- 作者: Robert E. Bellas; Yen Li
- 作者服務機構: a Department of Biochemistry, Boston University School of Medicine, Boston, Mass., b Center for Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, Mass., c New England Regional Primate Research Center, Harvard Medical School, Southborough, Mass., d Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Md., USA
- 中文摘要: --
- 英文摘要: Sequence analysis of the acutely lethal pbj 14 strain of simian immunodeficiency virus (SIVpbj14) clone revealed among other differences from its less pathogenic counterparts a duplication of its binding site for nuclear factor kappa B (NF-κB) in its long terminal repeats (LTR). We have investigated whether introducing a similar duplication into the pathogenic molecular clone SIVmac239 would alter its biological properties. We compared an SIV which possessed 2 NF-κB sites to the wild type, a single NF-κB site virus, with respect to its ability to replicate in vitro in established CD4+ T cell lines, primary peripheral blood mononuclear cells (PBMCs), and primary alveolar macrophages. The virus containing 2 NF-κB sites exhibited no apparent difference from wild type in established cell lines 174xCEM, MT-2 and MT-4, or in primary PBMC or tissue macrophage cultures. However, the 2 κB virus replicated well in the established cell line C8166, while the wild type, 1 κB virus replicated very poorly in this cell type, suggesting that duplication of the NF-κB site is capable of overcoming a block to efficient replication of SIVmac239 in C8166 cells. Interestingly, Em*, a macrophage tropic SIVmac that differs from SIVmac239 by 9 amino acids in the envelope region yet possesses only one NF-κB binding site, also replicates well in C8166. The data suggest that the replication of wild type SIVmac239 is restricted in C8166 cells, but that this restriction can be overcome either by changes in the LTR or by changes in the envelope region.
- 中文關鍵字: --
- 英文關鍵字: Lentivirus; Electrophorectic mobility shift assay; Transcription; ELISA; AIDS