Abstract

Inter-host transmission of pathogenic arboviruses such as dengue virus (DENV) and Zika virus (ZIKV) requires systemic infection of the mosquito vector. Successful systemic infection requires initial viral entry and proliferation in the midgut cells of the mosquito followed by dissemination to secondary tissues and eventual entry into salivary glands1. Lack of arbovirus proliferation in midgut cells has been observed in several Aedes aegypti strains2, but the midgut antiviral responses underlying this phenomenon are not yet fully understood. We report here that there is a rapid induction of apoptosis (RIA) in the Aedes aegypti midgut epithelium within 2 hours of infection with DENV-2 or ZIKV in both in vivo blood-feeding and ex vivo midgut infection models. Inhibition of RIA led to increased virus proliferation in the midgut, implicating RIA as an innate immune mechanism mediating midgut infection in this mosquito vector.

Highlights

  • Inter-host transmission of pathogenic arboviruses such as dengue virus (DENV) and Zika virus (ZIKV) requires systemic infection of the mosquito vector

  • The present study explores whether this rapid induction of apoptosis (RIA) response and its limiting effect occurs in vector mosquitoes infected with medically relevant Flaviviruses

  • Using adult female Orlando (ORL) strain A. aegypti, we assayed for signs of apoptosis following exposure to a naive blood meal or a blood meal containing either DENV-2 NGC (DENV serotype 2 New Guinea C strain) or ZIKV-PR

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Summary

Introduction

Inter-host transmission of pathogenic arboviruses such as dengue virus (DENV) and Zika virus (ZIKV) requires systemic infection of the mosquito vector. Previous work on apoptosis following viral infection in the adult mosquito midgut has focused on 24+ hours post infection (hpi)[16,17,18,19,20,21,22,23,24].

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