tetano
Editor, Senior Moderator
Apoptosis. 2019 Oct 30. doi: 10.1007/s10495-019-01575-3. [Epub ahead of print] [h=1]Influenza A virus-induced apoptosis and virus propagation.[/h]
Ampomah PB[SUP]1,[/SUP][SUP]2[/SUP], Lim LHK[SUP]3,[/SUP][SUP]4[/SUP].
[h=3]Author information[/h] 1 Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, 28 Medical Drive, Singapore, 117456, Singapore. 2 NUS Immunology Program, Life Sciences Institute, National University of Singapore, Singapore, 117456, Singapore. 3 Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, 28 Medical Drive, Singapore, 117456, Singapore. linalim@nus.edu.sg. 4 NUS Immunology Program, Life Sciences Institute, National University of Singapore, Singapore, 117456, Singapore. linalim@nus.edu.sg.
[h=3]Abstract[/h] Influenza A viruses (IAVs) are respiratory pathogens that cause severe morbidity and mortality worldwide. They affect cellular processes such as proliferation, protein synthesis, autophagy, and apoptosis. Although apoptosis is considered an innate cellular response to invading infectious pathogens, IAVs have evolved to encode viral proteins that modulate host cellular apoptosis in ways that support efficient viral replication and propagation. An understanding of the modulation of host responses is essential to the development of novel therapeutics for the treatment of IAV infections. In this review, we discuss the IAV lifecycle, biology, and strategies employed by the virus to modulate apoptosis to enhance viral survival and establish an infection.
[h=4]KEYWORDS:[/h] Apoptosis; Cell death; Influenza virus; Interferons; Virus propagation
PMID: 31667646 DOI: 10.1007/s10495-019-01575-3
Ampomah PB[SUP]1,[/SUP][SUP]2[/SUP], Lim LHK[SUP]3,[/SUP][SUP]4[/SUP].
[h=3]Author information[/h] 1 Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, 28 Medical Drive, Singapore, 117456, Singapore. 2 NUS Immunology Program, Life Sciences Institute, National University of Singapore, Singapore, 117456, Singapore. 3 Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, 28 Medical Drive, Singapore, 117456, Singapore. linalim@nus.edu.sg. 4 NUS Immunology Program, Life Sciences Institute, National University of Singapore, Singapore, 117456, Singapore. linalim@nus.edu.sg.
[h=3]Abstract[/h] Influenza A viruses (IAVs) are respiratory pathogens that cause severe morbidity and mortality worldwide. They affect cellular processes such as proliferation, protein synthesis, autophagy, and apoptosis. Although apoptosis is considered an innate cellular response to invading infectious pathogens, IAVs have evolved to encode viral proteins that modulate host cellular apoptosis in ways that support efficient viral replication and propagation. An understanding of the modulation of host responses is essential to the development of novel therapeutics for the treatment of IAV infections. In this review, we discuss the IAV lifecycle, biology, and strategies employed by the virus to modulate apoptosis to enhance viral survival and establish an infection.
[h=4]KEYWORDS:[/h] Apoptosis; Cell death; Influenza virus; Interferons; Virus propagation
PMID: 31667646 DOI: 10.1007/s10495-019-01575-3