The Experts below are selected from a list of 291 Experts worldwide ranked by ideXlab platform
P.a. Van Rijn - One of the best experts on this subject based on the ideXlab platform.
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African Horse Sickness Virus
Reference Module in Life Sciences, 2019Co-Authors: P.a. Van RijnAbstract:African Horse Sickness is an infectious, non-contagious, arthropod-borne disease of Equidae caused by African Horse Sickness virus transmitted by biting culicoides midges. African Horse Sickness is endemic in Africa but outbreaks outside the African continent have been reported. The disease is characterized by changes in respiratory and circulatory functions and exhibits different forms. The mortality is >90% for naive domestic Horses. In contrast, infected zebra and African donkey display mild or no clinical signs and a mortality of 5%–10%. Nine serotypes of African Horse Sickness virus have been recognized showing no or poor cross-protection with each other.
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requirements and comparative analysis of reverse genetics for bluetongue virus btv and African Horse Sickness virus ahsv
Virology Journal, 2016Co-Authors: P.a. Van Rijn, Sandra G P Van De Water, Femke Feenstra, Rene G P Van GennipAbstract:Background Bluetongue virus (BTV) and African Horse Sickness virus (AHSV) are distinct arthropod borne virus species in the genus Orbivirus (Reoviridae family), causing the notifiable diseases Bluetongue and African Horse Sickness of ruminants and equids, respectively. Reverse genetics systems for these orbiviruses with their ten-segmented genome of double stranded RNA have been developed. Initially, two subsequent transfections of in vitro synthesized capped run-off RNA transcripts resulted in the recovery of BTV. Reverse genetics has been improved by transfection of expression plasmids followed by transfection of ten RNA transcripts. Recovery of AHSV was further improved by use of expression plasmids containing optimized open reading frames.
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vp2 exchange and ns3 ns3a deletion in African Horse Sickness virus ahsv in development of disabled infectious single animal vaccine candidates for ahsv
Journal of Virology, 2015Co-Authors: Sandra G P Van De Water, P.a. Van Rijn, Christiaan A Potgieter, Rene G P Van Gennip, Isabel M WrightAbstract:African Horse Sickness virus (AHSV) is a virus species in the genus Orbivirus of the family Reoviridae. There are nine serotypes of AHSV showing different levels of cross neutralization. AHSV is transmitted by species of Culicoides biting 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 endemic Culicoides species 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 replication in 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. IMPORTANCE African Horse Sickness virus is transmitted by species of Culicoides biting 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 endemic Culicoides species 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 replication in vitro. However, the potential spread of the virus by biting midges is supposed to be blocked, since the in vitro release 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.
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VP2 Exchange and NS3/NS3a Deletion in African Horse Sickness Virus (AHSV) in Development of Disabled Infectious Single Animal Vaccine Candidates for AHSV.
Journal of Virology, 2015Co-Authors: Sandra G P Van De Water, Christiaan A Potgieter, Rene G P Van Gennip, Isabel M Wright, P.a. Van RijnAbstract:African Horse Sickness virus (AHSV) is a virus species in the genus Orbivirus of the family Reoviridae. There are nine serotypes of AHSV showing different levels of cross neutralization. AHSV is transmitted by species of Culicoides biting 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 endemic Culicoides species 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 replication in 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. IMPORTANCE African Horse Sickness virus is transmitted by species of Culicoides biting 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 endemic Culicoides species 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 replication in vitro. However, the potential spread of the virus by biting midges is supposed to be blocked, since the in vitro release 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.
Philip Scott Mellor - One of the best experts on this subject based on the ideXlab platform.
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African Horse Sickness - African Horse Sickness.
Veterinary Research, 2020Co-Authors: Philip Scott Mellor, Christopher HamblinAbstract:African Horse Sickness virus (AHSV) causes a non-contagious, infectious insect-borne disease of equids and is endemic in many areas of sub-Saharan Africa and possibly Yemen in the Arabian Peninsula. However, periodically the virus makes excursions beyond its endemic areas and has at times extended as far as India and Pakistan in the east and Spain and Portugal in the west. The vectors are certain species of Culicoides biting midge the most important of which is the Afro-Asiatic species C. imicola. This paper describes the effects that AHSV has on its equid hosts, aspects of its epidemiology, and present and future prospects for control. The distribution of AHSV seems to be governed by a number of factors including the efficiency of control measures, the presence or absence of a long term vertebrate reservoir and, most importantly, the prevalence and seasonal incidence of the major vector which is controlled by climate. However, with the advent of climate-change the major vector, C. imicola, has now significantly extended its range northwards to include much of Portugal, Spain, Italy and Greece and has even been recorded from southern Switzerland. Furthermore, in many of these new locations the insect is present and active throughout the entire year. With the related bluetongue virus, which utilises the same vector species of Culicoides this has, since 1998, precipitated the worst outbreaks of bluetongue disease ever recorded with the virus extending further north in Europe than ever before and apparently becoming endemic in that continent. The prospects for similar changes in the epidemiology and distribution of AHSV are discussed.
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African Horse Sickness Viruses
Encyclopedia of Virology, 2020Co-Authors: Philip Scott Mellor, Peter P. C. MertensAbstract:African Horse Sickness virus (AHSV) is a dsRNA virus in the genus Orbivirus in the family Reoviridae. To date nine distinct serotypes of the virus have been identified. The vertebrate hosts are species of equid, although dogs may also occasionally be infected. Horses are severely affected and in naive populations, the virus causes a disease of major international significance with mortality rates frequently exceeding 90%. AHSV is enzootic in many areas of sub-Saharan Africa and possibly Yemen. However, periodically it makes major and rapid excursions beyond its enzootic areas, and has at times extended as far as the Indian subcontinent in the east and Spain and Portugal in the west but so far has failed to establish itself permanently in such locations. The virus replicates in and is transmitted between its equid hosts by insect vectors which are species of Culicoides biting midge. The most important of these is the Afro-Asiatic midge, Culicoides imicola which has recently been expanding its range northward in response to climate change. Control of AHSV relies upon accurate laboratory diagnosis, restrictions in animal movements from infected areas, vector control, and vaccination.
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African Horse Sickness virus history transmission and current status
Annual Review of Entomology, 2017Co-Authors: Simon Carpenter, Philip Scott Mellor, Assane Gueye Fall, Claire Garros, Gert J. VenterAbstract:African Horse Sickness virus (AHSV) is a lethal arbovirus of equids that is transmitted between hosts primarily by biting midges of the genus Culicoides (Diptera: Ceratopogonidae). AHSV affects draft, thoroughbred, and companion Horses and donkeys in Africa, Asia, and Europe. In this review, we examine the impact of AHSV critically and discuss entomological studies that have been conducted to improve understanding of its epidemiology and control. The transmission of AHSV remains a major research focus and we critically review studies that have implicated both Culicoides and other blood-feeding arthropods in this process. We explore AHSV both as an epidemic pathogen and within its endemic range as a barrier to development, an area of interest that has been underrepresented in studies of the virus to date. By discussing AHSV transmission in the African republics of South Africa and Senegal, we provide a more balanced view of the virus as a threat to equids in a diverse range of settings, thus leading to a d...
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adaptive strategies of African Horse Sickness virus to facilitate vector transmission
Veterinary Research, 2009Co-Authors: Anthony J Wilson, Philip Scott Mellor, Camille Szmaragd, Peter P. C. MertensAbstract:African Horse Sickness virus (AHSV) is an orbivirus that is usually transmitted between its equid hosts by adult Culicoides midges. In this article, we review the ways in which AHSV may have adapted to this mode of transmission. The AHSV particle can be modified by the pH or proteolytic enzymes of its immediate environment, altering its ability to infect different cell types. The degree of pathogenesis in the host and vector may also represent adaptations maximising the likelihood of successful vectorial transmission. However, speculation upon several adaptations for vectorial transmission is based upon research on related viruses such as bluetongue virus (BTV), and further direct studies of AHSV are required in order to improve our understanding of this important virus.
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African Horse Sickness
Veterinary Research, 2004Co-Authors: Philip Scott Mellor, Christopher HamblinAbstract:African Horse Sickness virus (AHSV) causes a non-contagious, infectious insect-borne disease of equids and is endemic in many areas of sub-Saharan Africa and possibly Yemen in the Arabian Peninsula. However, periodically the virus makes excursions beyond its endemic areas and has at times extended as far as India and Pakistan in the east and Spain and Portugal in the west. The vectors are certain species of Culicoides biting midge the most important of which is the Afro- Asiatic species C. imicola. This paper describes the effects that AHSV has on its equid hosts, aspects of its epidemiology, and present and future prospects for control. The distribution of AHSV seems to be governed by a number of factors including the efficiency of control measures, the presence or absence of a long term vertebrate reservoir and, most importantly, the prevalence and seasonal incidence of the major vector which is controlled by climate. However, with the advent of climatechange the major vector, C. imicola, has now significantly extended its range northwards to include much of Portugal, Spain, Italy and Greece and has even been recorded from southern Switzerland. Furthermore, in many of these new locations the insect is present and active throughout the entire year. With the related bluetongue virus, which utilises the same vector species of Culicoides this has, since 1998, precipitated the worst outbreaks of bluetongue disease ever recorded with the virus extending further north in Europe than ever before and apparently becoming endemic in that continent. The prospects for similar changes in the epidemiology and distribution of AHSV are discussed.
Sandra G P Van De Water - One of the best experts on this subject based on the ideXlab platform.
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requirements and comparative analysis of reverse genetics for bluetongue virus btv and African Horse Sickness virus ahsv
Virology Journal, 2016Co-Authors: P.a. Van Rijn, Sandra G P Van De Water, Femke Feenstra, Rene G P Van GennipAbstract:Background Bluetongue virus (BTV) and African Horse Sickness virus (AHSV) are distinct arthropod borne virus species in the genus Orbivirus (Reoviridae family), causing the notifiable diseases Bluetongue and African Horse Sickness of ruminants and equids, respectively. Reverse genetics systems for these orbiviruses with their ten-segmented genome of double stranded RNA have been developed. Initially, two subsequent transfections of in vitro synthesized capped run-off RNA transcripts resulted in the recovery of BTV. Reverse genetics has been improved by transfection of expression plasmids followed by transfection of ten RNA transcripts. Recovery of AHSV was further improved by use of expression plasmids containing optimized open reading frames.
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vp2 exchange and ns3 ns3a deletion in African Horse Sickness virus ahsv in development of disabled infectious single animal vaccine candidates for ahsv
Journal of Virology, 2015Co-Authors: Sandra G P Van De Water, P.a. Van Rijn, Christiaan A Potgieter, Rene G P Van Gennip, Isabel M WrightAbstract:African Horse Sickness virus (AHSV) is a virus species in the genus Orbivirus of the family Reoviridae. There are nine serotypes of AHSV showing different levels of cross neutralization. AHSV is transmitted by species of Culicoides biting 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 endemic Culicoides species 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 replication in 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. IMPORTANCE African Horse Sickness virus is transmitted by species of Culicoides biting 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 endemic Culicoides species 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 replication in vitro. However, the potential spread of the virus by biting midges is supposed to be blocked, since the in vitro release 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.
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VP2 Exchange and NS3/NS3a Deletion in African Horse Sickness Virus (AHSV) in Development of Disabled Infectious Single Animal Vaccine Candidates for AHSV.
Journal of Virology, 2015Co-Authors: Sandra G P Van De Water, Christiaan A Potgieter, Rene G P Van Gennip, Isabel M Wright, P.a. Van RijnAbstract:African Horse Sickness virus (AHSV) is a virus species in the genus Orbivirus of the family Reoviridae. There are nine serotypes of AHSV showing different levels of cross neutralization. AHSV is transmitted by species of Culicoides biting 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 endemic Culicoides species 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 replication in 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. IMPORTANCE African Horse Sickness virus is transmitted by species of Culicoides biting 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 endemic Culicoides species 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 replication in vitro. However, the potential spread of the virus by biting midges is supposed to be blocked, since the in vitro release 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.
Rene G P Van Gennip - One of the best experts on this subject based on the ideXlab platform.
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requirements and comparative analysis of reverse genetics for bluetongue virus btv and African Horse Sickness virus ahsv
Virology Journal, 2016Co-Authors: P.a. Van Rijn, Sandra G P Van De Water, Femke Feenstra, Rene G P Van GennipAbstract:Background Bluetongue virus (BTV) and African Horse Sickness virus (AHSV) are distinct arthropod borne virus species in the genus Orbivirus (Reoviridae family), causing the notifiable diseases Bluetongue and African Horse Sickness of ruminants and equids, respectively. Reverse genetics systems for these orbiviruses with their ten-segmented genome of double stranded RNA have been developed. Initially, two subsequent transfections of in vitro synthesized capped run-off RNA transcripts resulted in the recovery of BTV. Reverse genetics has been improved by transfection of expression plasmids followed by transfection of ten RNA transcripts. Recovery of AHSV was further improved by use of expression plasmids containing optimized open reading frames.
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vp2 exchange and ns3 ns3a deletion in African Horse Sickness virus ahsv in development of disabled infectious single animal vaccine candidates for ahsv
Journal of Virology, 2015Co-Authors: Sandra G P Van De Water, P.a. Van Rijn, Christiaan A Potgieter, Rene G P Van Gennip, Isabel M WrightAbstract:African Horse Sickness virus (AHSV) is a virus species in the genus Orbivirus of the family Reoviridae. There are nine serotypes of AHSV showing different levels of cross neutralization. AHSV is transmitted by species of Culicoides biting 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 endemic Culicoides species 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 replication in 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. IMPORTANCE African Horse Sickness virus is transmitted by species of Culicoides biting 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 endemic Culicoides species 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 replication in vitro. However, the potential spread of the virus by biting midges is supposed to be blocked, since the in vitro release 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.
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VP2 Exchange and NS3/NS3a Deletion in African Horse Sickness Virus (AHSV) in Development of Disabled Infectious Single Animal Vaccine Candidates for AHSV.
Journal of Virology, 2015Co-Authors: Sandra G P Van De Water, Christiaan A Potgieter, Rene G P Van Gennip, Isabel M Wright, P.a. Van RijnAbstract:African Horse Sickness virus (AHSV) is a virus species in the genus Orbivirus of the family Reoviridae. There are nine serotypes of AHSV showing different levels of cross neutralization. AHSV is transmitted by species of Culicoides biting 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 endemic Culicoides species 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 replication in 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. IMPORTANCE African Horse Sickness virus is transmitted by species of Culicoides biting 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 endemic Culicoides species 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 replication in vitro. However, the potential spread of the virus by biting midges is supposed to be blocked, since the in vitro release 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.
Christiaan A Potgieter - One of the best experts on this subject based on the ideXlab platform.
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consensus sequence of 27 African Horse Sickness virus genomes from viruses collected over a 76 year period 1933 to 2009
Genome Announcements, 2015Co-Authors: Christiaan A Potgieter, Isabella M Wright, Alberdina A Van DijkAbstract:ABSTRACT We announce the complete consensus genome sequence of 27 African Horse Sickness viruses, representing all nine African Horse Sickness virus (AHSV) serotypes from historical and recent isolates collected over a 76-year period (1933 to 2009). The data set includes the sequence of the virulent Office International des Epizooties AHSV reference strains which are not adapted to cell culture.
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vp2 exchange and ns3 ns3a deletion in African Horse Sickness virus ahsv in development of disabled infectious single animal vaccine candidates for ahsv
Journal of Virology, 2015Co-Authors: Sandra G P Van De Water, P.a. Van Rijn, Christiaan A Potgieter, Rene G P Van Gennip, Isabel M WrightAbstract:African Horse Sickness virus (AHSV) is a virus species in the genus Orbivirus of the family Reoviridae. There are nine serotypes of AHSV showing different levels of cross neutralization. AHSV is transmitted by species of Culicoides biting 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 endemic Culicoides species 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 replication in 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. IMPORTANCE African Horse Sickness virus is transmitted by species of Culicoides biting 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 endemic Culicoides species 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 replication in vitro. However, the potential spread of the virus by biting midges is supposed to be blocked, since the in vitro release 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.
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VP2 Exchange and NS3/NS3a Deletion in African Horse Sickness Virus (AHSV) in Development of Disabled Infectious Single Animal Vaccine Candidates for AHSV.
Journal of Virology, 2015Co-Authors: Sandra G P Van De Water, Christiaan A Potgieter, Rene G P Van Gennip, Isabel M Wright, P.a. Van RijnAbstract:African Horse Sickness virus (AHSV) is a virus species in the genus Orbivirus of the family Reoviridae. There are nine serotypes of AHSV showing different levels of cross neutralization. AHSV is transmitted by species of Culicoides biting 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 endemic Culicoides species 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 replication in 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. IMPORTANCE African Horse Sickness virus is transmitted by species of Culicoides biting 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 endemic Culicoides species 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 replication in vitro. However, the potential spread of the virus by biting midges is supposed to be blocked, since the in vitro release 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.
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characterising non structural protein ns4 of African Horse Sickness virus
PLOS ONE, 2015Co-Authors: Lizahn Zwart, Christiaan A Potgieter, Sarah J Clift, Vida Van StadenAbstract:African Horse Sickness is a serious equid disease caused by the orbivirus African Horse Sickness virus (AHSV). The virus has ten double-stranded RNA genome segments encoding seven structural and three non-structural proteins. Recently, an additional protein was predicted to be encoded by genome segment 9 (Seg-9), which also encodes VP6, of most orbiviruses. This has since been confirmed in bluetongue virus and Great Island virus, and the non-structural protein was named NS4. In this study, in silico analysis of AHSV Seg-9 sequences revealed the existence of two main types of AHSV NS4, designated NS4-I and NS4-II, with different lengths and amino acid sequences. The AHSV NS4 coding sequences were in the +1 reading frame relative to that of VP6. Both types of AHSV NS4 were expressed in cultured mammalian cells, with sizes close to the predicted 17–20 kDa. Fluorescence microscopy of these cells revealed a dual cytoplasmic and nuclear, but not nucleolar, distribution that was very similar for NS4-I and NS4-II. Immunohistochemistry on heart, spleen, and lung tissues from AHSV-infected Horses showed that NS4 occurs in microvascular endothelial cells and mononuclear phagocytes in all of these tissues, localising to the both the cytoplasm and the nucleus. Interestingly, NS4 was also detected in stellate-shaped dendritic macrophage-like cells with long cytoplasmic processes in the red pulp of the spleen. Finally, nucleic acid protection assays using bacterially expressed recombinant AHSV NS4 showed that both types of AHSV NS4 bind dsDNA, but not dsRNA. Further studies will be required to determine the exact function of AHSV NS4 during viral replication.
