HIV-1 infection affects the expression of host cell factor TSG101 and Alix.
- Author:
Hui-liang HU
1
;
Zhe-feng MENG
;
Xiao-yan ZHANG
;
Jian-xin LU
Author Information
1. Wenzhou Medical College, Wenzhou 325000, China. hhlhzp@163.com
- Publication Type:Journal Article
- MeSH:
Calcium-Binding Proteins;
genetics;
metabolism;
Cell Cycle Proteins;
genetics;
metabolism;
DNA-Binding Proteins;
genetics;
metabolism;
Endosomal Sorting Complexes Required for Transport;
genetics;
metabolism;
Gene Expression Regulation;
HEK293 Cells;
HIV-1;
physiology;
Humans;
Jurkat Cells;
Leukocytes, Mononuclear;
metabolism;
virology;
RNA, Messenger;
genetics;
metabolism;
Transcription Factors;
genetics;
metabolism
- From:
Chinese Journal of Virology
2011;27(2):129-134
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the effects of HIV-1 infection on the expression of host factors TSG101 (Tumor Susceptibility Gene 101) and Alix (ALG-2-interacting protein X). HIV-1 infectious clone pNL4-3 was used to infect TZM-bl, PM1, Jurkat cell lines and human peripheral blood mononuclear cells (PBMC). Twenty-four hours post-infection, the infected or uninfected cells were harvested respectively for extraction of total RNAs and total cellular proteins, which were subsequently used in RT-PCR and Western-blotting respectively to quantify TSG101 and Alix, respectively. Our data showed that HIV-1 infection resulted in various influences on the expression of TSG101 and Alix in the cell lines and the primary PBMC. A down-regulation was mainly observed in the cell lines, whereas an up-regulation of TSG101 was identified in primary PBMC. Three patterns were observed for down-regulation, including dual down-regulation of TSG101 and Alix for Jurkat cells, single down-regulation of Alix for TZM-bl cells and marginal or no influence on PM1 cells. The dual down-regulation of Alix and TSG101 in Jurkat cells coincided with less expression of HIV-1 p24 protein. This is the first-line evidence that HIV-1 infection affects the expression of host factors TSG101 and Alix, the down-regulation of these molecules may influence the HIV-1 replication. The underlying mechanism remains to be addressed.
