scholarly journals An Early Block in the Replication of the Atypical Bluetongue Virus Serotype 26 in Culicoides Cells Is Determined by Its Capsid Proteins

Viruses ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 919
Author(s):  
Marc Guimerà Busquets ◽  
Gillian D. Pullinger ◽  
Karin E. Darpel ◽  
Lyndsay Cooke ◽  
Stuart Armstrong ◽  
...  
Keyword(s):  
Bluetongue Virus ◽  
Mammalian Cells ◽  
Reverse Genetics ◽  
Reassortant Virus ◽  
Biting Midges ◽  
Potential Barriers ◽  
Virus Serotype ◽  
Vertebrate Hosts ◽  
Viral Determinants ◽  
Culicoides Biting Midges

Arboviruses such as bluetongue virus (BTV) replicate in arthropod vectors involved in their transmission between susceptible vertebrate-hosts. The “classical” BTV strains infect and replicate effectively in cells of their insect-vectors (Culicoides biting-midges), as well as in those of their mammalian-hosts (ruminants). However, in the last decade, some “atypical” BTV strains, belonging to additional serotypes (e.g., BTV-26), have been found to replicate efficiently only in mammalian cells, while their replication is severely restricted in Culicoides cells. Importantly, there is evidence that these atypical BTV are transmitted by direct-contact between their mammalian hosts. Here, the viral determinants and mechanisms restricting viral replication in Culicoides were investigated using a classical BTV-1, an “atypical” BTV-26 and a BTV-1/BTV-26 reassortant virus, derived by reverse genetics. Viruses containing the capsid of BTV-26 showed a reduced ability to attach to Culicoides cells, blocking early steps of the replication cycle, while attachment and replication in mammalian cells was not restricted. The replication of BTV-26 was also severely reduced in other arthropod cells, derived from mosquitoes or ticks. The data presented identifies mechanisms and potential barriers to infection and transmission by the newly emerged “atypical” BTV strains in Culicoides.

scholarly journals Measurement of the Infection and Dissemination of Bluetongue Virus in Culicoides Biting Midges Using a Semi-Quantitative RT-PCR Assay and Isolation of Infectious Virus

PLoS ONE ◽  
2013 ◽  
Vol 8 (8) ◽  
pp. e70800 ◽  
Author(s):  
Eva Veronesi ◽  
Frank Antony ◽  
Simon Gubbins ◽  
Nick Golding ◽  
Alison Blackwell ◽  
...  
Keyword(s):  
Bluetongue Virus ◽  
Infectious Virus ◽  
Rt Pcr ◽  
Pcr Assay ◽  
Biting Midges ◽  
Culicoides Biting Midges

Indoor and outdoor winter activity of Culicoides biting midges, vectors of bluetongue virus, in Italy

2017 ◽  
Vol 32 (1) ◽  
pp. 70-77 ◽  
Author(s):  
A. MAGLIANO ◽  
P. SCARAMOZZINO ◽  
S. RAVAGNAN ◽  
F. MONTARSI ◽  
G. DA ROLD ◽  
...  
Keyword(s):  
Bluetongue Virus ◽  
Biting Midges ◽  
Winter Activity ◽  
Culicoides Biting Midges ◽  
Indoor And Outdoor

scholarly journals The VP3 Protein of Bluetongue Virus Associates with the MAVS Complex and Interferes with the RIG-I-Signaling Pathway

Viruses ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 230
Author(s):  
Marie Pourcelot ◽  
Rayane Amaral Moraes ◽  
Aurore Fablet ◽  
Emmanuel Bréard ◽  
Corinne Sailleau ◽  
...  
Keyword(s):  
Bluetongue Virus ◽  
Type I Interferon ◽  
Type I ◽  
Adapter Protein ◽  
Structural Protein ◽  
Innate Response ◽  
Biting Midges ◽  
Domestic Ruminants ◽  
Infected Cells ◽  
Culicoides Biting Midges

Bluetongue virus (BTV), an arbovirus transmitted by Culicoides biting midges, is a major concern of wild and domestic ruminants. While BTV induces type I interferon (alpha/beta interferon [IFN-α/β]) production in infected cells, several reports have described evasion strategies elaborated by this virus to dampen this intrinsic, innate response. In the present study, we suggest that BTV VP3 is a new viral antagonist of the IFN-β synthesis. Indeed, using split luciferase and coprecipitation assays, we report an interaction between VP3 and both the mitochondrial adapter protein MAVS and the IRF3-kinase IKKε. Overall, this study describes a putative role for the BTV structural protein VP3 in the control of the antiviral response.

DNA barcode identification and molecular detection of bluetongue virus in Culicoides biting midges (Diptera: Ceratopogonidae) from western Thailand

Acta Tropica ◽  
2021 ◽  
pp. 106147
Author(s):  
Yuki Fujisawa ◽  
Thanyaporn Homat ◽  
Arunrat Thepparat ◽  
Tanasak Changbunjong ◽  
Kripitch Sutummaporn ◽  
...  
Keyword(s):  
Bluetongue Virus ◽  
Molecular Detection ◽  
Dna Barcode ◽  
Biting Midges ◽  
Culicoides Biting Midges

scholarly journals Diversity of Transmission Outcomes Following Co-Infection of Sheep with Strains of Bluetongue Virus Serotype 1 and 8

2020 ◽  
Vol 8 (6) ◽  
pp. 851 ◽  
Author(s):  
Eva Veronesi ◽  
Karin Darpel ◽  
Simon Gubbins ◽  
Carrie Batten ◽  
Kyriaki Nomikou ◽  
...  
Keyword(s):  
Bluetongue Virus ◽  
Policy Implications ◽  
Transmission Model ◽  
Biting Midges ◽  
The United Kingdom ◽  
Virus Rna ◽  
Virus Serotype ◽  
Serotype 1 ◽  
Low Passage

Bluetongue virus (BTV) causes an economically important disease, bluetongue (BT), in susceptible ruminants and is transmitted primarily by species of Culicoides biting midges (Diptera: Ceratopogonidae). Since 2006, northern Europe has experienced multiple incursions of BTV through a variety of routes of entry, including major outbreaks of strains of BTV serotype 8 (BTV-8) and BTV serotype 1 (BTV-1), which overlapped in distribution within southern Europe. In this paper, we examined the variation in response to coinfection with strains of BTV-1 and BTV-8 using an in vivo transmission model involving Culicoides sonorensis, low passage virus strains, and sheep sourced in the United Kingdom. In the study, four sheep were simultaneously infected using BTV-8 and BTV-1 intrathoracically inoculated C. sonorensis and co-infections of all sheep with both strains were established. However, there were significant variations in both the initiation and peak levels of virus RNA detected throughout the experiment, as well as in the infection rates in the C. sonorensis that were blood-fed on experimentally infected sheep at peak viremia. This is discussed in relation to the potential for reassortment between these strains in the field and the policy implications for detection of BTV strains.

scholarly journals PB2 Protein of a Highly Pathogenic Avian Influenza Virus Strain A/chicken/Yamaguchi/7/2004 (H5N1) Determines Its Replication Potential in Pigs

2008 ◽  
Vol 83 (4) ◽  
pp. 1572-1578 ◽  
Author(s):  
Rashid Manzoor ◽  
Yoshihiro Sakoda ◽  
Naoki Nomura ◽  
Yoshimi Tsuda ◽  
Hiroichi Ozaki ◽  
...  
Keyword(s):  
Avian Influenza ◽  
Mammalian Cells ◽  
Reverse Genetics ◽  
Single Gene ◽  
Polymerase Activity ◽  
Influenza Viruses ◽  
Upper Respiratory Tract ◽  
Reassortant Virus ◽  
Range Restriction

ABSTRACT It has been shown that not all but most of the avian influenza viruses replicate in the upper respiratory tract of pigs (H. Kida et al., J. Gen. Virol. 75:2183-2188, 1994). It was shown that A/chicken/Yamaguchi/7/2004 (H5N1) [Ck/Yamaguchi/04 (H5N1)] did not replicate in pigs (N. Isoda et al., Arch. Virol. 151:1267-1279, 2006). In the present study, the genetic basis for this host range restriction was determined using reassortant viruses generated between Ck/Yamaguchi/04 (H5N1) and A/swine/Hokkaido/2/1981 (H1N1) [Sw/Hokkaido/81 (H1N1)]. Two in vivo-generated single-gene reassortant virus clones of the H5N1 subtype (virus clones 1 and 2), whose PB2 gene was of Sw/Hokkaido/81 (H1N1) origin and whose remaining seven genes were of Ck/Yamaguchi/04 (H5N1) origin, were recovered from the experimentally infected pigs. The replicative potential of virus clones 1 and 2 was further confirmed by using reassortant virus (rg-Ck-Sw/PB2) generated by reverse genetics. Interestingly, the PB2 gene of Ck/Yamaguchi/04 (H5N1) did not restrict the replication of Sw/Hokkaido/81 (H1N1), as determined by using reassortant virus rg-Sw-Ck/PB2. The rg-Sw-Ck/PB2 virus replicated to moderate levels and for a shorter duration than parental Sw/Hokkaido/81 (H1N1). Sequencing of two isolates recovered from the pigs inoculated with rg-Sw-Ck/PB2 revealed either the D256G or the E627K amino acid substitution in the PB2 proteins of the isolates. The D256G and E627K mutations enhanced viral polymerase activity in the mammalian cells, correlating with replication of virus in pigs. These results indicate that the PB2 protein restricts the growth of Ck/Yamaguchi/04 (H5N1) in pigs.

scholarly journals Retrospective Analysis of the Bluetongue Outbreak in Serbia

2017 ◽  
Vol 40 (1) ◽  
pp. 21-27 ◽  
Author(s):  
Spomenka Djurić ◽  
Predrag Simeunović ◽  
Milorad Mirilović ◽  
Jevrosima Stevanović ◽  
Uroš Glavinić ◽  
...  
Keyword(s):  
Bluetongue Virus ◽  
Control Measure ◽  
Infected Sheep ◽  
Economic Losses ◽  
Biting Midges ◽  
Domestic Ruminants ◽  
Investigation Period ◽  
Bluetongue Disease ◽  
Culicoides Biting Midges ◽  
Veterinary Institute

Abstract Bluetongue, a vector-born disease caused by the Bluetongue virus (BTV) and transmitted by Culicoides biting midges, is considered to be one of the most important diseases of domestic ruminants. The first outbreak of bluetongue in Serbia was reported in 2001, when BTV serotype 9 was identified in sampled materials. In 2014, outbreak of BTV-4 in Serbia caused considerable economic losses affecting sheep, cattle and goats. During this outbreak, BTV-4 was recorded in 644 outbreaks within 49 municipalities, part of 17 administrative regions. From the total number of sheep kept in areas affected by bluetongue (n=1 748 110), 2 083 cases (0.2%) were proven to be BTV-4 infected. Total of 206 infected cattle and 24 infected goats were reported during this investigation period, which represents 0.06% and 0.03% of the total number of cattle and goats kept in affected areas, respectively. The highest incidence of infected sheep, cattle and goats was recorded on the territory covered by veterinary institute of Nis. Recorded lethality in cattle, sheep and goats was 18.45% (n=38), 48.10% (n=1002) and 54.17% (n=13), respectively. The peak of the outbreak was in September and October when 94.43% of the confirmed positive cases, regardless of the species, was recorded. Monitoring of bluetongue disease in Serbia relies on active surveillance programmes aimed at: (i) identification and tracing of susceptible and potentially infected animals and (ii) detection, distribution and prevalence of insect vectors. Vaccination of sheep is planned to be implemented as a control measure against bluetongue in Serbia.

Expression and secretion of Bluetongue virus serotype 8 (BTV-8)VP2 outer capsid protein by mammalian cells

2010 ◽  
Vol 169 (2) ◽  
pp. 420-424 ◽  
Author(s):  
A. Capocefalo ◽  
V. Franceschi ◽  
P.P. Mertens ◽  
J. Castillo-Olivares ◽  
S. Cavirani ◽  
...  
Keyword(s):  
Capsid Protein ◽  
Bluetongue Virus ◽  
Mammalian Cells ◽  
Outer Capsid Protein ◽  
Virus Serotype ◽  
Outer Capsid

scholarly journals VP2 Exchange and NS3/NS3a Deletion in African Horse Sickness Virus (AHSV) in Development of Disabled Infectious Single Animal Vaccine Candidates for AHSV

2015 ◽  
Vol 89 (17) ◽  
pp. 8764-8772 ◽  
Author(s):  
Sandra G. P. van de Water ◽  
René G. P. van Gennip ◽  
Christiaan A. Potgieter ◽  
Isabel M. Wright ◽  
Piet A. van Rijn
Keyword(s):  
Mammalian Cells ◽  
Reverse Genetics ◽  
African Horse Sickness ◽  
African Horse Sickness Virus ◽  
Vaccine Platform ◽  
Biting Midges ◽  
Content Type ◽  
Vp2 Protein ◽  
Single Animal

ABSTRACTAfrican horse sickness virus (AHSV) is a virus species in the genusOrbivirusof the familyReoviridae. There are nine serotypes of AHSV showing different levels of cross neutralization. AHSV is transmitted by species ofCulicoidesbiting midges and causes African horse sickness (AHS) in equids, with a mortality rate of up to 95% in naive horses. AHS has become a serious threat for countries outside Africa, since endemicCulicoidesspecies in moderate climates appear to be competent vectors for the related bluetongue virus (BTV). To control AHS, live-attenuated vaccines (LAVs) are used in Africa. We used reverse genetics to generate “synthetic” reassortants of AHSV for all nine serotypes by exchange of genome segment 2 (Seg-2). This segment encodes VP2, which is the serotype-determining protein and the dominant target for neutralizing antibodies. Single Seg-2 AHSV reassortants showed similar cytopathogenic effects in mammalian cells but displayed different growth kinetics. Reverse genetics for AHSV was also used to study Seg-10 expressing NS3/NS3a proteins. We demonstrated that NS3/NS3a proteins are not essential for AHSV replicationin vitro. NS3/NS3a of AHSV is, however, involved in the cytopathogenic effect in mammalian cells and is very important for virus release from cultured insect cells in particular. Similar to the concept of the bluetongue disabled infectious single animal (BT DISA) vaccine platform, an AHS DISA vaccine platform lacking NS3/NS3a expression was developed. Using exchange of genome segment 2 encoding VP2 protein (Seg-2[VP2]), we will be able to develop AHS DISA vaccine candidates for all current AHSV serotypes.IMPORTANCEAfrican horse sickness virus is transmitted by species ofCulicoidesbiting midges and causes African horse sickness in equids, with a mortality rate of up to 95% in naive horses. African horse sickness has become a serious threat for countries outside Africa, since endemicCulicoidesspecies in moderate climates are supposed to be competent vectors. By using reverse genetics, viruses of all nine serotypes were constructed by the exchange of Seg-2 expressing the serotype-determining VP2 protein. Furthermore, we demonstrated that the nonstructural protein NS3/NS3a is not essential for virus replicationin vitro. However, the potential spread of the virus by biting midges is supposed to be blocked, since thein vitrorelease of the virus was strongly reduced due to this deletion. VP2 exchange and NS3/NS3a deletion in African horse sickness virus were combined in the concept of a disabled infectious single animal vaccine for all nine serotypes.

Sign in / Sign up

Export Citation Format

Share Document