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40. Interactions between Classical swine fever virus and host cells
Abstracts.
14
Room
A.
Tuesday
26th
March
2002
11~45-12~00
38. Foot and month disease in Cumbria - a day in the life. HOLLIMAN. VLA
Pen&h,
Merrythought,
Cnlthwnite,
Foot and mouth disease had a devastating impact on the agricultural scene in Cumbria, with over 570,000 animals killed on almost 900 infected premises. At one stage over 250 vets were working 7 days a week, 12 hours a day in an attempt to contain the outbreak. The role of the vet on farm encompassed
Room
A.” Penrith,
CA11
9RR
many duties from initial inspection of stock through to slaughter and including overall control of detox teams, slaughtermen, field officers and many ancillary workers. This talk highlights many of these aspects, with emphasis on disease diagnosis.
A. 12~00-12~30
39. KEYNOTE:
Classical and African swine fever: an update PATON, D.J.,:” WILKINSON,
Institute
for Animal
health,
Pirbright
Luboratory,
A small RNA virus of the genus Pestivirus and family Flaviviridne causes classical swine fever, which is also known as hog cholera. African swine fever is caused by a large DNA virus, which is the only member of the family Asfurviridne. Both diseases may be manifest by a haemorrhagic fever with a high mortality although less virulent viruses can be associated with milder disease with much less specific signs of illness. The diseases are also highly contagious, may infect wild boar as well as domestic pigs and may be spread by swill feeding. For these reasons both diseases are placed on the list A of the Office International des Epizooties, signifying their importance for international trade. Classical swine fever is present in parts of Europe, Asia and South and Central America, different genetic variants being associated with particular regions. Excellent live vaccines are available and efforts are
Room
Cumhria,
A.
Ash
Road,
P.J. Pirbright,
Waking,
Surrey
GU24
ONF
continuing to produce effective marker vaccines. In Western Europe, eradication has been based on a non-vaccination policy that has been partially successful. Reservoirs of infection in wild boar and periodic imports of infected products continue to spark off new cases. which have recentlv flared un in Suain. African swine fever was originally an infection of wart hogs and ticks localised to Southern Africa. Once infected, domestic pigs can maintain and spread the disease with or without the agency of tick vectors. In the last forty years outbreaks of African swine fever have also occurred in Europe, South America and the Caribbean. No effective vaccine is available. In Europe, African swine fever now occurs only in Sardinia, following eradication from the Iberian Peninsula in the early 1990s. Recently the range of the disease has been extended to include West Africa.
12.30-12.45
40. Interactions between Classical swine fever virus and host cells BENSAUDE, ‘Virology
Department,
E.,*:“’ SWEETMAN,
D.,2 PATON, D..J.,2 DREW, T.W.,’ WILEMAN,
Veterinary 21nstitute
Agency, Woodhnm Lane, Health, Ash Road, Pirbright.
Laboratories for Animal
Classical swine fever virus (CSFV) is a small, enveloped single stranded RNA virus in the Pestivirus genus. Infection with virulent strains of CSFV results in an acute haemorrhagic disease of pigs, characterised by disseminated intravascular coagulation, thronbocytopenia and lymphopenia, whilst infection with moderate virulent strains can lead to persistent infection. The virus replicates to high levels in macrophages, vascular endothelial cells and cpithelial cells. In view of the central role of vascular endothelial cells in the pathogenesis of the disease, WC investigated the response of these cells to CSFV infection. Primary porcine aortic endothelial cells (PAEC) were infcctcd with CSFV Alfort 187.
T.,2 POWELL,
New Haw, Addlestone, Surrey, Surrey, UK GU14 ONF
UK
P.’ KTl5
3 NB,
Expression of proinflammatory and antiviral cytokines after CSFV infection was analysed by relative quantitative RT-PCR and ELISA. Another characteristic of CSFV is its ability to persist in cell culture. To investigate the mechanisms underlying pcrsistence, we treated uninfected and persistently infected cells with pIpC (synthetic dsRNA). Double stranded RNA is a major intermediate of viral replication, as well as a well characterised inducer of apoptosis. We demonstrated that cells persistently infected with CSFV were protected against pIpC induced apoptosis. This suggests that one of the mechanisms allowing viral persistence in cell culture is by preventing ds RNA induced apoptosis.
14
Room
A.
Tuesday
26th
March
2002
11~45-12~00
38. Foot and month disease in Cumbria - a day in the life. HOLLIMAN. VLA
Pen&h,
Merrythought,
Cnlthwnite,
Foot and mouth disease had a devastating impact on the agricultural scene in Cumbria, with over 570,000 animals killed on almost 900 infected premises. At one stage over 250 vets were working 7 days a week, 12 hours a day in an attempt to contain the outbreak. The role of the vet on farm encompassed
Room
A.” Penrith,
CA11
9RR
many duties from initial inspection of stock through to slaughter and including overall control of detox teams, slaughtermen, field officers and many ancillary workers. This talk highlights many of these aspects, with emphasis on disease diagnosis.
A. 12~00-12~30
39. KEYNOTE:
Classical and African swine fever: an update PATON, D.J.,:” WILKINSON,
Institute
for Animal
health,
Pirbright
Luboratory,
A small RNA virus of the genus Pestivirus and family Flaviviridne causes classical swine fever, which is also known as hog cholera. African swine fever is caused by a large DNA virus, which is the only member of the family Asfurviridne. Both diseases may be manifest by a haemorrhagic fever with a high mortality although less virulent viruses can be associated with milder disease with much less specific signs of illness. The diseases are also highly contagious, may infect wild boar as well as domestic pigs and may be spread by swill feeding. For these reasons both diseases are placed on the list A of the Office International des Epizooties, signifying their importance for international trade. Classical swine fever is present in parts of Europe, Asia and South and Central America, different genetic variants being associated with particular regions. Excellent live vaccines are available and efforts are
Room
Cumhria,
A.
Ash
Road,
P.J. Pirbright,
Waking,
Surrey
GU24
ONF
continuing to produce effective marker vaccines. In Western Europe, eradication has been based on a non-vaccination policy that has been partially successful. Reservoirs of infection in wild boar and periodic imports of infected products continue to spark off new cases. which have recentlv flared un in Suain. African swine fever was originally an infection of wart hogs and ticks localised to Southern Africa. Once infected, domestic pigs can maintain and spread the disease with or without the agency of tick vectors. In the last forty years outbreaks of African swine fever have also occurred in Europe, South America and the Caribbean. No effective vaccine is available. In Europe, African swine fever now occurs only in Sardinia, following eradication from the Iberian Peninsula in the early 1990s. Recently the range of the disease has been extended to include West Africa.
12.30-12.45
40. Interactions between Classical swine fever virus and host cells BENSAUDE, ‘Virology
Department,
E.,*:“’ SWEETMAN,
D.,2 PATON, D..J.,2 DREW, T.W.,’ WILEMAN,
Veterinary 21nstitute
Agency, Woodhnm Lane, Health, Ash Road, Pirbright.
Laboratories for Animal
Classical swine fever virus (CSFV) is a small, enveloped single stranded RNA virus in the Pestivirus genus. Infection with virulent strains of CSFV results in an acute haemorrhagic disease of pigs, characterised by disseminated intravascular coagulation, thronbocytopenia and lymphopenia, whilst infection with moderate virulent strains can lead to persistent infection. The virus replicates to high levels in macrophages, vascular endothelial cells and cpithelial cells. In view of the central role of vascular endothelial cells in the pathogenesis of the disease, WC investigated the response of these cells to CSFV infection. Primary porcine aortic endothelial cells (PAEC) were infcctcd with CSFV Alfort 187.
T.,2 POWELL,
New Haw, Addlestone, Surrey, Surrey, UK GU14 ONF
UK
P.’ KTl5
3 NB,
Expression of proinflammatory and antiviral cytokines after CSFV infection was analysed by relative quantitative RT-PCR and ELISA. Another characteristic of CSFV is its ability to persist in cell culture. To investigate the mechanisms underlying pcrsistence, we treated uninfected and persistently infected cells with pIpC (synthetic dsRNA). Double stranded RNA is a major intermediate of viral replication, as well as a well characterised inducer of apoptosis. We demonstrated that cells persistently infected with CSFV were protected against pIpC induced apoptosis. This suggests that one of the mechanisms allowing viral persistence in cell culture is by preventing ds RNA induced apoptosis.