Abstract
Protein modifications dynamically occur and regulate biological processes in all organisms. Towards understanding the significance of protein modifications in influenza virus infection, we performed a global mass spectrometry screen followed by bioinformatics analyses of acetylation, methylation and allysine modification in human lung epithelial cells in response to influenza A virus infection. We discovered 8 out of 10 major viral proteins and 245 out of 2280 host proteins detected to be differentially modified by three modifications in infected cells. Some of the identified proteins were modified on multiple amino acids residues and by more than one modification; the latter occurred either on different or same residues. Most of the modified residues in viral proteins were conserved across >40 subtypes of influenza A virus, and influenza B or C viruses and located on the protein surface. Importantly, many of those residues have already been determined to be critical for the influenza A virus. Similarly, many modified residues in host proteins were conserved across influenza A virus hosts like humans, birds, and pigs. Finally, host proteins undergoing the three modifications clustered in common functional networks of metabolic, cytoskeletal, and RNA processes, all of which are known to be exploited by the influenza A virus.
Highlights
Deacetylases in influenza A virus (IAV) infection [19]. These findings indicated that the host acetylation machinery plays a pro-viral role during IAV infection and, potentially, both viral and host proteins are differentially modified by acetylation to facilitate this
Eight Viral Proteins Were Modified by Acetylation, Methylation and/or Allysine
The role and significance of lysine acetylation and lysine/arginine methylation have been extensively studied in histones modifications and their influence on gene expression
Summary
The influenza virus is a globally prevalent human respiratory pathogen, with recurring epidemic and pandemic potentials. The influenza A virus (IAV) will be impossible to eradicate because of its intrinsic evolving nature, zoonotic potential, and broad host range which includes migratory birds. IAV is an obligate intracellular pathogen and exploits the host machinery to multiply and cause flu [1]. IAV employs viral proteins and exploits host proteins to execute multiple crucial functions, such as anterograde and retrograde intracellular trafficking, RNA processing, and antagonism of host antiviral response. Many of these functions involve numerous protein-protein, protein-nucleic acid, and protein-lipid interactions. The dysregulation or imbalance of protein modifications is a hallmark of various human diseases [2,3]
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