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Journal of Virology, April 2001, p. 3383-3390, Vol. 75, No. 7
Program of Cell Biology, Department of
Medicine, National Jewish Medical and Research Center, and
Department of Medicine, University of Colorado Health Science
Center, Denver, Colorado 80206
Received 23 September 2000/Accepted 9 January 2001
Human cytomegalovirus (HCMV) evades healthy immune responses during
infection, and this evasion may allow HCMV to establish latency in the
host. The human vasculature has been recognized as a site of HCMV
infection and may also be a site of latent HCMV infection. As the
interface between circulating cells and underlying parenchymal
cells, the vascular endothelium provides signals for local reaction of
inflammatory cells. We propose that HCMV down-regulates expression of
the proinflammatory chemokine RANTES from the infected endothelium, which may result in reduced recruitment of mononuclear cells to the site of infection. Abortive HCMV infection of
primary endothelial cells with the clinical isolate HCMV 4010, under
conditions in which viral gene expression could not occur,
induced high levels of RANTES expression. Replicative HCMV
infection, however, induced cells in parallel cultures to
express significantly lower levels of RANTES. Expression of the
chemokines interleukin 8 and MCP-1 by endothelial cells was found
to be unaffected by replicative HCMV infection and thus may not
play an important role during early HCMV infection of the endothelium.
HCMV may regulate RANTES expression from
endothelial cells as a mechanism to evade the local immune response to infection.
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.7.3383-3390.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Viral Regulation of RANTES Expression during Human
Cytomegalovirus Infection of Endothelial Cells
*
Corresponding author. Mailing address: Department of
Medicine, National Jewish Medical and Research Center, 1400 Jackson
St., Denver, CO 80206. Phone: (303) 398-1420. Fax: (303) 270-2319. E-mail: billstroms{at}njc.org.
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