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Impact of HMGB1/TLR ligand complexes on HIV-1 replication: possible role for flagellin during HIV-1 infection
Department of Infectious Diseases, Institution of Medicine, Karolinska University Hospital, Stockholm, Sweden .
Department of Infectious Diseases, Institution of Medicine, Karolinska University Hospital, Stockholm, Sweden .ORCID iD: 0000-0003-0902-508X
Department of Clinical Microbiology, Institution of Laboratory Medicine, Karolinska University Hospital, Stockholm, Sweden .
Department of Infectious Diseases, Oslo University Hospital Ullevål, Oslo, Norway .
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2012 (English)In: International Journal of Microbiology, ISSN 1687-918X, E-ISSN 1687-9198, 263836- p.Article in journal (Refereed) Published
Abstract [en]

Objective: We hypothesized that HMGB1 in complex with bacterial components, such as flagellin, CpG-ODN, and LPS, promotes HIV-1 replication. Furthermore, we studied the levels of antiflagellin antibodies during HIV-1-infection.

Methods: Chronically HIV-1-infected U1 cells were stimulated with necrotic extract/recombinant HMGB1 in complex with TLR ligands or alone. HIV-1 replication was estimated by p24 antigen in culture supernatants 48-72 hours after stimulation. The presence of systemic anti-flagellin IgG was determined in 51 HIV-1-infected patients and 19 controls by immunoblotting or in-house ELISA.

Results: Flagellin, LPS, and CpG-ODN induced stronger HIV-1 replication when incubated together with necrotic extract or recombinant HMGB1 than activation by any of the compounds alone. Moreover, the stimulatory effect of necrotic extract was inhibited by depletion of HMGB1. Elevated levels of anti-flagellin antibodies were present in plasma from HIV-1-infected patients and significantly decreased during 2 years of antiretroviral therapy.

Conclusions: Our findings implicate a possible role of HGMB1-bacterial complexes, as a consequence of microbial translocation and cell necrosis, for immune activation in HIV-1 pathogenesis. We propose that flagellin is an important microbial product, that modulates viral replication and induces adaptive immune responses in vivo.

Place, publisher, year, edition, pages
2012. 263836- p.
National Category
Infectious Medicine
Research subject
Infectious Diseases
Identifiers
URN: urn:nbn:se:oru:diva-41996DOI: 10.1155/2012/263836PubMedID: 22719767Scopus ID: 2-s2.0-84863676731OAI: oai:DiVA.org:oru-41996DiVA: diva2:792887
Available from: 2015-03-05 Created: 2015-01-16 Last updated: 2015-05-13Bibliographically approved

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CiteExportLink to record
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