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Zika virus (ZIKV) is transmitted primarily to humans through Aedes mosquitoes. In the vector, infection does not lead to adverse health effects, whereas the virus can cause various symptoms
and induce apoptotic cell death in humans. Thaker et al. investigated the underlying mechanism of the differential effects and showed that infection of human foreskin fibroblasts increased
glucose utilization in the tricarboxylic acid cycle. By contrast, in mosquito cells, the virus increased glucose use in the pentose phosphate pathway. Infection resulted in increased AMP:ATP
ratios in human cells, an effect that was not seen in mosquito cells. The change in nucleotide levels in infected human cells led to the activation of AMP-activated protein kinase-mediated
signalling, which promotes apoptosis and cell death. The findings suggest that ZIKA differentially reprogrammes glucose metabolism in humans and mosquitoes, which affects host cell death and
survival.
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