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Dengue virus infection promotes translocation of High Mobility Group Box 1 protein from the nucleus to the cytosol in dendritic cells, upregulates cytokine production and modulates viral replication.

¹ Walter Reed Army Institute of Research;
² Department of Microbiology and Immunology, Georgetown University School of;
³ Division of Viral Diseases, Walter Reed Army Institute of Research, Silver Spring, MD 20910;
⁴ Division of Retrovirology, Walter Reed Army Institute of Research, Rockville, MD;
⁵ Viral Diseases Dept., Naval Medical Research Center, 503 Robert Grant Ave, Silver Spring, MD 20910

⁶ E-mail: edwin.kamau{at}amedd.army.mil

High mobility group box 1 (HMGB1) protein functions in regulation of transcription, cellular activation and pro-inflammatory responses. However, the potential role of HMGB1 during viral infection has not been investigated. This study attempted to elucidate whether HMGB1-mediated inflammatory response contributes to the pathogenesis of DENV infection. Our data showed that HMGB1 was released at low DENV infection levels (MOI of 1) under non-necrotic conditions by human dendritic cells (DCs). When DENV-infected DCs were co-cultured with autologous T cells, there was increased production of HMGB1 by both cell types. HMGB1 regulated TNF-, IL-6, IL-8 and IFN- secretion in DENV infected DCs. Additionally, increased HMGB1 production was associated with reduced DENV replication titers in DCs. These results suggest that HMGB1 production likely influences DENV infection in susceptible hosts.

Received 1 December 2008; accepted 9 April 2009.