Fig. 2

Aedes mosquito–microbiota–arbovirus interactions may modulate vectorial competence. Some viral regulatory strategies include the following: Modulation of physical barriers in midgut epithelial cells (MEC). Serratia marcescens by releasing Sm enhancin protein and the fungus Talaromyces by suppressing the expression of digestive enzymes (trypsin) in the midgut of Aedes can promote susceptibility to DENV infection. Activation of immune response signaling pathways and release of antipathogenic components. Wolbachia in the presence of arboviruses can induce antimicrobial peptides (AMP), melanization, and the production of reactive oxygen species (ROS), among others, that restrict arboviral activity. Release of antipathogenic compounds. Chromobacterium sp. Panama (Csp_P), by degrading the arbovirus coat protein, limits the replication of DENV and ZIKV, while Serratia odorifera participates in the interaction between P40 polypeptide and prohibitin, proteins associated with DENV and CHIKV infection in Aedes. Red boxes indicate interactions that increase vector competence (susceptibility to virus infection). Blue boxes indicate interactions that decrease vector competence (resistance to virus infection). CHIKV chikungunya virus, ZIKV Zika virus, DENV dengue virus, ROS reactive oxygen species, AMP antimicrobial peptides, miRNA microRNA, MEC midgut epithelial cells, P40 polyvinentide P40, Pr prohibitin. Figure created with BioRender.com