Wolbachia is an endosymbiotic bacterium present in a broad range of arthropod hosts, including Aedes mosquitoes, that has been used in vector control strategies to reduce arbovirus transmission. Zika virus, a flavivirus transmitted by Aedes mosquitoes, can cause severe neurological complications in adults and microcephaly in newborns. While Wolbachia is known to restrict ZIKV within mosquitoes, the molecular mechanisms underlying its antiviral effects remain to be fully characterized. Previous studies have associated both ZIKV replication and Wolbachia density with autophagy. This study hypothesizes that Wolbachia proteins modulate host autophagy, thereby restricting ZIKV replication. To investigate this, bacterial proteins associated with the host autophagosomal marker ATG8 were identified in Aedes albopictus (C6/36) cells. The impact of inhibiting these bacterial proteins on ZIKV replication was assessed by suppressing their expression in Wolbachia-positive cell lines using nucleic acid inhibitors. Inhibition of bacterial proteins, including outer membrane proteins, porins, and protein kinases, reduced Wolbachia-mediated protection and increased ZIKV infection in Wolbachia-positive cells. To evaluate whether specific bacterial proteins confer cellular resistance to ZIKV in mammalian cell lines, Wolbachia genes of interest were transfected into VERO and HEK293T cells. Expression of proteins in mammalian cells prior to viral infection resulted in a significant reduction in ZIKV. These findings indicate that autophagy-related Wolbachia proteins contribute to the restriction of ZIKV in mosquito cells and in mammalian cells. These results provide insight into the mechanisms of Wolbachia-mediated inhibition of arboviruses in Aedes mosquitoes and underscore the potential of Wolbachia proteins as preventive, therapeutic, or vector-control agents.