Molecular epizootiology and evolution of vesicular stomatitis virus New Jersey

Molecular epizootiology and evolution of vesicular stomatitis virus New Jersey
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新泽西州水泡性口炎病毒的分子流行病学和进化

DOI:
10.1128/jvi.61.4.1029-1036.1987
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发表时间:
1987
影响因子:
5.4
通讯作者:
S. Nichol
S. Nichol
中科院分区:
医学2区
文献类型:
--
作者:
S. Nichol

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Vesicular stomatitis virus (VSV) has been shown previously to be capable of undergoing rapid mutational change during sequential experimental infections in various tissue culture cell systems (J. Holland, K. Spindler, F. Horodyski, E. Grabau, S. Nichol, and S. Vandepol, Science 215:1577-1585, 1982). The present study was undertaken to determine the degree of genetic diversity and evolution of the virus under natural infection conditions and to gain insight into the epizootiology of the disease. Between 1982 and 1985, numerous outbreaks of VSV of the New Jersey serotype were reported throughout regions of the United States and Mexico. A T1 RNase fingerprint analysis was performed on the RNA genomes of 43 virus isolates from areas of epizootic and enzootic virus activity. This indicates that virus populations were genetically relatively homogeneous within successive U.S. virus epizootics. The data included virus isolates from different epizootic stages, geographical locations, host animals, and host lesion sites. In contrast, only distant genome RNA T1 fingerprint similarities were observed among viruses of the different U.S. epizootics. However, Mexican viruses isolated before or concurrent with U.S. epizootics had very similar RNA genome fingerprints, suggesting that Mexico may have been the possible origin of virus initiating recent U.S. VSV New Jersey outbreaks. Comparison of T1 fingerprints of viruses with enzootic disease areas revealed a greater extent of virus genetic diversity in these areas relative to that observed in epizootic areas. The evolutionary significance of these findings and their relationship to experimental data on VSV evolution are discussed.
高感染复数有利于水泡性口炎病毒的快速和随机进化。
DOI: 10.1016/0042-6822(82)90068-x
发表时间: 1982
期刊: Virology
影响因子: 3.7
作者:
Spindler,KR;Horodyski,FM;Holland,JJ
通讯作者: Holland,JJ
DOI: 10.1126/science.7041255
发表时间: 1982-01-01
期刊: SCIENCE
影响因子: 56.9
作者:
HOLLAND, J;SPINDLER, K;VANDEPOL, S
通讯作者: VANDEPOL, S
水泡性口炎病毒连续未稀释传代过程中温度敏感突变体的产生和扩增。
DOI: 10.1016/0042-6822(81)90529-8
发表时间: 1981
期刊: Virology
影响因子: 3.7
作者:
Youngner,JS;Jones,EV;Kelly,M;Frielle,DW
通讯作者: Frielle,DW
从 L 细胞持续感染中分离出的水疱性口炎病毒基因组末端非编码区的碱基突变。
DOI: 10.1016/0042-6822(85)90363-0
发表时间: 1985
期刊: Virology
影响因子: 3.7
作者:
Wilusz,J;Youngner,JS;Keene,JD
通讯作者: Keene,JD
一类新型水泡性口炎病毒缺陷干扰颗粒的结构和起源。
DOI: 10.1093/nar/12.6.2775
发表时间: 1984
影响因子: 14.9
作者:
Nichol,ST;O'Hara,PJ;Holland,JJ;Perrault,J
通讯作者: Perrault,J