Sindbis Virus Infection Alters Blood Feeding Responses and DEET Repellency in Aedes aegypti (Diptera: Culicidae)

2012 ◽  
Vol 49 (2) ◽  
pp. 418-423 ◽  
Author(s):  
Whitney A. Qualls ◽  
Jonathan F. Day ◽  
Rui-De Xue ◽  
Doria F. Bowers
Keyword(s):  
Virus Infection ◽  
Aedes Aegypti ◽  
Sindbis Virus ◽  
Blood Feeding

Confocal Analysis of the Distribution and Persistence of Sindbis Virus (TaV-GFP) Infection in Midguts of Aedes aegypti Mosquitoes

2020 ◽  
Vol 26 (2) ◽  
pp. 267-274
Author(s):  
Jason J. Saredy ◽  
Florence Y. Chim ◽  
Zoë L. Lyski ◽  
Yani P. Ahearn ◽  
Doria F. Bowers
Keyword(s):  
Aedes Aegypti ◽  
Sindbis Virus ◽  
Fluorescent Protein ◽  
Blood Feeding ◽  
Target Tissue ◽  
Secondary Target ◽  
Posterior Midgut ◽  
Infected Cells ◽  
Green Fluorescent ◽  
Global Threat

AbstractBiological transmission of arthropod-borne viruses (arboviruses) to vertebrate hosts by hematophagous insects poses a global threat because such arboviruses can result in a range of serious public health infectious diseases. Sindbis virus (SINV), the prototype Alphavirus, was used to track infections in the posterior midgut (PMG) of Aedes aegypti adult mosquitoes. Females were fed viremic blood containing a virus reporter, SINV [Thosea asigna virus-green fluorescent protein (TaV-GFP)], that leaves a fluorescent signal in infected cells. We assessed whole-mount PMGs to identify primary foci, secondary target tissues, distribution, and virus persistence. Following a viremic blood meal, PMGs were dissected and analyzed at various days of post blood-feeding. We report that virus foci indicated by GFP in midgut epithelial cells resulted in a 9.8% PMG infection and a 10.8% dissemination from these infected guts. The number of virus foci ranged from 1 to 3 per individual PMG and was more prevalent in the PMG-middle > PMG-frontal > PMG-caudal regions. SINV TaV-GFP was first observed in the PMG (primary target tissue) at 3 days post blood-feeding, was sequestered in circumscribed foci, replicated in PMG peristaltic muscles (secondary target tissue) following dissemination, and GFP was observed to persist in PMGs for 30 days postinfection.

scholarly journals Sindbis Virus Infection in Non-Blood-Fed Hibernating Culex pipiens Mosquitoes in Sweden

Viruses ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 1441
Author(s):  
Alexander Bergman ◽  
Emma Dahl ◽  
Åke Lundkvist ◽  
Jenny C. Hesson
Keyword(s):  
Virus Infection ◽  
Culex Pipiens ◽  
Sindbis Virus ◽  
Virus Transmission ◽  
Blood Feeding ◽  
Northern Europe ◽  
Infection Status ◽  
Endemic Region ◽  
Viral Interactions ◽  
Mosquito Ecology

A crucial, but unresolved question concerning mosquito-borne virus transmission is how these viruses can remain endemic in regions where the transmission is halted for long periods of time, due to mosquito inactivity in, e.g., winter. In northern Europe, Sindbis virus (SINV) (genus alphavirus, Togaviridae) is transmitted among birds by Culex mosquitoes during the summer, with occasional symptomatic infections occurring in humans. In winter 2018–19, we sampled hibernating Culex spp females in a SINV endemic region in Sweden and assessed them individually for SINV infection status, blood-feeding status, and species. The results showed that 35 out of the 767 collected mosquitoes were infected by SINV, i.e., an infection rate of 4.6%. The vast majority of the collected mosquitoes had not previously blood-fed (98.4%) and were of the species Cx. pipiens (99.5%). This is the first study of SINV overwintering, and it concludes that SINV can be commonly found in the hibernating Cx. pipiens population in an endemic region in Sweden, and that these mosquitoes become infected through other means besides blood-feeding. Further studies on mosquito ecology and viral interactions are needed to elucidate the mechanisms of the persistence of these viruses over winter.

scholarly journals Aedes aegypti uses RNA interference in defense against Sindbis virus infection

2008 ◽  
Vol 8 (1) ◽  
pp. 47 ◽  
Author(s):  
Corey L Campbell ◽  
Kimberly M Keene ◽  
Douglas E Brackney ◽  
Ken E Olson ◽  
Carol D Blair ◽  
...  
Keyword(s):  
Rna Interference ◽  
Virus Infection ◽  
Aedes Aegypti ◽  
Sindbis Virus

scholarly journals Effects of Manipulating Apoptosis on Sindbis Virus Infection of Aedes aegypti Mosquitoes

2012 ◽  
Vol 86 (12) ◽  
pp. 6546-6554 ◽  
Author(s):  
H. Wang ◽  
T. Gort ◽  
D. L. Boyle ◽  
R. J. Clem
Keyword(s):  
Virus Infection ◽  
Aedes Aegypti ◽  
Sindbis Virus

scholarly journals Temperature modulates innate immunity in Aedes aegypti during chikungunya virus infection

2020 ◽  
Vol 101 ◽  
pp. 489
Author(s):  
B.R. Wimalasiri-Yapa ◽  
F. Frentiu ◽  
L. Stassen ◽  
R. Gumiel
Keyword(s):  
Innate Immunity ◽  
Virus Infection ◽  
Aedes Aegypti ◽  
Chikungunya Virus

scholarly journals Alpha/Beta Interferons Potentiate Virus-Induced Apoptosis through Activation of the FADD/Caspase-8 Death Signaling Pathway

2000 ◽  
Vol 74 (3) ◽  
pp. 1513-1523 ◽  
Author(s):  
Siddharth Balachandran ◽  
P. Christopher Roberts ◽  
Todd Kipperman ◽  
Kapil N. Bhalla ◽  
Richard W. Compans ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Sindbis Virus ◽  
Influenza Virus Infection ◽  
Dominant Negative ◽  
Caspase 8 ◽  
Signaling Complex ◽  
Dependent Protein ◽  
Induced Apoptosis ◽  
Dominant Negative Variant

ABSTRACT Interferon (IFN) mediates its antiviral effects by inducing a number of responsive genes, including the double-stranded RNA (dsRNA)-dependent protein kinase, PKR. Here we report that inducible overexpression of functional PKR in murine fibroblasts sensitized cells to apoptosis induced by influenza virus, while in contrast, cells expressing a dominant-negative variant of PKR were completely resistant. We determined that the mechanism of influenza virus-induced apoptosis involved death signaling through FADD/caspase-8 activation, while other viruses such as vesicular stomatitis virus (VSV) and Sindbis virus (SNV) did not significantly provoke PKR-mediated apoptosis but did induce cytolysis of fibroblasts via activation of caspase-9. Significantly, treatment with IFN-α/β greatly sensitized the fibroblasts to FADD-dependent apoptosis in response to dsRNA treatment or influenza virus infection but completely protected the cells against VSV and SNV replication in the absence of any cellular destruction. The mechanism by which IFN increases the cells' susceptibility to lysis by dsRNA or certain virus infection is by priming cells to FADD-dependent apoptosis, possibly by regulating the activity of the death-induced signaling complex (DISC). Conversely, IFN is also able to prevent the replication of viruses such as VSV that avoid triggering FADD-mediated DISC activity, by noncytopathic mechanisms, thus preventing destruction of the cell.

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