Cann A J, Zack J A, Go A S, Arrigo S J, Koyanagi Y, Green P L, Koyanagi Y, Pang S, Chen I S
Department of Medicine, University of California-Los Angeles, School of Medicine 90024-1678.
J Virol. 1990 Oct;64(10):4735-42. doi: 10.1128/JVI.64.10.4735-4742.1990.
Different strains of human immunodeficiency virus type 1 (HIV-1) vary in the ability to replicate in cells that bear the HIV-1 receptor, CD4. The mechanism responsible for these cell tropism differences is unknown. We examined different isolates of HIV-1 with regard to replication in specific tumor-derived CD4-positive T-cell lines and normal peripheral blood lymphocytes. To investigate early events in the virus life cycle at low multiplicities of infection, we used a modification of the polymerase chain reaction method. Use of a molecularly cloned primary HIV-1 isolate, HIV-1 JR-CSF, restricted for replication in T-cell lines, demonstrated that little or no viral DNA or RNA was synthesized in nonpermissive cells after infection. However, transfection of proviral DNA resulted in efficient transient virus production from these cells. Therefore, we conclude that at least one block to infection for HIV-1 strains in nonpermissive T cells occurs at a point in entry or uncoating before provirus formation.
1型人类免疫缺陷病毒（HIV-1）的不同毒株在携带HIV-1受体CD4的细胞中复制的能力有所不同。造成这些细胞嗜性差异的机制尚不清楚。我们研究了不同的HIV-1分离株在特定肿瘤来源的CD4阳性T细胞系和正常外周血淋巴细胞中的复制情况。为了在低感染复数下研究病毒生命周期中的早期事件，我们对聚合酶链反应方法进行了改进。使用一种分子克隆的原发性HIV-1分离株HIV-1 JR-CSF（其在T细胞系中的复制受限），结果表明感染后在非允许细胞中几乎没有合成病毒DNA或RNA。然而，转染前病毒DNA导致这些细胞高效瞬时产生病毒。因此，我们得出结论，对于非允许T细胞中的HIV-1毒株，至少有一个感染阻断发生在病毒前体形成之前的进入或脱壳阶段。
