Pathogenicity and kinetics of virus propagation in swine infected with the cytopathogenic classical swine fever virus containing defective interfering particles

被引:8
作者
Aoki, H
Ishikawa, K
Sekiguchi, H
Suzuki, S
Fukusho, A
机构
[1] Natl Vet Assay Lab, Assay Div 1, Tokyo 1858511, Japan
[2] Natl Inst Anim Hlth, Kyushu Res Stn, Kagoshima, Japan
关键词
D O I
10.1007/s00705-002-0907-2
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
To analyze the pathogenicity and in vivo kinetics of the cytopathogenic (cp) classical swine fever virus (CSFV) WB82 strain, which is composed of cp defective interfering (DI) particles and noncytopathogenic (noncp) helper virus (WB82/E+ strain), WB82 and WB82/E+ strains were administered separately to domestic pigs. After inoculation with either strain, all pigs showed typical symptoms of classical swine fever (CSF), such as leucopenia and high fever. There were few differences in clinical signs and survival times between each group. However, the appearance of some symptoms of CSF had a tendency to be delayed following infection with the WB82 strain, when compared with the WB82/E+ strain. Virus isolation and detection of subgenomic (sg) and full-length viral (flv) RNA by RT-PCR was carried out using sera, 10% homogenized organs and oral, nasal and rectal swabs. Both noncytopathogenic helper virus and cp DI particles were detected in samples from pigs infected with the WB82 strain, but only noncp phenotype virus was isolated from pigs infected with the WB82/E+ strain. Interestingly, the cp DI particles appeared six to seven days later than helper virus in sera from pigs infected with the WB82 strain. Although active cp DI particles could not be isolated from swabs, sg RNA as well as flv RNA was detected in swabs from animals infected with the WB82 strain. These results suggest that progeny cp DI particles are replicated from parent DI particles after noncp virus replication, and subsequently discharged from infected animals. Furthermore, propagation of DI particles or replication of sg RNA, following propagation of helper virus, appears to inhibit the appearance of CSF symptoms induced by virulent helper CSFV.
引用
收藏
页码:297 / 310
页数:14
相关论文
共 34 条
[1]  
[Anonymous], 1975, ANN REP NAT VET ASSA
[2]   Characterization of classical swine fever virus associated with defective interfering particles containing a cytopathogenic subgenomic RNA isolated from wild boar [J].
Aoki, H ;
Ishikawa, K ;
Sakoda, Y ;
Sekiguchi, H ;
Kodama, M ;
Suzuki, S ;
Fukusho, A .
JOURNAL OF VETERINARY MEDICAL SCIENCE, 2001, 63 (07) :751-758
[3]   EXPERIMENTAL PRODUCTION OF FATAL MUCOSAL DISEASE IN CATTLE [J].
BROWNLIE, J ;
CLARKE, MC ;
HOWARD, CJ .
VETERINARY RECORD, 1984, 114 (22) :535-536
[4]  
DECASTRO MP, 1973, IN VITRO CELL DEV B, V9, P8
[5]   PREVENTION OF DEATH IN SEMLIKI FOREST VIRUS-INFECTED MICE BY ADMINISTRATION OF DEFECTIVE-INTERFERING SEMLIKI FOREST VIRUS [J].
DIMMOCK, NJ ;
KENNEDY, SIT .
JOURNAL OF GENERAL VIROLOGY, 1978, 39 (MAY) :231-242
[6]   PROTECTION OF MICE FROM LETHAL INFLUENZA - EVIDENCE THAT DEFECTIVE INTERFERING VIRUS MODULATES THE IMMUNE-RESPONSE AND NOT VIRUS MULTIPLICATION [J].
DIMMOCK, NJ ;
BECK, S ;
MCLAIN, L .
JOURNAL OF GENERAL VIROLOGY, 1986, 67 :839-850
[7]   PROPHYLAXIS AND IMMUNIZATION IN MICE BY USE OF VIRUS-FREE DEFECTIVE-T-PARTICLES TO PROTECT AGAINST INTRACEREBRAL INFECTION BY VESICULAR STOMATITIS-VIRUS [J].
DOYLE, M ;
HOLLAND, JJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1973, 70 (07) :2105-2108
[8]   The development of early vs. late onset mucosal disease is a consequence of two different pathogenic mechanisms [J].
Fritzemeier, J ;
Haas, L ;
Liebler, E ;
Moennig, V ;
GreiserWilke, I .
ARCHIVES OF VIROLOGY, 1997, 142 (07) :1335-1350
[9]   REVERSE PLAQUE-FORMATION BY HOG-CHOLERA VIRUS OF GPE-STRAIN INDUCING HETEROLOGOUS INTERFERENCE [J].
FUKUSHO, A ;
OGAWA, N ;
YAMAMOTO, H ;
SAWADA, M ;
SAZAWA, H .
INFECTION AND IMMUNITY, 1976, 14 (02) :332-336
[10]   MEDIATORS OF PROTECTION AGAINST LETHAL SYSTEMIC VESICULAR STOMATITIS-VIRUS INFECTION IN HAMSTERS - DEFECTIVE INTERFERING PARTICLES, POLYINOSINATE-POLYCYTIDYLATE, AND INTERFERON [J].
FULTZ, PN ;
SHADDUCK, JA ;
KANG, CY ;
STREILEIN, JW .
INFECTION AND IMMUNITY, 1982, 37 (02) :679-686