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Influenza A virus-induced apoptosis and virus propagation

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Abstract

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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(Adapted from Viral control of mitochondrial apoptosis [67])

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Funding

Funding for this study was provided by grants from the National Medical Research Council in Singapore (NMRC/CBRG/056/2014) awarded to LHKL. PAB was supported by a NUS-SINGA graduate scholarship.

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Correspondence to Lina H. K. Lim.

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Ampomah, P.B., Lim, L.H.K. Influenza A virus-induced apoptosis and virus propagation. Apoptosis 25, 1–11 (2020). https://doi.org/10.1007/s10495-019-01575-3

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