Abstract
In the last years, proteomics has represented a valuable approach to elucidate key aspects in the regulation of type I/III interferons (IFNs) and autophagy, two main processes involved in the response to viral infection, to unveil the molecular strategies that viruses have evolved to counteract these processes. Besides their main metabolic roles, mitochondria are well recognized as pivotal organelles in controlling signaling pathways essential to restrain viral infections. In particular, a major role in antiviral defense is played by mitochondrial antiviral signaling (MAVS) protein, an adaptor protein that coordinates the activation of IFN inducing pathways and autophagy at the mitochondrial level. Here, we provide an overview of how mass spectrometry-based studies of protein–protein interactions and post-translational modifications (PTMs) have fostered our understanding of the molecular mechanisms that control the mitochondria-mediated antiviral immunity.
Highlights
Mitochondria are the powerhouse of the cell due to their primary contribution in cell respiration
PHBs were shown to form a complex with mitochondrial antiviral signaling (MAVS) oligomers, which includes the AAA(+) ATPase proteins Caseinolytic Peptidase B (CLPB) Homolog and ATPase Family AAA Domain Containing 3A (ATAD3A), establishing a bridge between the outer mitochondrial membrane (OMM) and inner mitochondrial membrane (IMM) that is required for the efficient activation of the retinoic acid-inducible gene I (RIG-I) signaling pathway (Yoshinaka et al, 2019)
We found that hepatitis C virus (HCV) NS5A interacts with the mitochondrial protein LRPPRC and represses the antiviral response by promoting LRPPRC association with MAVS, which results in a reduced association of MAVS with TRAF proteins (Refolo et al, 2019)
Summary
Mitochondria are the powerhouse of the cell due to their primary contribution in cell respiration. Several pathogen-activated pathways are influenced by mitochondria, this role is to be attributed mainly to the mitochondrial localization of the signaling adaptor mitochondrial antiviral signaling (MAVS) protein, a key mediator of the innate immune response during RNA viral infection (Vazquez and Horner, 2015).
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