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CD4+淋巴细胞中HIV复制的差异与β趋化因子的产生无关。

Differences in HIV replication in CD4+ lymphocytes are not related to beta-chemokine production.

作者信息

Greco G, Barker E, Levy J A

机构信息

Department of Medicine and Cancer Research Institute, University of California, San Francisco 94143-1270, USA.

出版信息

AIDS Res Hum Retroviruses. 1998 Nov 1;14(16):1407-11. doi: 10.1089/aid.1998.14.1407.

Abstract

CD4+ T lymphocytes from different donors vary in their ability to replicate different isolates of HIV. Beta-chemokines have been shown to reduce the rate of HIV replication in cultured cells. We now demonstrate, using CD4+ cells from 19 different donors, that the variations in viral replication observed in CD4+ lymphocytes are not due to endogenous production of beta-chemokines by the cells. Instead of finding a correlation of high-level beta-chemokine production with low-level replication of virus, we found either no consistent relationship between these two parameters or a correlation between high-level beta-chemokine production and high-level virus replication. This observation was made with both chemokine-sensitive and chemokine-resistant HIV isolates. Thus, other mechanisms appear to be involved in the variability in HIV replication in cultured CD4+ cells.

摘要

来自不同供体的CD4 + T淋巴细胞在复制不同HIV分离株的能力上存在差异。β趋化因子已被证明可降低培养细胞中HIV的复制速率。我们现在使用来自19个不同供体的CD4 +细胞证明,在CD4 +淋巴细胞中观察到的病毒复制差异并非由于细胞内源性产生β趋化因子所致。我们没有发现高水平β趋化因子产生与低水平病毒复制之间的相关性,而是发现这两个参数之间要么没有一致的关系,要么存在高水平β趋化因子产生与高水平病毒复制之间的相关性。对趋化因子敏感和趋化因子抗性的HIV分离株均有此观察结果。因此,其他机制似乎参与了培养的CD4 +细胞中HIV复制的变异性。

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