Viral and cellular gene expression in CD4+ human lymphoid cell lines infected by the simian immunodeficiency virus, SIV/Mne.
Viral and cellular gene expression in CD4+ human lymphoid cell lines infected by the simian immunodeficiency virus, SIV/Mne.
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被猿猴免疫缺陷病毒 SIV/Mne 感染的 CD4 人淋巴细胞系中的病毒和细胞基因表达。
DOI：
10.1016/0042-6822(91)90130-4
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发表时间：
1991
期刊：
影响因子：
3.7
通讯作者：
Katze,MG
中科院分区：
文献类型：
--
作者：
Agy,MB;Foy,K;Gale,MJ;Benveniste,RE;Clark,EA;Katze,MG
我们的实验室已经对人类和猿类免疫缺陷病毒HIV-1和SIWMne分别感染的CD4+人类淋巴样细胞系的细胞和病毒基因表达进行了分析。本研究的目的是：(I)检测SIWMne感染对宿主大分子合成的影响，并将结果与HIV-1系统中的结果进行比较；(Ii)探讨容易感染HIV-1的CD4+淋巴细胞中SIV/Mne感染受到限制的机制。首先，我们确定SIV不会选择性地阻止宿主的大分子合成，不像HIV-1，HIV-1既会导致细胞蛋白质合成的选择性抑制，也会导致细胞mRNAs的降解。在感染SIV/Mne的细胞中，没有观察到这种选择性的细胞mRNA稳定性或蛋白质合成的降低。使用一组CD4+人类细胞系观察到SIV和HIV-1之间的其他差异。当HIV-1感染所有细胞系时，SIWMne仅有效感染MT-4、C8166和174×CEM细胞系。病毒DNA的聚合酶链式反应分析表明，反复感染CEM或Jurkat细胞的努力均未成功。HUT 78细胞支持只有通过聚合酶链式反应分析才能检测到的有限感染。这些数据表明，在不敏感的细胞系中阻止病毒复制还处于早期阶段。有趣的是，所有SIV敏感细胞都被病毒转化，HTLV-1转化C8166和MT-4，Epstein-Barr病毒转化174×CEM。流式细胞仪分析显示，所有易感细胞均表达B7/BB1和CD40两种B细胞相关标志。这些观察结果综合起来突出了HIV和SIV病毒之间的差异，并表明为了有效地复制，SIV/Mne可能需要额外的细胞表面分子，由转化病毒提供的辅助因子，或者两者之间复杂的相互作用。
Our laboratory has undertaken an analysis of cellular and viral gene expression in CD4+ human lymphoid cell lines infected by the human and simian immunodeficiency viruses, HIV-1 and SIWMne, respectively. The purpose of the current study was to: (i) examine the effects of SIWMne infection on host macromolecular synthesis and compare the results to those in the HIV-1 system; and (ii) investigate the mechanisms responsible for the restriction of SIV/Mne infection in CD4 positive lymphoid cells which are readily infected by HIV-1. First we determined that SIV does not impose selective blocks on host macromolecular synthesis, unlike HIV-1, which induces both the selective inhibition of cellular protein synthesis and the degradation of cellular mRNAs Agy, M., Wambach, M., Foy, K., and Katze, M. G., 1990. No such selective reduction in cellular mRNA stability or protein synthesis was observed in cells infected by SIV/Mne. Additional differences between SIV and HIV-1 were observed using a panel of CD4+ human cell lines. While HIV-1-infected all cell lines, SIWMne efficiently infected only the MT-4, C8166, and 174 × CEM cell lines. Repeated efforts to infect CEM or Jurkat cells were unsuccessful as determined by PCR analysis of viral DNA. HUT 78 cells supported a limited infection detectable only by PCR analysis. These data suggest the block in viral replication in the nonsusceptible cell lines is at an early step. Interestingly, all the SIV susceptible cells were virally transformed, C8166 and MT-4 by HTLV-1, and 174 × CEM by Epstein-Barr virus. Furthermore FACS analysis revealed that all susceptible cells expressed two B cell associated markers, B7/BB1 and CD40. These observations taken together highlight differences between the HIV and SIV viruses, and suggest that for efficient replication, SIV/Mne may require an additional cell surface molecule, cofactors provided by transforming viruses, or a complex interplay between the two.