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Cellular Immune Activation in Children with Acute Dengue Virus Infections Is Modulated by Apoptosis
Author(s) -
Khin Saw Aye Myint,
Timothy P. Endy,
Duangrat Mongkolsirichaikul,
Choompun Manomuth,
Siripen Kalayanarooj,
David W. Vaughn,
Ananda Nisalak,
Sharone Green,
Alan L. Rothman,
Francis A. Ennis,
Daniel H. Libraty
Publication year - 2006
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/506451
Subject(s) - dengue fever , apoptosis , peripheral blood mononuclear cell , dengue virus , immunology , immune system , virus , fas receptor , virology , innate immune system , medicine , biology , programmed cell death , in vitro , biochemistry
Apoptosis is an important modulator of cellular immune responses during systemic viral infections. Peripheral-blood mononuclear cell (PBMC) apoptosis and plasma soluble levels of CD95, a mediator of apoptosis, were determined in sequential samples from children participating in a prospective study of dengue virus (DV) infections. During the period of defervescence, levels of PBMC apoptosis were higher in children developing dengue hemorrhagic fever (DHF), the most severe form of illness, than in those with dengue fever (DF) and other, nondengue, febrile illnesses. CD8(+) T lymphocytes made up approximately half of the peak circulating apoptotic PBMCs in DHF and DF. Maximum plasma levels of soluble CD95 were also higher in children with DHF than in those with DF. The level of PBMC apoptosis correlated with dengue disease severity. Apoptosis appears to be involved in modulation of the innate and adaptive immune responses to DV infection and is likely involved in the evolution of immune responses in other viral hemorrhagic fevers.

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