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.