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This Article Full Text Full Text (PDF) All Versions of this Article: vir.0.009027-0v1 90/8/1827    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Google Scholar Articles by Kamau, E. Articles by Palmer, D. R. PubMed PubMed Citation Articles by Kamau, E. Articles by Palmer, D. R. Agricola Articles by Kamau, E. Articles by Palmer, D. R.

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 virus replication

¹ Division of Viral Diseases, Walter Reed Army Institute of Research, Silver Spring, MD 20910, USA
² Department of Microbiology and Immunology, Georgetown University School of Medicine, Washington, DC 20057, USA
³ Division of Retrovirology, Walter Reed Army Institute of Research, Rockville, MD 21910, USA
⁴ Viral and Rickettsial Diseases Department, Naval Medical Research Center, 503 Robert Grant Avenue, Silver Spring, MD 20910, USA

Correspondence
Edwin Kamau
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 the HMGB1-mediated inflammatory response contributes to the pathogenesis of dengue virus (DENV) infection. Our data showed that HMGB1 was released at low DENV infection levels (m.o.i. 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 tumour necrosis factor alpha, interleukin (IL)-6, IL-8 and alpha interferon secretion in DENV-infected DCs. Additionally, increased HMGB1 production was associated with reduced DENV replication titres in DCs. These results suggest that HMGB1 production influences DENV infection in susceptible hosts.