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Blood, 15 October 2002, Vol. 100, No. 8, pp. 2867-2873
IMMUNOBIOLOGY
Latent cytomegalovirus down-regulates major histocompatibility
complex class II expression on myeloid progenitors
Barry Slobedman,
Edward S. Mocarski,
Ann M. Arvin,
Elizabeth D. Mellins, and
Allison Abendroth
From the Center for Virus Research, Westmead Millennium
Institute and University of Sydney, Westmead, Australia, and the
Departments of Microbiology & Immunology and of Pediatrics, Stanford
University School of Medicine, CA.
Following primary infection, human cytomegalovirus (CMV)
establishes a lifelong latent infection in bone marrow-derived
myeloid lineage cells. Although downmodulation of major
histocompatibility complex (MHC) class I and class II protein levels
occurs during active viral replication, little is known about the
modulation of these proteins during latent infection. When analyzed by
flow cytometry, latently infected adherent cells collected from
granulocyte macrophage progenitor (GM-P) cultures exhibited a striking
reduction in MHC class II antigen present on the cell surface starting
very early after exposure to virus that continued for more than 2 weeks. In comparison, cell surface levels of the monocyte cell surface marker CD14 remained unaltered in these cells. A recombinant virus (RV798) lacking the virus genes US2-US11 retained the ability to
downmodulate MHC class II levels during latent infection. Immunoblot and immunofluorescent antibody staining analyses showed that the reduction in MHC class II surface levels during latency was associated with a block in protein trafficking. HLA-DR was retained within cytoplasmic vesicles that also contained HLA-DM. Thus, downmodulation remained independent of all previously characterized MHC class I and
class II immunomodulatory viral gene products and involved a mechanism
not previously ascribed to any viral function. These data show that
latent infection is accompanied by reduced cell surface expression of
MHC class II proteins, a strategy that would afford the virus escape
from immunosurveillance and increase the chances for lifelong
latent infection.
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