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Chinese Journal of Virology ; (6): 388-394, 2015.
Article in Chinese | WPRIM | ID: wpr-296272

ABSTRACT

Human immunodeficiency virus (HIV)-1 infection changes transcriptional profiles and regulates. the factors and machinery of the host that facilitate viral replication. Our previous study suggested that the serine/threonine kinase citron kinase (citK) promotes HIV-1 egress. To ascertain if HIV-1 infection affects citK expression in primary cells, peripheral blood mononuclear cells were infected with vesicular stomatitis virus G protein (VSV-G)-pseudotyped HIV-1 vector NL4-3-luc viruses, which resulted in remarkably increased expression of citK. citK overexpression led to a more than two-fold increase in HIV-1 production, whereas a significant decrease was observed when citK was depleted in CD4+ T cells. Infection with HIV-1 pseudoviruses induced increases in the mRNA and protein levels of citK by 2. 5- and 2. 7-fold in HEK293T cells, respectively. By cloning the 5-kb promoter of citK into a luciferase reporter system and transfecting the construct into HEK293T cells, enhanced luciferase activity was observed during HIV-1 infection. Taken together, these data demonstrate that HIV-1 infection upregulates citK expression at the transcriptional level, and thereby renders the host more susceptible to invasion by HIV-1.


Subject(s)
Humans , CD4-Positive T-Lymphocytes , Virology , Cloning, Molecular , Gene Expression Regulation, Enzymologic , HEK293 Cells , HIV-1 , Physiology , Intracellular Signaling Peptides and Proteins , Genetics , Protein Serine-Threonine Kinases , Genetics , Up-Regulation , Virus Replication
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