IN-VITRO AND IN-VIVO STUDY OF THE ECTROMELIA VIRUS HOMOLOG OF THE VACCINIA VIRUS K1L HOST-RANGE GENE
IN-VITRO AND IN-VIVO STUDY OF THE ECTROMELIA VIRUS HOMOLOG OF THE VACCINIA VIRUS K1L HOST-RANGE GENE
复制标题
DOI：
10.1006/viro.1993.1525
复制
发表时间：
1993-10-01
期刊：
影响因子：
3.7
通讯作者：
BULLER, RML
中科院分区：
文献类型：
--
作者：
CHEN, W;DRILLIEN, R;BULLER, RML
缺肢病病毒编码的蛋白质与牛痘病毒宿主范围基因K1 L的产物同源，除了在羧基末端有8个保守和2个非保守取代以及一个额外的苏氨酸残基。与牛痘病毒基因不同，缺肢症病毒同源物未能支持RK-13细胞中的最佳病毒复制，并且似乎有效表达20倍损失。这种较低的表达水平不是由于病毒的遗传背景、K1 L RNA转录、K1 L RNA前导序列或K1 L RNA或蛋白质的稳定性。感染RK-13细胞与缺肢症或牛痘病毒突变体缺乏一个完整的K1 L基因导致瞬时表达的早期基因，随后由病毒和宿主蛋白质合成的快速和不可逆的停止。感染的疾病易感ANCR或抗C57 BL/6小鼠与K1 L缺乏缺肢病病毒产生的发病机制模式与野生型难以区分，这表明缺肢病病毒同源的痘苗病毒K1 L是不重要的缺肢病病毒在体内复制和传播。
Ectromelia virus encodes a protein which is homologous to the product of the vaccinia virus host range gene, K1L, except for eight conservative and two non-conservative substitutions and an additional threonine residue at the carboxyl terminus. Unlike the vaccinia virus gene, the ectromelia virus homolog failed to support optimal virus replication in RK-13 cells and appeared to be expressed 20-fold loss efficiently. This lower level of expression was not due to the genetic background of the virus, K1L RNA transcription, sequence of the K1L RNA leader, or stability of K1L RNA or protein. Infections of RK-13 cells with ectromelia or vaccinia virus mutants lacking an intact K1L gene resulted in transient expression of early genes followed by a rapid and irreversible cessation of both virus and host protein synthesis. Infections of the disease-susceptible ANCR or -resistant C57BL/6 mice with the K1L-lacking ectromelia virus yielded a pathogenesis pattern indistinguishable from wild-type, suggesting that the ectromelia virus homolog of vaccinia virus K1L is not important for ectromelia virusin vivoreplication and spread.