Host cell-dependent alterations in envelope components of human immunodeficiency virus type 1 virions
Host cell-dependent alterations in envelope components of human immunodeficiency virus type 1 virions
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DOI：
10.1128/jvi.71.5.3444-3450.1997
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发表时间：
1997-05-01
影响因子：
5.4
通讯作者：
ZollaPazner, S
中科院分区：
文献类型：
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作者：
Bastiani, L;Laal, S;ZollaPazner, S
除了gp 41和gp 120之外，一系列细胞粘附分子存在于人类免疫缺陷病毒1型（HIV-1）的包膜上。为了检查宿主细胞在病毒体获得这些分子中的作用，将实验室适应的分离株和原代分离株依次传代到不同的宿主细胞中。通过病毒结合酶联免疫吸附测定法检查从各种宿主细胞获得的病毒是否存在10种不同的细胞衍生分子。在外周血单个核细胞中培养的病毒后代表达了大多数测试的粘附分子，其中LFA-1的水平最高。当病毒传代到CEM-SS或SupT 1细胞中时，病毒包膜上的大多数粘附分子的表达丧失。相反，当病毒传代到MT 2细胞中时，病毒后代具有高水平的LFA-3、ICAM-1和主要组织相容性复合物I类和II类。这些研究首次证明了HIV-1原代分离株包膜上粘附分子分布的宿主细胞依赖性。还描述了几种以前未被鉴定为实验室或原代分离株包膜成分的粘附分子的存在。此外，我们表明，病毒体的粘附分子的配置文件是收购，或丢失，在一个通道内，并保持与随后的通道在相同的细胞类型。
In addition to gp41 and gp120, an array of cell adhesion molecules is present on the envelope of human immunodeficiency virus type 1 (HIV-1). To examine the role of the host cell in the acquisition of these molecules by virions, both laboratory-adapted and primary isolates were sequentially passaged into different host cells. Viruses obtained from the various host cells were examined for the presence of 10 different cell-derived molecules by a virus binding enzyme-linked immunosorbent assay. Virus progeny raised in peripheral blood mononuclear cells expressed most of the adhesion molecules tested, with the level of LFA-1 being the highest. When viruses were passaged into CEM-SS or SupT1 cells, the expression of most of the adhesion molecules on the virus envelope was lost. In contrast, when viruses were passaged into MT2 cells, the virus progeny bore high levels of LFA-3, ICAM-1, and major histocompatibility complex classes I and II. These studies demonstrate for the first time the host cell dependence of the adhesion molecule profile present on the envelope of primary isolates of HIV-1. The presence of several adhesion molecules that have not previously been identified as components of the envelope of either laboratory or primary isolates is also described. In addition, we show that the adhesion molecule profile of the virions is acquired, or lost, within one passage and is maintained with subsequent passages in the same cell type.