CD4 mRNA expression in CD19-positive B cells and its suppression by the Epstein-Barr virus.
CD4 mRNA expression in CD19-positive B cells and its suppression by the Epstein-Barr virus.
复制标题
CD19 阳性 B 细胞中 CD4 mRNA 的表达及其受到 Epstein-Barr 病毒的抑制。
DOI：
10.1006/viro.1994.1083
复制
发表时间：
1994
期刊：
影响因子：
3.7
通讯作者：
Henderson,EE
中科院分区：
文献类型：
--
作者：
Zhang,RD;Henderson,EE
我们检查了 HIV-1 IIIB 毒株和 Epstein-Barr 病毒 (EBV) 在同种细胞类型感染过程中的协同作用。为了获得由同质细胞类型组成的细胞群，通过流式细胞术从人扁桃体中纯化 CD19 阳性 B 淋巴细胞。 CD19阳性淋巴细胞不表达可检测的表面CD4抗原。然而，通过与聚合酶链式反应偶联的逆转录以及使用反义核糖核酸探针的点印迹杂交，可以在 CD19 阳性淋巴细胞中检测到 CD4 mRNA。 CD19 阳性淋巴细胞中 CD4 mRNA 的转录受到 EBV B95-8 株感染的抑制，并在 B95-8 转化的淋巴母细胞系中丢失。相反，EBV P3HR-1K株对CD4 mRNA水平没有影响。通过与 SupT1 细胞共培养后逆转录酶的积累和合胞体诱导来测量，HIV-1 可以感染 CD19 分选的 B 细胞。 OKT4a 抗体可阻断携带 CD19 的淋巴细胞的 HIV-1 感染。预感染 B95-8 后，HIV-1 在 CD19 阳性 B 淋巴细胞中复制的能力下降，但感染 P3HR-1K 后则没有下降。这些结果以及 EBNA-2 表达载体的结果表明，人 B 细胞中 CD4 mRNA 和 HIV-1 感染的下调是 EBV 核抗原 EBNA-2 的功能。天然 CD19 阳性 B 淋巴细胞表达足够的 CD4 受体 mRNA 以允许 HIV-1 感染，这一事实增强了 B 细胞中 HIV-1 复制直接参与 AIDS 发病机制的可能性。此外，EBV 感染可能会调节 HIV-1 感染的能力，并在共感染个体的 B 淋巴细胞中建立潜伏感染。
We have examined for synergy between the IIIB strain of HIV-1 and Epstein-Barr virus (EBV) during infection of a homogeneous cell type. In order to obtain a cell population consisting of a homogeneous cell type, CD19-positive B lymphocytes were purified from human tonsils by flow cytometry. CD19-positive lymphocytes did not express detectable surface CD4 antigen. However, CD4 mRNA could be detected in CD19-positive lymphocytes by reverse transcription coupled to polymerase chain reaction and by dot blot hybridization using an antisense riboprobe. Transcription of CD4 mRNA in CD19-positive lymphocytes was suppressed by infection with the B95-8 strain of EBV and lost in B95-8-transformed lymphoblastoid cell lines. In contrast, the P3HR-1K strain of EBV had no effect on the level of CD4 mRNA. HIV-1 could infect CD19-sorted B cells as measured by accumulation of reverse transcriptase and syncytia induction after coculture with SupT1 cells. HIV-1 infection of CD19-bearing lymphocytes was blocked by OKT4a antibodies. The ability of HIV-1 to replicate in CD19-positive B lymphocytes declined following preinfection with B95-8 but not with P3HR-1K. These results as well as results with an EBNA-2 expression vector suggest that down-regulation of both CD4 mRNA and HIV-1 infection in human B cells is a function of EBV nuclear antigen EBNA-2. The fact that native CD19-positive B lymphocytes express sufficient CD4 receptor mRNA to allow HIV-1 infection strengthens the possibility that HIV-1 replication in B cells directly participates in AIDS pathogenesis. In addition, infection with EBV may modulate the ability of HIV-1 to infect and establish a latent infection in B lymphocytes in co-infected individuals.