Nagendra A R, Smith C W, Wyde P R
Department of Microbiology and Immunology, Baylor College of Medicine, Houston, Texas 77030, USA.
J Virol. 1995 Jul;69(7):4357-63. doi: 10.1128/JVI.69.7.4357-4363.1995.
Measles virus (MV), human immunodeficiency virus, Epstein-Barr virus, and other leukotropic viruses can modulate the expression of leukocyte function antigen 1 (LFA-1) on the surface of infected and nearby leukocytes. This ability to induce changes in LFA-1 expression may play an important role in the pathogenesis of these viruses. However, the mechanism(s) involved in virus-mediated regulation of LFA-1 is unknown. Evidence is presented in this report that it is the MV hemagglutinin (H) protein that initiates up-regulation of LFA-1 expression in leukocyte cultures infected with this virus. Indeed, comparison of the abilities of different MV strains to modulate LFA-1 expression, examination of published nucleotide sequences for the H proteins of different vaccine strains, and competitive inhibition assays using oligopeptides homologous or heterologous to a region of the H protein gene encompassing amino acid 116 (from the amino terminus) all suggest that it is this portion of the H protein that is responsible for MV-induced alteration of LFA-1. These comparisons also support the hypothesis that there is a relationship between the abilities of different MV strains to alter LFA-1 expression and their pathogenic potentials.
麻疹病毒(MV)、人类免疫缺陷病毒、爱泼斯坦-巴尔病毒及其他亲白细胞病毒可调节受感染及附近白细胞表面白细胞功能抗原1(LFA-1)的表达。诱导LFA-1表达变化的这种能力可能在这些病毒的发病机制中起重要作用。然而,病毒介导的LFA-1调节机制尚不清楚。本报告提供的证据表明,正是MV血凝素(H)蛋白启动了感染该病毒的白细胞培养物中LFA-1表达的上调。事实上,比较不同MV毒株调节LFA-1表达的能力、检查不同疫苗毒株H蛋白的已发表核苷酸序列,以及使用与包含第116位氨基酸(从氨基端起)的H蛋白基因区域同源或异源的寡肽进行竞争性抑制试验,均表明正是H蛋白的这一部分负责MV诱导的LFA-1改变。这些比较也支持了这样一种假说,即不同MV毒株改变LFA-1表达的能力与其致病潜力之间存在关联。