Browne H, Churcher M, Minson T
Department of Pathology, University of Cambridge, United Kingdom.
J Virol. 1992 Nov;66(11):6784-7. doi: 10.1128/JVI.66.11.6784-6787.1992.
The UL18 open reading frame of human cytomegalovirus (HCMV) (which encodes a product homologous to major histocompatibility complex class I heavy chains) has been disrupted by insertion of the beta-galactosidase gene under control of the major HCMV early promoter. The recombinant virus delta UL18 showed no phenotypic differences from wild-type HCMV in terms of single-step growth curves or particle/infectivity ratios, indicating that the UL18 gene product is dispensable for the growth of HCMV in human fibroblasts in vitro. The synthesis of the mature cellular class I heterodimer is shut down in cells infected at a high multiplicity with wild-type HCMV, and a similar effect was seen in delta UL18-infected fibroblasts, suggesting that although the UL18 gene product can associate with beta 2 microglobulin, it is not directly involved in the disruption of class I assembly.
人类巨细胞病毒(HCMV)的UL18开放阅读框(其编码一种与主要组织相容性复合体I类重链同源的产物)已被在主要HCMV早期启动子控制下插入的β-半乳糖苷酶基因破坏。重组病毒δUL18在单步生长曲线或颗粒/感染性比率方面与野生型HCMV没有表型差异,这表明UL18基因产物对于HCMV在人成纤维细胞中的体外生长是可有可无的。在以高感染复数感染野生型HCMV的细胞中,成熟细胞I类异二聚体的合成被关闭,并且在感染δUL18的成纤维细胞中也观察到类似的效果,这表明尽管UL18基因产物可以与β2微球蛋白结合,但它并不直接参与I类装配的破坏。