Pingen, M, Bryden, SB, Pondeville, E et al. (6 more authors) (2016) Host Inflammatory Response to Mosquito Bites Enhances the Severity of Arbovirus Infection. Immunity, 44 (6). pp. 1455-1469. ISSN 1074-7613
Abstract
Aedes aegypti mosquitoes are responsible for trans- mitting many medically important viruses such as those that cause Zika and dengue. The inoculation of viruses into mosquito bite sites is an important and common stage of all mosquito-borne virus infec- tions. We show, using Semliki Forest virus and Bunyamwera virus, that these viruses use this inflam- matory niche to aid their replication and dissemina- tion in vivo. Mosquito bites were characterized by an edema that retained virus at the inoculation site and an inflammatory influx of neutrophils that coordi- nated a localized innate immune program that inad- vertently facilitated virus infection by encouraging the entry and infection of virus-permissive myeloid cells. Neutrophil depletion and therapeutic blockade of inflammasome activity suppressed inflammation and abrogated the ability of the bite to promote infec- tion. This study identifies facets of mosquito bite inflammation that are important determinants of the subsequent systemic course and clinical outcome of virus infection.
Metadata
Item Type: | Article |
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Authors/Creators: |
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Copyright, Publisher and Additional Information: | © 2016 The Author(s). Published by Elsevier. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/). |
Keywords: | Inflammation; Virology; Infectious disease; Mosquitoes; Chemokine; Skin |
Dates: |
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Institution: | The University of Leeds |
Academic Units: | The University of Leeds > Faculty of Medicine and Health (Leeds) > School of Medicine (Leeds) > Leeds Institute of Cancer and Pathology (LICAP) > Oncology and Cancer Research - Labs (Leeds) |
Depositing User: | Symplectic Publications |
Date Deposited: | 23 Jun 2016 13:45 |
Last Modified: | 23 Jun 2016 13:47 |
Published Version: | http://dx.doi.org/10.1016/j.immuni.2016.06.002 |
Status: | Published |
Publisher: | Elsevier (Cell Press) |
Identification Number: | 10.1016/j.immuni.2016.06.002 |
Open Archives Initiative ID (OAI ID): | oai:eprints.whiterose.ac.uk:101334 |