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Rheumatology/Immunology and Allergy, Department of Medicine, Tri-Service General Hospital;
Graduate Institute of Life Science;
Institute of Biology and Anatomy; and
Department of Parasitology and Tropical Medicine, National Defense Medical Center, Taiwan, Republic of China;
¶ School of Medical Technology, College of Medicine and Division of Infectious Disease, National Taiwan University, Taiwan, Republic of China; and
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Immunology Division, Cheng-Hsin Rehabilitation Medical Center, Taiwan, Republic of China.
Dengue virus (DV) infection is a major problem in public health. It
can cause fatal diseases such as Dengue hemorrhagic fever and Dengue
shock syndrome. Dendritic cells (DC) are professional APCs required for
establishing a primary immune response. Here, we investigated the role
of human PBMC-derived DC in DV infection. Using different techniques,
including plaque assay, flow cytometry analysis, nested RT-PCR, and
confocal microscope and electron microscope examinations, we show that
DV can enter cultured human DC and produce virus particles. After
entrance, DV could be visualized in cystic vesicles, vacuoles, and the
endoplasmic reticulum. The DV-infected DC also showed proliferation and
hypertrophy of the endoplasmic reticulum as well as the swollen
mitochondria. In addition, the DV-stimulated DC could express
maturation markers such as B7-1, B7-2, HLA-DR, CD11b, and CD83.
Furthermore, the infection of DC by DV induced production of TNF-
and IFN-
, but not IL-6 and IL-12. Although DC underwent spontaneous
apoptosis in the absence of feeding cytokines, this process appeared to
be delayed after DV infection. Our observations provide important
information in understanding the pathogenesis of DV
infection.
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