Kim H J, Lee K, O'Rear J J
Department of Molecular Genetics and Microbiology, UMDNJ-Robert Wood Johnson Medical School, Piscataway 08854.
Virology. 1994 Jan;198(1):336-40. doi: 10.1006/viro.1994.1037.
A series of linker scanning and deletion mutations has been constructed in the 5' leader sequence of HIV-1. One virus with a 13-base-linker substitution upstream of the 5' major splice site was as impaired in its ability to replicate as a virus with a large deletion, which included these 13 bases, and was less efficient in packaging its genomic RNA than viruses carrying mutations between the 5' major splice site and the gag translation initiation site. These observations have led to the identification of a conserved pattern of repeated sequence elements associated with sequences experimentally defined as necessary for encapsidation of Moloney murine leukemia virus, spleen necrosis virus, avian leukosis-sarcoma viruses, and human immunodeficiency virus type 1.
已在HIV-1的5'前导序列中构建了一系列接头扫描和缺失突变。一种在5'主要剪接位点上游有13个碱基接头替代的病毒，其复制能力与一个包含这13个碱基的大片段缺失病毒一样受损，并且在包装其基因组RNA方面比携带5'主要剪接位点和gag翻译起始位点之间突变的病毒效率更低。这些观察结果导致鉴定出一种保守的重复序列元件模式，该模式与实验定义为莫洛尼鼠白血病病毒、脾坏死病毒、禽白血病-肉瘤病毒和1型人类免疫缺陷病毒包装所必需的序列相关。
