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Memórias do Instituto Oswaldo Cruz
Fundação Oswaldo Cruz, Fiocruz
ISSN: 1678-8060 EISSN: 1678-8060
Vol. 104, No. 8, 2009, pp. 1091-1099
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Bioline Code: oc09223
Full paper language: English
Document type: Research Article
Document available free of charge
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Memórias do Instituto Oswaldo Cruz, Vol. 104, No. 8, 2009, pp. 1091-1099
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Dengue-2 infection and the induction of apoptosis in human primary monocytes
Torrentes-Carvalho, Amanda; Azeredo, Elzinandes L; Reis, Alessandro S; Gandini, Mariana; Barbosa, Luciana S & Kubelka, Claire F
Abstract
Monocytes/macrophages are important targets for dengue virus (DENV) replication; they induce inflammatory
mediators and are sources of viral dissemination in the initial phase of the disease. Apoptosis is an active process of
cellular destruction genetically regulated, in which a complex enzymatic pathway is activated and may be trigged by
many viral infections. Since the mechanisms of apoptotic induction in DENV-infected target cells are not yet defined,
we investigated the virus-cell interaction using a model of primary human monocyte infection with DENV-2 with the
aim of identifying apoptotic markers. Cultures analyzed by flow cytometry and confocal microscopy yielded DENV
antigen positive cells with rates that peaked at the second day post infection (p.i.), decayed afterwards and produced
the apoptosis-related cytokines TNF-α and IL-10. Phosphatidylserine, an early marker for apoptosis, was increased
at the cell surface and the Fas death receptor was upregulated at the second day p.i. at significantly higher rates in
DENV infected cell cultures than controls. However, no detectable changes were observed in the expression of the
anti-apoptotic protein Bcl-2 in infected cultures. Our data support virus modulation of extrinsic apoptotic factors in
the in vitro model of human monocyte DENV-2 infection. DENV may be interfering in activation and death mechanisms
by inducing apoptosis in target cells.
Keywords
dengue - apoptosis - monocytes - human
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