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Tytuł pozycji:

Spondweni virus causes fetal harm in Ifnar1 -/- mice and is transmitted by Aedes aegypti mosquitoes.

Tytuł:
Spondweni virus causes fetal harm in Ifnar1 mice and is transmitted by Aedes aegypti mosquitoes.
Autorzy:
Jaeger AS; Department of Veterinary and Biomedical Sciences, University of Minnesota, Twin Cities, United States.
Weiler AM; Wisconsin National Primate Research Center, University of Wisconsin-Madison, United States.
Moriarty RV; Wisconsin National Primate Research Center, University of Wisconsin-Madison, United States.
Rybarczyk S; Wisconsin National Primate Research Center, University of Wisconsin-Madison, United States.
O'Connor SL; Wisconsin National Primate Research Center, University of Wisconsin-Madison, United States; Department of Pathology and Laboratory Medicine, University of Wisconsin-Madison, United States.
O'Connor DH; Wisconsin National Primate Research Center, University of Wisconsin-Madison, United States; Department of Pathology and Laboratory Medicine, University of Wisconsin-Madison, United States.
Seelig DM; Department of Veterinary Clinical Sciences, University of Minnesota, Twin Cities, United States.
Fritsch MK; Department of Pathology and Laboratory Medicine, University of Wisconsin-Madison, United States.
Friedrich TC; Wisconsin National Primate Research Center, University of Wisconsin-Madison, United States; Department of Pathobiological Sciences, University of Wisconsin-Madison, United States.
Aliota MT; Department of Veterinary and Biomedical Sciences, University of Minnesota, Twin Cities, United States. Electronic address: .
Źródło:
Virology [Virology] 2020 Aug; Vol. 547, pp. 35-46. Date of Electronic Publication: 2020 May 24.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Original Publication: New York, Academic Press.
MeSH Terms:
Aedes/*virology
Flavivirus/*physiology
Flavivirus Infections/*virology
Mosquito Vectors/*virology
Receptor, Interferon alpha-beta/*genetics
Aedes/physiology ; Animals ; Disease Models, Animal ; Female ; Flavivirus/genetics ; Flavivirus Infections/genetics ; Flavivirus Infections/metabolism ; Flavivirus Infections/mortality ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mosquito Vectors/physiology ; Receptor, Interferon alpha-beta/deficiency
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Grant Information:
P51 OD011106 United States OD NIH HHS; R01 AI132563 United States AI NIAID NIH HHS; R21 AI131454 United States AI NIAID NIH HHS; T32 AI083196 United States AI NIAID NIH HHS
Contributed Indexing:
Keywords: Aedes aegypti; Arbovirus; Congenital zika syndrome; Flavivirus; Spondweni virus; Vector competence; Zika virus
Substance Nomenclature:
0 (Ifnar1 protein, mouse)
156986-95-7 (Receptor, Interferon alpha-beta)
Entry Date(s):
Date Created: 20200621 Date Completed: 20210205 Latest Revision: 20240328
Update Code:
20240329
PubMed Central ID:
PMC7246013
DOI:
10.1016/j.virol.2020.05.005
PMID:
32560903
Czasopismo naukowe
Spondweni virus (SPONV) is the most closely related known flavivirus to Zika virus (ZIKV). Its pathogenic potential and vector specificity have not been well defined. SPONV has been found predominantly in Africa, but was recently detected in a pool of Culex quinquefasciatus mosquitoes in Haiti. Here we show that SPONV can cause significant fetal harm, including demise, comparable to ZIKV, in a mouse model of vertical transmission. Following maternal inoculation, we detected infectious SPONV in placentas and fetuses, along with significant fetal and placental histopathology, together suggesting vertical transmission. To test vector competence, we exposed Aedes aegypti and Culex quinquefasciatus mosquitoes to SPONV-infected bloodmeals. Aedes aegypti could efficiently transmit SPONV, whereas Culex quinquefasciatus could not. Our results suggest that SPONV has the same features that made ZIKV a public health risk.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.)

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