Abstract
Over the last decade, there has been significant advances in the understanding of the cross-talk between metabolism and immune responses. It is now evident that immune cell effector function strongly depends on the metabolic pathway in which cells are engaged in at a particular point in time, the activation conditions, and the cell microenvironment. It is also clear that some metabolic intermediates have signaling as well as effector properties and, hence, topics such as immunometabolism, metabolic reprograming, and metabolic symbiosis (among others) have emerged. Viruses completely rely on their host's cell energy and molecular machinery to enter, multiply, and exit for a new round of infection. This review explores how viruses mimic, exploit or interfere with host cell metabolic pathways and how, in doing so, they may evade immune responses. It offers a brief outline of key metabolic pathways, mitochondrial function and metabolism-related signaling pathways, followed by examples of the mechanisms by which several viral proteins regulate host cell metabolic activity.
Highlights
Several recent comprehensive reviews have highlighted the key role of eukaryotic cell metabolism in immunity (Ganeshan and Chawla, 2014; O’Neill and Pearce, 2016; O’Neill et al, 2016)
Energetic and biosynthetic metabolism is fueled by carbon sources, including glucose and glutamine (DeBerardinis and Cheng, 2010), which are taken up by the cells by glucose and glutamine transporters, respectively (Bhutia and Ganapathy, 2016; Navale and Paranjape, 2016)
BamH1-Hright reading frame (BHRF1) accumulates in the outer mitochondrial membrane (OMM) of B lymphocytes, preventing apoptosis and promoting survival of Epstein Barr virus (EBV)-infected cells, viral persistence, and replication; BHRF presents homology with the transmembrane domains of some eukaryotic Bcl2 family members (Kvansakul et al, 2017; Cavallari et al, 2018); and Zebra protein (BZLF1) has the capacity to interact with Mitochondrial single-stranded DNA binding protein (mtSSB), which is required for the replication of the mitochondrial genome, and partially redirects mtSSB from mitochondria to the nucleus (LaJeunesse et al, 2005; Cavallari et al, 2018)
Summary
Several recent comprehensive reviews have highlighted the key role of eukaryotic cell metabolism in immunity (Ganeshan and Chawla, 2014; O’Neill and Pearce, 2016; O’Neill et al, 2016). BHRF1 accumulates in the outer mitochondrial membrane (OMM) of B lymphocytes, preventing apoptosis and promoting survival of EBV-infected cells, viral persistence, and replication; BHRF presents homology with the transmembrane domains of some eukaryotic Bcl2 family members (Kvansakul et al, 2017; Cavallari et al, 2018); and BZLF1 has the capacity to interact with mtSSB (mitochondrial single-stranded DNA-binding protein), which is required for the replication of the mitochondrial genome, and partially redirects mtSSB from mitochondria to the nucleus (LaJeunesse et al, 2005; Cavallari et al, 2018).
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