Down-regulation of HIV-1 Infection by Inhibition of the MAPK Signaling Pathway
10.1007/s12250-011-3184-y
- Author:
Jian GONG
;
Xihui SHEN
;
Chao CHEN
;
Hui QIU
;
Rongge YANG
- Publication Type:Journal Article
- Keywords:
HIV-1 inhibition;
Mitogen-activated protein kinase(MAPK);
Extracellular signal-regulated kinase(ERK);
Jun N-terminal kinase(JNK);
p38;
LTR activation
- From:
Virologica Sinica
2011;26(2):114-122
- CountryChina
- Language:Chinese
-
Abstract:
The human immunodeficiency virus type 1(HIV-1)can interact with and exploit the host cellular machinery to replicate and propagate itself.Numerous studies have shown that the Mitogen-activated protein kinase(MAPK)signal pathway can positively regulate the replication of HIV-1,but exactly how each MAPK pathway affects HIV-1 infection and replication is not understood.In this study,we used the Extracellular signal-regulated kinase(ERK)pathway inhibitor,PD98059,the Jun N-terminal kinase(JNK)pathway inhibitor,SP600125,and the p38 pathway inhibitor,SB203580,to investigate the roles of these pathways in HIV-1replication.We found that application of PD98059 results in a strong VSV-G pseudotyped HIV-1NL4-3 luciferase reporter virus and HIV-1NL4-3 virus inhibition activity.In addition,SB203580 and SP600125 also elicited marked VSV-G pseudotyped HIV-1NL4-3 luciferase reporter virus inhibition activity but no HIV-1NL4-3 virus inhibition activity.We also found that SB203580 and SP600125 can enhance the HIV-1 inhibition activity of PD98059when cells were treated with all three MAPK pathway inhibitors in combination.Finally,we show that HIV-1virus inhibition activity of the MAPK pathway inhibitors was the result of the negative regulation of HIV-1 LTR promoter activity.
