HIV-1 infection up-regulating expression of interferon-stimulated gene 15 in cell lines.
- Author:
Huan-mei WU
1
;
Jun SUN
2
;
Zhe-feng MENG
2
;
Xiao-yan ZHANG
2
;
Jian-qing XU
2
Author Information
1. Shanghai Public Health Clinical Center Affiliated to Fudan University, Shanghai 201508, China. dianan7@163.com
2. Shanghai Public Health Clinical Center Affiliated to Fudan University, Shanghai 201508, China.
- Publication Type:Journal Article
- MeSH:
Base Sequence;
Cell Line;
Cytokines;
genetics;
metabolism;
HIV Infections;
genetics;
metabolism;
virology;
HIV-1;
physiology;
Humans;
Interferons;
metabolism;
Molecular Sequence Data;
Ubiquitins;
genetics;
metabolism;
Up-Regulation
- From:
Chinese Journal of Virology
2013;29(5):480-487
- CountryChina
- Language:Chinese
-
Abstract:
To investigate whether HIV-1 infection affects expression of interferon-stimulated gene 15 (ISG15) and determine the antiviral effect of ISG15 in vitro, ISG15 expression at transcription and protein level and supernatant p24 of HIV-1 was detected in various HIV-1 infected or transfected cell lines, respec tively. HIV-1 molecular clone pNL4-3 was used to transfect 293T, TZM-bl and HeLa cells while HIV-1 pseudo-typed virus was used to infect Jurkat, MT-1 and THP-1 cells. After twenty-four hours post infection or transfection, cells were harvested for extraction of total RNAs and subsequently used in real time PCR for quantification of ISG15 transcriptional expression. After forty-eight hours post infection or transfection, cells were harvested for extraction of total proteins to detect ISG15 protein expression. A significant up-regulation of ISG15 at transcription level was observed in HIV-1 infected or transfected cell lines, particulaly in THP-1 and TZM-bl cells. Up-regulation of ISG15 protein was observed only in TZM-bl cell. Cotransfection of ISG15 and HIV-1 indicated that ISG15 inhibited production of HIV-1 progeny virus in a dose and time depend manner in 293T cell but not TZM-bl cell. These results revealed upregulating ISG15 expression in transcriptional level and potential antagonistic mechanism against ISG15 by HIV-1 infection, simultanelusly.
