Big news in flavivirus research! A new iScience study, led by Laurent Chatel-Chaix’s team, reveals how dengue (DENV) and Zika (ZIKV) viruses orchestrate a sophisticated cellular hijacking (1). These viruses alter the communication between the cell’s power plant, the mitochondria, and its factory, the endoplasmic reticulum (ER).
The key? They disrupt almost half of ER-mitochondria contact sites (ERMC) – think of ERMC as the powerlines for communication between the two organelles. It’s like these viruses are rewiring the cell to steal its ATP (the cell’s energy), leaving essential functions in the dark while powering their own replication rave. Key ERMC tethering complexes, including RRBP1 and SYNJ2BP proteins, are supposed to keep the power flowing smoothly, but both DENV and ZIKV are disrupting their expressions in the infected cell, thus interfering with the mitochondrial respiratory metabolism. In doing so, not only these viruses hijack host cells by redirecting energy and metabolism to synthesize viral components, but they also suppress the induction of apoptosis, consequently ensuring extended replication and spread.
The bright side in all this: we’ve found their weakness! Unraveling a new specific mechanism of action means a potential new target to develop prevention or curative strategies. The next step would be to investigate if the same disruption occurs in vivo.
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