Synergy between human immunodeficiency virus type 1 and Epstein-Barr virus in T lymphoblastoid cell lines.
Synergy between human immunodeficiency virus type 1 and Epstein-Barr virus in T lymphoblastoid cell lines.
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T 淋巴母细胞系中 1 型人类免疫缺陷病毒和 Epstein-Barr 病毒之间的协同作用。
DOI：
10.1089/aid.1997.13.161
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Henderson,EE
中科院分区：
文献类型：
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作者：
Zhang,RD;Guan,M;Park,Y;Tawadros,R;Yang,JY;Gold,B;Wu,B;Henderson,EE
通过间接荧光标记在四种 CD4 阳性细胞系中的三种上检测到 EBV 受体 CR2 (CD21)，并通过使用基于逆转录的聚合酶链式反应发现了其相应的 mRNA。为了确定 CD4 阳性细胞上的 CR2 是否具有功能，分析了它们被 EBV 感染的能力。 EBV B95.8 株感染后，表达 CR2 的 CD4 阳性细胞中可以检测到 EBV DNA、EBV 核抗原 2 (EBNA-2A) 和 EBV 编码的小 RNA (EBER1) 转录物。对末端区域的分析表明，EBV 基因组在感染后保持线性，并且拷贝数随着时间的推移而减少。由于CD4阳性细胞系是HIV-1感染的靶标，因此分析了EBV感染对HIV-1表达的影响。当 CD4 阳性细胞与 EBV B95.8 株共感染时，HIV-1 复制上调，但 P3HR-1K 则不然。这些结果表明 EBNA-2 参与 T 淋巴母细胞系中 HIV-1 表达的上调。为了检验这一假设，将 EBNA-2 表达载体转染至 T 淋巴母细胞系中，并测量 HIV-1 表达。首先，EBNA-2 1型表达增强了Tat对HIV-1长末端重复序列（LTR）的反式激活，当CD4阳性细胞被编码完整EBNA-2的EBV（菌株B95.8）感染时，Tat对HIV-1 LTR的反式激活也增强，但被删除EBNA-2的P3HR-1K感染则不增强。此外，通过逆转录酶活性的积累和合胞体诱导来测量，稳定表达 EBNA-2 的 CD4 阳性细胞克隆支持增强的 HIV-1 复制。这提供了直接证据表明EBV感染可以增强T细胞中的HIV-1复制。这种体外现象是否会导致体内疾病进展仍有待确定。
CR2 (CD21), the EBV receptor, was detected on three of four CD4-positive cell lines by indirect fluorescent labeling, and its corresponding mRNA was found by use of the reverse transcription-based polymerase chain reaction. To determine whether CR2 on CD4-positive cells was functional, their ability to be infected by EBV was analyzed. EBV DNA, EBV nuclear antigen 2 (EBNA-2A), and EBV-encoded small RNA (EBER1) transcripts could be detected in CR2-expressing CD4-positive cells following infection by the B95.8 strain of EBV. Analysis of the terminal region showed the EBV genome remained linear following infection, and copy number decreased with time. Since CD4-positive cell lines are targets for HIV-1 infection, the effects of EBV infection on HIV-1 expression were analyzed. HIV-1 replication was upregulated when CD4-positive cells were coinfected with EBV strain B95.8 but not P3HR-1K. These results suggested that EBNA-2 is involved in upregulation of HIV-1 expression in T lymphoblastoid cell lines. To test this hypothesis an EBNA-2-expression vector was transfected into T lymphoblastoid cell lines and HIV-1 expression measured. First,trans-activation of HIV-1 long terminal repeat (LTR) by Tat was enhanced by EBNA-2 type 1 expression,trans-Activation of the HIV-1 LTR by Tat was also enhanced when CD4-positive cells were infected by EBV (strain B95.8) encoding an intact EBNA-2, but not by P3HR-1K with a deleted EBNA-2. In addition, CD4-positive cell clones stably expressing EBNA-2 supported enhanced HIV-1 replication as measured by accumulation of reverse transcriptase activity and syncytium induction. This provides direct evidence that EBV infection can enhance HIV-1 replication in T cells. Whether thisin vitrophenomenon contributes to disease progressionin vivoremains to be determined.