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How Influenza Virus Uses Host Cell Pathways during Uncoating

期刊

CELLS
卷 10, 期 7, 页码 -

出版社

MDPI
DOI: 10.3390/cells10071722

关键词

influenza; capsid uncoating; HDAC6; ubiquitin; EPS8; TNPO1; pandemic; M1; virus-host interaction

资金

  1. Novartis Research Foundation
  2. European Research Council-ERC Synergy [856581]
  3. European Research Council (ERC) [856581] Funding Source: European Research Council (ERC)

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Influenza is a zoonotic respiratory disease of major public health interest due to its pandemic potential. Cellular cues contribute to viral conformational changes during host cell entry, aiding in critical events such as fusion with late endosomes and viral genome release into the cytosol.
Influenza is a zoonotic respiratory disease of major public health interest due to its pandemic potential, and a threat to animals and the human population. The influenza A virus genome consists of eight single-stranded RNA segments sequestered within a protein capsid and a lipid bilayer envelope. During host cell entry, cellular cues contribute to viral conformational changes that promote critical events such as fusion with late endosomes, capsid uncoating and viral genome release into the cytosol. In this focused review, we concisely describe the virus infection cycle and highlight the recent findings of host cell pathways and cytosolic proteins that assist influenza uncoating during host cell entry.

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