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Mediators of Inflammation
Volume 2014 (2014), Article ID 697837, 11 pages
Research Article

Hantaan Virus Infection Induces CXCL10 Expression through TLR3, RIG-I, and MDA-5 Pathways Correlated with the Disease Severity

1Department of Immunology, The Fourth Military Medical University, 169 Changle West Road, Xi’an 710032, China
2Department of Blood Transfusion, Xijing Hospital, The Fourth Military Medical University, Xi’an 710032, China
3Department of Infectious Disease, Tangdu Hospital, The Fourth Military Medical University, Xi’an 710032, China

Received 19 October 2013; Revised 28 December 2013; Accepted 11 January 2014; Published 23 February 2014

Academic Editor: Beatriz De las Heras

Copyright © 2014 Yusi Zhang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Hantaan virus (HTNV) is a major agent causing hemorrhagic fever with renal syndrome (HFRS). Although the pathogenesis of HFRS is unclear, some reports have suggested that the abundant production of proinflammatory cytokines and uncontrolled inflammatory responses may contribute to the development of HFRS. CXCL10 is one of these cytokines and is found to be involved in the pathogenesis of many virus infectious diseases. However, the role of CXCL10 in the pathogenesis of HFRS and the molecular regulation mechanism of CXCL10 in HTNV infection remain unknown. In this study, we report that CXCL10 expresses highly in the HFRS patients’ sera and the elevated CXCL10 is positively correlated with the severity of HFRS. We find that HTNV, a single-strand RNA virus, can act as a double-strand RNA to activate the TLR3, RIG-I, and MDA-5 signaling pathways. Through the downstream transcription factors of these pathways, NF-κB and IRF7, which bind directly to the CXCL10’s promoter, the expression of CXCL10 is increased. Our results may help to better understand the role of CXCL10 in the development of HFRS and may provide some novel insights into the immune response of HTNV infection.