Abstract
Aedes aegypti is the primary vector of several medically relevant arboviruses including dengue virus (DENV) types 1–4. Ae. aegypti transmits DENV by inoculating virus-infected saliva into host skin during probing and feeding. Ae. aegypti saliva contains over one hundred unique proteins and these proteins have diverse functions, including facilitating blood feeding. Previously, we showed that Ae. aegypti salivary gland extracts (SGEs) enhanced dissemination of DENV to draining lymph nodes. In contrast, HPLC-fractionation revealed that some SGE components inhibited infection. Here, we show that D7 proteins are enriched in HPLC fractions that are inhibitory to DENV infection, and that recombinant D7 protein can inhibit DENV infection in vitro and in vivo. Further, binding assays indicate that D7 protein can directly interact with DENV virions and recombinant DENV envelope protein. These data reveal a novel role for D7 proteins, which inhibits arbovirus transmission to vertebrates through a direct interaction with virions.
Highlights
Dengue virus (DENV) is a mosquito-borne arbovirus that is transmitted primarily by the species Aedes aegypti
Previous data suggests that antibodies against D7 protein from Culex spp. can increase West Nile virus infection
We show that recombinant Ae. aegypti D7 protein can inhibit DENV infection in vitro and in vivo, and that D7 can bind to DENV virions
Summary
Dengue virus (DENV) is a mosquito-borne arbovirus that is transmitted primarily by the species Aedes aegypti. Conventional vaccines are in development and regulatory approval has been granted in a few countries. Development of a conventional DENV vaccine has been difficult due to the co-circulation of four serotypes [3, 4]. It is critical that conventional vaccines elicit robust antibody titers to avoid antibody-dependent enhancement, which occurs during a sub-neutralizing response. It is theoretically possible to target mosquito saliva or midgut proteins to block either transmission or acquisition of DENV [3, 5, 6]. This strategy would not be subject to antibody-dependent enhancement or viral genetic drift
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