The inhibition mechanism of Wolbachia on mosquito-borne RNA virus replication as seen through lipid metabolism regulation.

Mosquito-borne RNA viruses, including but not limited to the dengue virus (DENV), Zika virus (ZIKV), and chikungunya virus (CHIKV), pose serious threats to global public health. Current countermeasure approaches are frequently plagued by insufficient coverage, susceptibility to drug resistance, and poor sustainability. Wolbachia, a natural symbiont within mosquitoes, has been shown to block the replication and transmission of mosquito-borne RNA viruses. In recent years, increasing attention has focused on the mechanism of its antiviral action, which involves the regulation of host lipid metabolism. Here, we systematically reviewed the mechanisms by which mosquito-borne RNA viruses disrupt normal lipid metabolism in host cells, elucidating how these viruses rely on host lipids to achieve invasion and form replication complexes. Multiple pathways of Wolbachia disrupting lipid metabolism are highlighted, including rearranging the host lipid environment, competing with viruses for key metabolic resources, regulating mitochondrial-lipid droplet interactions, and altering membrane fluidity. The translational medicine and public health applications of Wolbachia strains were explored, holding potential for advancing novel antiviral strategies based on metabolic disruption.