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. 2018 Feb 15;14(2):e1006853. doi: 10.1371/journal.ppat.1006853

Fig 10. DENV infection perturbs cellular energy production from lipids.

Fig 10

The schematic shows the carnitine shuttle translocating fatty acyl-CoA from the cytosol into the mitochondrial matrix for fatty acid degradation (β-oxidation) and two hypotheses (I and II) to explain the accumulation of medium-chain length acyl-carnitines and the diversion of FA-CoAs during DENV infection. Hypothesis I represents a pathway where an accumulation of acyl-carnitines is observed because β-oxidation in the mitochondria is inhibited or blocked by infection. Hypothesis II represents a pathway that leads to mitochondrial overload during infection due to increased energetic demands. Abbreviations: CPTI, carnitine palmitoyl transferase I; CPTII, carnitine palmitoyl transferase II; and FA-CoA, fatty acyl-CoA. Red arrows represent the hypothesized flow of intermediates occurring during infection.