Chen W, Drillien R, Spehner D, Buller R M
Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892.
Virology. 1993 Oct;196(2):682-93. doi: 10.1006/viro.1993.1525.
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 less 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 virus in vivo replication and spread.
痘苗病毒宿主范围基因K1L的产物有一个与之同源的蛋白质，该蛋白质由痘苗病毒编码，除了有八个保守性和两个非保守性取代以及在羧基末端有一个额外的苏氨酸残基。与痘苗病毒基因不同，痘苗病毒同源物在RK-13细胞中不能支持最佳病毒复制，其表达效率似乎低20倍。这种较低的表达水平并非由于病毒的遗传背景、K1L RNA转录、K1L RNA前导序列或K1L RNA或蛋白质的稳定性。用缺乏完整K1L基因的痘苗病毒突变体感染RK-13细胞，会导致早期基因的瞬时表达，随后病毒和宿主蛋白质合成迅速且不可逆地停止。用缺乏K1L的痘苗病毒感染易感疾病的ANCR或抗性C57BL/6小鼠，其发病模式与野生型无异，这表明痘苗病毒K1L的痘苗病毒同源物对痘苗病毒在体内的复制和传播并不重要。
