agriculture and Forestry University, Fuzhou, 350002, China. 4 Institute of Microbiology, University of Agriculture Faisalabad, 38000, Pakistan. 5 School of Science and Technology, Orebro University, SE-70182, Orebro, Sweden. 6 Institute of Microbiology, University of Agriculture Faisalabad, 38000, Pakistan. Electronic address: sajjadrahmanuaf@gmail.com.
[h=3]Abstract[/h] Influenza viruses cause mild to severe infections in animals and humans worldwide with significant morbidity and mortality. Infection of eukaryotic cells with influenza A viruses triggers the induction of innate immune system through the interaction between pattern recognition receptors (PRRs) and pathogen associated molecular patterns (PAMPs), which culminate in the induction of interferons (IFNs). Consequently, IFNs bind to their cognate receptors on the cellular membrane and activate the signaling pathway for transcriptional regulation of interferon-stimulated genes (ISGs) through Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway. Cumulative actions of these ISGs establish an antiviral state of the host. Several ISGs have been described, which play critical roles to inhibit the infection and replication of influenza A viruses at multiple steps of virus life cycle. In this review, the dynamics and redundancy of these ISGs against influenza A viruses are discussed. Additionally, current understanding and molecular mechanisms that are underlying the roles of ISGs in pathogenesis of influenza virus are critically reviewed.
Copyright ? 2019. Published by Elsevier Ltd.
[h=4]KEYWORDS:[/h] Influenza virus; Innate immunity; Interferon stimulated genes; JAK-STAT signaling; Non-coding RNA
PMID: 31830579 DOI: 10.1016/j.micpath.2019.103919
Goraya MU[SUP]1[/SUP], Zaighum F[SUP]2[/SUP], Sajjad N[SUP]3[/SUP], Anjum FR[SUP]4[/SUP], Sakhawat I[SUP]5[/SUP], Rahman SU[SUP]6[/SUP].
[h=3]Author information[/h] 1 Institute of Microbiology, University of Agriculture Faisalabad, 38000, Pakistan. Electronic address: goraya_uaf@yahoo.com. 2 Bahauddin Zakariya University, Multan, Pakistan. 3 College of Life Sciences, Fujian Agriculture and Forestry University, Fuzhou, 350002, China. 4 Institute of Microbiology, University of Agriculture Faisalabad, 38000, Pakistan. 5 School of Science and Technology, Orebro University, SE-70182, Orebro, Sweden. 6 Institute of Microbiology, University of Agriculture Faisalabad, 38000, Pakistan. Electronic address: sajjadrahmanuaf@gmail.com.
[h=3]Abstract[/h] Influenza viruses cause mild to severe infections in animals and humans worldwide with significant morbidity and mortality. Infection of eukaryotic cells with influenza A viruses triggers the induction of innate immune system through the interaction between pattern recognition receptors (PRRs) and pathogen associated molecular patterns (PAMPs), which culminate in the induction of interferons (IFNs). Consequently, IFNs bind to their cognate receptors on the cellular membrane and activate the signaling pathway for transcriptional regulation of interferon-stimulated genes (ISGs) through Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway. Cumulative actions of these ISGs establish an antiviral state of the host. Several ISGs have been described, which play critical roles to inhibit the infection and replication of influenza A viruses at multiple steps of virus life cycle. In this review, the dynamics and redundancy of these ISGs against influenza A viruses are discussed. Additionally, current understanding and molecular mechanisms that are underlying the roles of ISGs in pathogenesis of influenza virus are critically reviewed.
Copyright ? 2019. Published by Elsevier Ltd.
[h=4]KEYWORDS:[/h] Influenza virus; Innate immunity; Interferon stimulated genes; JAK-STAT signaling; Non-coding RNA
PMID: 31830579 DOI: 10.1016/j.micpath.2019.103919