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不同的机制导致了KG-1和HL-60细胞系对逆转录病毒感染的相对抗性。

Different mechanisms account for the relative resistance of KG-1 and HL-60 cell lines to retrovirus infection.

作者信息

Collins S J

机构信息

Molecular Medicine Program, Fred Hutchinson Cancer Research Center, Seattle, Washington 98104.

出版信息

J Virol. 1988 Nov;62(11):4346-8. doi: 10.1128/JVI.62.11.4346-4348.1988.

DOI:10.1128/JVI.62.11.4346-4348.1988
PMID:3172344
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC253870/
Abstract

I infected three different human leukemic cell lines (K562, KG-1, and HL-60) with an amphotropic retrovirus vector (designated PA317/N2) which confers G418 resistance and contains the Moloney murine leukemia virus long terminal repeat. Compared with K562 cells, both KG-1 and HL-60 cells were relatively resistant to infection with this retrovirus vector. In HL-60 cells, this resistance appeared to result from diminished viral DNA synthesis, while in KG-1 cells there was a block to the genomic integration of the viral DNA.

摘要

我用一种嗜异性逆转录病毒载体（命名为PA317/N2）感染了三种不同的人类白血病细胞系（K562、KG-1和HL-60），该载体赋予对G418的抗性并含有莫洛尼鼠白血病病毒长末端重复序列。与K562细胞相比，KG-1和HL-60细胞对这种逆转录病毒载体的感染相对抗性较强。在HL-60细胞中，这种抗性似乎是由于病毒DNA合成减少所致，而在KG-1细胞中则存在病毒DNA基因组整合的障碍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecd7/253870/0294af4dcb72/jvirol00090-0443-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecd7/253870/0294af4dcb72/jvirol00090-0443-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecd7/253870/0294af4dcb72/jvirol00090-0443-a.jpg

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