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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Human Cytomegalovirus: Coordinating Cellular Stress, Signaling, and Metabolic Pathways
Thomas Shenk1, James C Alwine2
1Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544.
Abstract:
Viruses face a multitude of challenges when they infect a host cell. Cells have evolved innate defenses to protect against pathogens, and an infecting virus may induce a stress response that antagonizes viral replication. Further, the metabolic, oxidative, and cell cycle state may not be conducive to the viral infection. But viruses are fabulous manipulators, inducing host cells to use their own characteristic mechanisms and pathways to provide what the virus needs. This article centers on the manipulation of host cell metabolism by human cytomegalovirus (HCMV). We review the features of the metabolic program instituted by the virus, discuss the mechanisms underlying these dramatic metabolic changes, and consider how the altered program creates a synthetic milieu that favors efficient HCMV replication and spread.
Insights
Human cytomegalovirus (HCMV) expertly manipulates host cell metabolism to overcome cellular defenses. This reprogramming creates an optimal environment for viral replication and spread.
Area of Science:
- Virology
- Cell Biology
- Metabolic Engineering
Background:
- Host cells possess innate defenses against viral infections.
- Viruses must overcome cellular stress and metabolic states unfavorable for replication.
- Viruses are adept at hijacking host cell machinery.
Purpose of the Study:
- To review the metabolic reprogramming induced by human cytomegalovirus (HCMV).
- To discuss the mechanisms driving these metabolic alterations.
- To explore how HCMV-induced metabolic changes favor viral replication and spread.
Main Methods:
- Review of existing literature on HCMV and host cell metabolism.
- Analysis of viral strategies for manipulating host metabolic pathways.
- Discussion of the interplay between viral infection and cellular metabolic state.
Main Results:
- HCMV institutes a distinct metabolic program within infected host cells.
- Specific mechanisms employed by HCMV to alter host metabolism are identified.
- The altered metabolic milieu created by HCMV is conducive to efficient viral replication.
Conclusions:
- HCMV effectively manipulates host cell metabolism to its advantage.
- Understanding these metabolic alterations is key to comprehending HCMV pathogenesis.
- Targeting HCMV-induced metabolic changes may offer therapeutic strategies.
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