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Review
. 2019 Apr 18:9:95.
doi: 10.3389/fcimb.2019.00095. eCollection 2019.

Virus Control of Cell Metabolism for Replication and Evasion of Host Immune Responses

María Maximina B Moreno-Altamirano  1 , Simon E Kolstoe  2 , Francisco Javier Sánchez-García  1
Affiliations
Review

Virus Control of Cell Metabolism for Replication and Evasion of Host Immune Responses

María Maximina B Moreno-Altamirano et al. Front Cell Infect Microbiol. .

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.

Keywords: cell metabolism; immune response; mitochondria; viral evasion; viruses.

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Figures

Figure 1
Figure 1
Eukaryotic cell metabolism. Bioenergetic and biosynthetic pathways interconnect glycolysis, glutaminolysis, PPP (pentose phospahate pathway), TCA (tricarboxylic acid cycle), FAO (fatty acid oxidation), fatty acid synthesis, aminoacid synthesis, metabolic sensors such as the AMPK, mTORC1, and mTORC2 pathways, and are also dependent on calcium homeostasis, mitochondrial membrane potential and mitochondrial dynamics. All together they influence cell function and may be the targets of several viruses.
Figure 2
Figure 2
Antiviral immune responses. Type I interferons, cell cytotoxicity, neutrophil extracellular traps and neutralizing antibodies protect against viral infections, each type of response has a metabolic hallmark. Viruses may target specific metabolic pathways for immune evasion.?, not known.
See this image and copyright information in PMC

References

    1. Akira S., Takeda K. (2004). Toll-like receptor signalling. Nat. Rev. Immunol. 4,499–511. 10.1038/nri1391 - DOI - PubMed
    1. Aldabe R., Irurzun A., Carrasco L. (1997). Poliovirus protein 2BC increase cytosolic free calcium concentrations. J. Virol. 71, 6214–6217. - PMC - PubMed
    1. Arnoult D., Soares F., Tattoli S., Girardin S. E. (2011). Mitochondria in innate immunology. EMBO Rep. 12, 901–910. 10.1038/embor.2011.157 - DOI - PMC - PubMed
    1. Barber D. L., Wherry E. J., Masopust D., Zhu B., Allison J. P., Sharpe A. H., et al. . (2006). Restoring function in exhausted CD8 T cells during chronic viral infection. Nature 439, 682–687. 10.1038/nature04444 - DOI - PubMed
    1. Barber G. N. (2015). STING: infection, inflammation and cancer. Nat. Rev. Immunol. 15, 760–770. 10.1038/nri3921 - DOI - PMC - PubMed

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