Please use this identifier to cite or link to this item:
https://doi.org/10.1007/s10495-019-01575-3
Title: | Influenza A virus-induced apoptosis and virus propagation | Authors: | Ampomah, Patrick B Lim, Lina HK |
Keywords: | Science & Technology Life Sciences & Biomedicine Biochemistry & Molecular Biology Cell Biology Influenza virus Apoptosis Cell death Virus propagation Interferons CRM1-MEDIATED NUCLEAR EXPORT NF-KAPPA-B NS1 PROTEIN NITRIC-OXIDE MITOCHONDRIAL PROTEIN MESSENGER-RNAS CELLS RESPOND C-TERMINUS INDUCTION NEURAMINIDASE |
Issue Date: | 1-Feb-2020 | Publisher: | SPRINGER | Citation: | Ampomah, Patrick B, Lim, Lina HK (2020-02-01). Influenza A virus-induced apoptosis and virus propagation. APOPTOSIS 25 (1-2) : 1-11. ScholarBank@NUS Repository. https://doi.org/10.1007/s10495-019-01575-3 | Abstract: | © 2019, Springer Science+Business Media, LLC, part of Springer Nature. 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. | Source Title: | APOPTOSIS | URI: | https://scholarbank.nus.edu.sg/handle/10635/176820 | ISSN: | 13608185 1573675X |
DOI: | 10.1007/s10495-019-01575-3 |
Appears in Collections: | Staff Publications Elements |
Show full item record
Files in This Item:
File | Description | Size | Format | Access Settings | Version | |
---|---|---|---|---|---|---|
Influenza A virus.pdf | 643.13 kB | Adobe PDF | OPEN | Post-print | View/Download |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.