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Journal of Virology, August 1999, p. 6582-6589, Vol. 73, No. 8
INSERM U 395, Toulouse,
France,1 and Louis Jeantet Laboratory of
Molecular Genetics, Department of Genetics and Microbiology, University
of Geneva Medical School, Geneva, Switzerland2
Received 1 March 1999/Accepted 14 May 1999
Human cytomegalovirus (HCMV), a betaherpesvirus, is a pathogen
which escapes immune recognition through various mechanisms. In this
paper, we show that HCMV down regulates gamma interferon (IFN-
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Copyright © 1999, American Society for Microbiology. All rights reserved.
Escape of Human Cytomegalovirus from
HLA-DR-Restricted CD4+ T-Cell Response Is Mediated by
Repression of Gamma Interferon-Induced Class II Transactivator
Expression
)-induced HLA-DR expression in U373 MG astrocytoma cells due to
a defect downstream of STAT1 phosphorylation and nuclear translocation.
Repression of class II transactivator (CIITA) mRNA expression is
detected within the first hours of IFN-
-HCMV coincubation and
results in the absence of HLA-DR synthesis. This defect leads to the
absence of presentation of the major immediate-early protein IE1 to
specific CD4+ T-cell clones when U373 MG cells, used as
antigen-presenting cells, are treated with IFN-
plus HCMV. However,
presentation of endogenously synthesized IE1 can be restored when U373
MG cells are transfected with CIITA prior to infection with HCMV.
Altogether, the data indicate that the defect induced by HCMV resides
in the activation of the IFN-
-responsive promoter of CIITA. This is the first demonstration of a viral inhibition of CIITA expression.
*
Corresponding author. Mailing address: INSERM U 395, CHU Purpan, BP 3028, 31024 Toulouse Cedex, France. Phone: 33 5 62 74 83 76. Fax: 33 5 62 74 83 86. E-mail:
davignon{at}purpan.inserm.fr.
This work is dedicated to the memory of our friend and colleague
Claude de Préval.
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