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Characteristics of dengue virus‐infected peripheral blood mononuclear cell death that correlates with the severity of illness
Author(s) -
Jaiyen Yanin,
Masrinoul Promsin,
Kalayanarooj Siripen,
Pulmanausahakul Rojjanaporn,
Ubol Sukathida
Publication year - 2009
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.2009.00148.x
Subject(s) - apoptosis , peripheral blood mononuclear cell , dengue virus , immunology , dengue fever , biology , programmed cell death , innate immune system , immune system , virology , in vitro , biochemistry
The pathogenic mechanism of the severe form of dengue is complicated. Recent reports indicate that apoptotic death of various tissues or organs may be associated with vascular leakage, and ultimately leads to the death of DENV‐infected patients. In the present study, we provide additional evidence supporting the detrimental role of apoptosis in DENV infection. A comparison of the rate of apoptosis in PBMCs isolated from patients suffering DF, a mild form of the disease, and the rate in patients with DHF, a life‐threatening disease, revealed that PBMCs from DHF patients underwent apoptosis at a significantly higher rate than those suffering from DF alone. This suggests that the severity of natural DENV infection correlates with PBMC apoptosis. In addition, this cell death was induced not only by DENV itself, but also by the apoptotic activities of pro‐inflammatory cytokines, such as TNF‐α, and IL‐1β, that were upregulated in DHF patients. The death of these mononuclear cells that function in an innate immune system may explain the higher viral load in DHF patients than in DF patients. Interestingly, a gene expression profile pattern elucidated that apoptosis occurring during natural DENV infection involved mainly the extrinsic apoptosis pathway, which is mediated via both caspase‐dependent and caspase‐independent mechanisms. In conclusion, our data highlight the adverse effect of apoptosis induced by DENV and by pro‐inflammatory cytokines during natural DENV infection.