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 Wolbachia prevalence in the vector species Culex pipiens and Culex torrentium in a Sindbis virus-endemic region of Sweden

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Alexander Bergman ◽  
Jenny C. Hesson
Keyword(s):  
Culex Pipiens ◽  
Sindbis Virus ◽  
Vector Competence ◽  
Horizontal Transmission ◽  
Vector Species ◽  
Endemic Region ◽  
Species Determination ◽  
Terrestrial Arthropods ◽  
Endosymbiotic Bacteria ◽  
Vector Borne

Abstract Background Wolbachia pipientis are endosymbiotic bacteria present in a large proportion of terrestrial arthropods. The species is known to sometimes affect the ability of its host to transmit vector-borne pathogens. Central Sweden is endemic for Sindbis virus (SINV), where it is mainly transmitted by the vector species Culex pipiens and Culex torrentium, with the latter established as the main vector. In this study we investigated the Wolbachia prevalence in these two vector species in a region highly endemic for SINV. Methods Culex mosquitoes were collected using CDC light traps baited with carbon dioxide over 9 years at 50 collection sites across the River Dalälven floodplains in central Sweden. Mosquito genus was determined morphologically, while a molecular method was used for reliable species determination. The presence of Wolbachia was determined through PCR using general primers targeting the wsp gene and sequencing of selected samples. Results In total, 676 Cx. pipiens and 293 Cx. torrentium were tested for Wolbachia. The prevalence of Wolbachia in Cx. pipiens was 97% (95% CI 94.8–97.6%), while only 0.7% (95% CI 0.19–2.45%) in Cx. torrentium. The two Cx. torrentium mosquitoes that were infected with Wolbachia carried different types of the bacteria. Conclusions The main vector of SINV in the investigated endemic region, Cx. torrentium, was seldom infected with Wolbachia, while it was highly prevalent in the secondary vector, Cx. pipiens. The presence of Wolbachia could potentially have an impact on the vector competence of these two species. Furthermore, the detection of Wolbachia in Cx. torrentium could indicate horizontal transmission of the endosymbiont between arthropods of different species. Graphical abstract

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

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.

scholarly journals Age-Dependent Resistance to Lethal Alphavirus Encephalitis in Mice: Analysis of Gene Expression in the Central Nervous System and Identification of a Novel Interferon-Inducible Protective Gene, Mouse ISG12

2002 ◽  
Vol 76 (22) ◽  
pp. 11688-11703 ◽  
Author(s):  
Lucia Labrada ◽  
Xiao Huan Liang ◽  
Wei Zheng ◽  
Christine Johnston ◽  
Beth Levine
Keyword(s):  
Gene Expression ◽  
Central Nervous System ◽  
Nervous System ◽  
Virus Infection ◽  
Sindbis Virus ◽  
Expressed Sequence Tag ◽  
Severe Disease ◽  
Altered Expression ◽  
Age Dependent ◽  
Old Mice

ABSTRACT Several different mammalian neurotropic viruses produce an age-dependent encephalitis characterized by more severe disease in younger hosts. To elucidate potential factors that contribute to age-dependent resistance to lethal viral encephalitis, we compared central nervous system (CNS) gene expression in neonatal and weanling mice that were either mock infected or infected intracerebrally with a recombinant strain, dsTE12Q, of the prototype alphavirus Sindbis virus. In 1-day-old mice, infection with dsTE12Q resulted in rapidly fatal disease associated with high CNS viral titers and extensive CNS apoptosis, whereas in 4-week-old mice, dsTE12Q infection resulted in asymptomatic infection with lower CNS virus titers and undetectable CNS apoptosis. GeneChip expression comparisons of mock-infected neonatal and weanling mouse brains revealed developmental regulation of the mRNA expression of numerous genes, including some apoptosis regulatory genes, such as the proapoptotic molecules caspase-3 and TRAF4, which are downregulated during development, and the neuroprotective chemokine, fractalkine, which is upregulated during postnatal development. In parallel with increased neurovirulence and increased viral replication, Sindbis virus infection in 1-day-old mice resulted in both a greater number of host inflammatory genes with altered expression and greater changes in levels of host inflammatory gene expression than infection in 4-week-old mice. Only one inflammatory response gene, an expressed sequence tag similar to human ISG12, increased by a greater magnitude in infected 4-week-old mouse brains than in infected 1-day-old mouse brains. Furthermore, we found that enforced neuronal ISG12 expression results in a significant delay in Sindbis virus-induced death in neonatal mice. Together, our data identify genes that are developmentally regulated in the CNS and genes that are differentially regulated in the brains of different aged mice in response to Sindbis virus infection.

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