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The Warburg effect refers to a metabolic state in which cells preferentially use aerobic glycolysis rather than oxidative phosphorylation to generate ATP and macromolecules. A number of chronic inflammatory conditions are characterized by host cells that adopt a sustained, pathological Warburg-like metabolism. In cancer, previously healthy cells shift into a Warburg state centered on rapid energy production and increased cell proliferation that drives tumor formation. Macrophage in atherosclerotic plaque and in sarcoidosis granuloma can also harbor a Warburg-like phenotype that promotes an inflammatory milieu. The question of why host cells in patients with cancer and other chronic inflammatory conditions adapt a pathological Warburg-like metabolism is a matter of debate. This review/hypothesis piece explores how intracellular infection can contribute to this Warburg metabolism or related pathological metabolic states. We detail molecular mechanisms by which viral, bacterial, and protozoan intracellular pathogens can induce, or contribute to, a Warburg-like metabolism in infected host cells in order to meet their own replication and nutritional needs. We also discuss how host defense towards infection may impact cellular metabolic changes. We then provide examples of how many of these same intracellular pathogens have been identified in tumors, atherosclerotic lesions, granuloma, and other tissues containing cells with a Warburg or altered metabolism. Last, we examine further trends associated with infection and host cell metabolism, including how pathogen-driven hijacking of host cell lipid metabolism can support viral, bacterial, and parasite survival and replication.

Pathogens Hijack Host Cell Metabolism: Intracellular Infection as a Driver of the Warburg Effect in Cancer and Other Chronic Inflammatory Conditions