Abstract
Throughout various stages of its life cycle, influenza A virus relies heavily on host cellular machinery, including the post-translational modifications (PTMs) system. During infection, influenza virus interacts extensively with the cellular PTMs system to aid in its successful infection and dissemination. The complex interplay between viruses and the PTMs system induces global changes in PTMs of the host proteome as well as modifications of specific host or viral proteins. The most common PTMs include phosphorylation, ubiquitination, SUMOylation, acetylation, methylation, NEDDylation, and glycosylation. Many PTMs directly support influenza virus infection, whereas others contribute to modulating antiviral responses. In this review, we describe current knowledge regarding the role of PTMs in different stages of the influenza virus replication cycle. We also discuss the concerted role of PTMs in antagonizing host antiviral responses, with an emphasis on their impact on viral pathogenicity and host range.
Highlights
Influenza A viruses (IAV) are enveloped viruses containing eight single-stranded, negative-sense RNA gene segments
Nuclear export of viral ribonucleoproteins (vRNPs) requires sufficient amounts of HA and NA to be embedded in the plasma membrane, and this process is coordinated in part by protein kinase C α (PKCα)/mitogen-activated protein (MAP) kinase signaling cascade mediated by HA membrane accumulation (Pleschka et al, 2001; Marjuki et al, 2006)
As an obligatory intracellular parasite, influenza virus heavily depends on host cellular factors and host cellular machineries to accomplish its life cycle and establish a successful infection
Summary
Influenza A viruses (IAV) are enveloped viruses containing eight single-stranded, negative-sense RNA gene segments. SUMO can competitively bind the substrate proteins of ubiquitin Both ubiquitination and SUMOylation are widely involved in various cellular processes, including DNA damage repair, transcriptional regulation, protein function regulation, and protein–protein interaction, as well as in various signaling pathways, such as those linked to gene regulation, epigenetics, cell differentiation, protein degradation, and tumorigenesis; they play roles in viral replication and immune responses (Johnson, 2004; Pickart, 2004; Welchman et al, 2005). We discuss how the IAV usurps the PTMs system to evade host innate immune responses, accelerating viral pathogenesis
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