acute dengue virus 2 infection in gabonese patients is associated with an early innate immune response, including strong interferon alpha production急性感染登革病毒2加蓬患者与早期的先天免疫反应有关,包括强大的干扰素α生产.pdfVIP
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acute dengue virus 2 infection in gabonese patients is associated with an early innate immune response, including strong interferon alpha production急性感染登革病毒2加蓬患者与早期的先天免疫反应有关,包括强大的干扰素α生产
Becquart et al. BMC Infectious Diseases 2010, 10:356
/1471-2334/10/356
RESEARCH ARTICLE Open Access
Acute dengue virus 2 infection in Gabonese
patients is associated with an early innate
immune response, including strong interferon
alpha production
1,2*† 1,3† 1 4 1
Pierre Becquart , Nadia Wauquier , Dieudonné Nkoghe , Angélique Ndjoyi-Mbiguino , Cindy Padilla ,
Marc Souris5,6, Eric M Leroy1,2
Abstract
Background: Dengue is now a leading cause of morbidity and mortality throughout the tropics. We conducted
the first ex vivo study of dengue fever (DF) in African patients infected during the first Gabonese dengue virus 2
(DENV-2) outbreak in 2007, in order to investigate cytokine production, including the antiviral cytokine IFN-a,
reported to be a potent inhibitor of DENV replication in vitro.
Methods: Levels of 50 cytokines, chemokines and growth factors were measured in plasma from 36 patients with
DENV-2 infection, and in uninfected controls, using Luminex multiplex technology. The results were interpreted
according to the day of sampling after symptom onset. PBMC from six patients were also studied for T lymphocyte
cell surface marker expression by flow cytometry.
Results: Acute DENV-2 infection elicited high levels of several pro-inflammatory cytokines (IL-6 and IL-17),
chemokines (MIF, RANTES, IP-10 and MCP-1) and growth factors (G-CSF, GM-CSF and VEGF-A). We also observed
high levels of IFN-a for the first time in adult DF patients, and CD4+ and CD8+ T cell activation at symptom onset.
Conclusion: Acute DENV-2 infection in African patients elicits a strong innate response involving IFN-a production,
as well as an adaptive immune response.
Background
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