Journal
APOPTOSIS
Volume 25, Issue 1-2, Pages 1-11Publisher
SPRINGER
DOI: 10.1007/s10495-019-01575-3
Keywords
Influenza virus; Apoptosis; Cell death; Virus propagation; Interferons
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Funding
- National Medical Research Council in Singapore [NMRC/CBRG/056/2014]
- NUS-SINGA graduate scholarship
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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.
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