Votre navigateur est trop ancien pour afficher correctement ce site. Ceci en est la version simplifiée.




Dengue virus (DENV) transmission is initiated when a blood-feeding Aedes (Ae) aegypti mosquito injects saliva, together with the virus, into the epidermis of its mammalian host. Studies of DENV should, therefore, take into account the triad virus-vector-vertebrate host. We have used functional genomic and proteomic analyses, of the salivary glands of female Ae. Aegypti, to demonstrate that this compartment harbors a potent immune response against DENV, represented by the production of an antimicrobial peptide (AMP). This AMP was found to exert, in addition to its anti-bacterial activity, an anti-viral activity against DENV and Chikungunya. Our data demonstrate, for the first time, the permissiveness of human epidermal keratinocytes to DENV infection. Remarkably, DENV replication in keratinocytes contributes to the establishment of anti-viral innate immunity that might occur shortly after the mosquito bite. To investigate the role of Ae. aegypti saliva in DENV transmission to man, primary human keratinocytes were infected with DENV in the presence of Ae. aegypti salivary gland extract. We show that Ae. aegypti saliva enhances dengue virus infection of human keratinocytes by suppressing innate immune responses. Furthermore, we have found a 34-kDa protein, in the saliva of Ae.aegypti, that strongly enhances DENV replication by suppressing type-I IFN production. This study provides new insights into the role of Ae. aegypti salivary glands and saliva in DENV transmission. The data presented here provide novel targets for the control of DENV replication in mammalian hosts.

Key words: Aedes aegypti, dengue, saliva proteins, keratinocytes, innate immune, 34kDa, antimicrobial peptides.