Interferon-Stimulated Genes Response in Endothelial Cells Following Hantaan Virus Infection.
10.3346/jkms.2007.22.6.987
- Author:
In Wook KIM
1
;
Ji Young HWANG
;
Sung Kwang KIM
;
Jong Kyu KIM
;
Ho Sun PARK
Author Information
1. Department of Applied Microbiology, College of Natural Resources, Yeungnam University, Daegu, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Hantaan Virus;
IFN-alpha/beta;
IRF-3/7;
MxA;
Endothelial Cells
- MeSH:
ATP-Binding Cassette Transporters/*genetics;
Blotting, Western;
Cells, Cultured;
Endothelial Cells/metabolism/*virology;
GTP-Binding Proteins/*genetics;
*Gene Expression Regulation;
Hantaan virus/*immunology;
Histocompatibility Antigens Class I/analysis;
Humans;
Interferon Regulatory Factor-3/genetics;
Interferon Regulatory Factor-7/*genetics;
Interferons/*genetics;
RNA, Messenger/analysis
- From:Journal of Korean Medical Science
2007;22(6):987-992
- CountryRepublic of Korea
- Language:English
-
Abstract:
The regulation mechanism of interferon (IFN) and IFN-stimulated genes is a very complex procedure and is dependent on cell types and virus species. We observed molecular changes related to anti-viral responses in endothelial cells during Hantaan virus (HTNV) infection. We found that there are two patterns of gene expression, the first pattern of gene expression being characterized by early induction and short action, as in that of type I IFNs,' and the other being characterized by delayed induction and long duration, as those of IRF-7, MxA, and TAP-1/2. Even though there are significant differences in their induction folds, we found that all of IFN-alpha/beta , IRF- 3/7, MxA, and TAP-1/2 mRNA expressions reached the peak when the viral replication was most active, which took place 3 days of post infection (d.p.i.). In addition, an interesting phenomenon was observed; only one gene was highly expressed in paired genes such as IFN-alpha/beta??(3/277-folds), IRF-3/7 (2.2/29.4-folds), and TAP- 1/2 (26.2/6.1-folds). Therefore, IFN-beta, IRF-7, and TAP-1 seem to be more important for the anti-viral response in HTNV infection. MxA was increased to 296-folds at 3 d.p.i. and kept continuing 207-folds until 7 d.p.i.. The above results indicate that IFN-beta works for an early anti-viral response, while IRF7, MxA, and TAP-1 work for prolonged anti-viral response in HTNV infection.
