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Implications of the release of high-mobility group box 1 protein from dying cells during human immunodeficiency virus type 1 infection in vitro
Division of Clinical Microbiology, Department of Laboratory Medicine, Karolinska University Hospital, Stockholm, Sweden .
Division of Clinical Microbiology, Department of Laboratory Medicine, Karolinska University Hospital, Stockholm, Sweden; Division of Infectious Diseases, Department of Laboratory Medicine, Karolinska University Hospital, Stockholm, Sweden.
Department of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden .ORCID iD: 0000-0003-0902-508X
Center for Infectious Medicine, Department of Laboratory Medicine, Karolinska University Hospital, Stockholm, Sweden .
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2010 (English)In: Journal of General Virology, ISSN 0022-1317, E-ISSN 1465-2099, Vol. 91, no Pt 7, p. 1800-1809Article in journal (Refereed) Published
Abstract [en]

Plasma levels of high-mobility group box 1 protein (HMGB1) are elevated during the course of human immunodeficiency virus type 1 (HIV-1) infection and the molecule has an impact on virus replication. This study investigated the mode of cell death and release of HMGB1 during HIV-1 infection in vitro. MT4 cells and primary CD4(+) T cells were infected with HIV-1 isolates, and HMGB1 release was monitored in relation to cytopathic effects (CPE) and apoptosis. HMGB1 release from cells was analysed by Western blotting. For MT4 cells, an enzyme-linked immunosorbent spot (ELISPOT) assay was adapted to measure the release during necrosis. Lactate dehydrogenase (LDH) activity was quantified using a commercial assay. Flow cytometry was used to determine the level of infection and apoptosis. MT4 cells were > or =90 % infected at 48 h post-infection (p.i.). CPE was first observed at 60 h and correlated with release of HMGB1, LDH activity and caspase-3 (C3) activation. HMGB1 spots were clearly detected by ELISPOT assay at 72 h p.i. Annexin V and C3 staining showed that apoptosis was substantially involved in HIV-1-related cell death. Addition of Z-VAD (a caspase inhibitor) in a single dose at 24 or 40 h p.i. decreased both the number of caspase-positive cells and the release of HMGB1. Infection of primary CD4(+) T cells showed a 22 % (median) infection rate at 96 h. Related CPE corresponded to LDH and HMGB1 release. Both necrosis and apoptosis contributed to HMGB1 liberation during HIV-1-induced cell death and the protein could induce tumour necrosis factor-alpha release from peripheral mononuclear blood cells. These data imply that passive HMGB1 release contributes to the excessive immune activation characteristic of HIV-1 pathogenesis.

Place, publisher, year, edition, pages
2010. Vol. 91, no Pt 7, p. 1800-1809
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Medical Biotechnology Basic Medicine
Identifiers
URN: urn:nbn:se:oru:diva-41993DOI: 10.1099/vir.0.016915-0ISI: 000279747600018PubMedID: 20200191Scopus ID: 2-s2.0-77954168421OAI: oai:DiVA.org:oru-41993DiVA, id: diva2:792892
Note

Funding Agencies:

Swedish Medical Research Council

Swedish Foundation for Strategic Research

Swedish Physicians Against AIDS Research Fund 

Available from: 2015-03-05 Created: 2015-01-16 Last updated: 2018-04-25Bibliographically approved

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Abdurahman, Samir

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