Seoul virus suppresses NF-κB-mediated inflammatory responses of antigen presenting cells from Norway rats

Research output: Contribution to journalArticle

Abstract

Hantavirus infection reduces antiviral defenses, increases regulatory responses, and causes persistent infection in rodent hosts. To address whether hantaviruses alter the maturation and functional activity of antigen presenting cells (APCs), rat bone marrow-derived dendritic cells (BMDCs) and macrophages (BMDMs) were generated and infected with Seoul virus (SEOV) or stimulated with TLR ligands. SEOV infected both DCs and macrophages, but copies of viral RNA, viral antigen, and infectious virus titers were higher in macrophages. The expression of MHCII and CD80, production of IL-6, IL-10, and TNF-α, and expression of Ifnβ were attenuated in SEOV-infected APCs. Stimulation of APCs with poly I:C prior to SEOV infection increased the expression of activation markers and production of inflammatory cytokines and suppressed SEOV replication. Infection of APCs with SEOV suppressed LPS-induced activation and innate immune responses. Hantaviruses reduce the innate immune response potential of APCs derived from a natural host, which may influence persistence of these zoonotic viruses in the environment.

Original languageEnglish (US)
Pages (from-to)115-127
Number of pages13
JournalVirology
Volume400
Issue number1
DOIs
StatePublished - Apr 25 2010

Keywords

  • Dendritic cells
  • Hantavirus
  • Innate immunity
  • Interferon
  • MHC
  • Macrophage
  • Rodent
  • TNF
  • Toll-like receptor
  • Viral persistence

ASJC Scopus subject areas

  • Virology

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