Ebola and Marburg Viruses Replicate in Monocyte-Derived Dendritic Cells without Inducing the Production of Cytokines and Full Maturation

Catharine M. Bosio, M. Javad Aman, Case Grogan, Robert Hogan, Gordon Ruthel, Diane Negley, Mansour Mohamadzadeh, Sina Bavari, Alan Schmaljohn

Research output: Contribution to journalArticlepeer-review

236 Scopus citations

Abstract

Ebola virus (EBOV) and Marburg virus (MARV) cause rapidly progressive hemorrhagic fever with high mortality and may possess specialized mechanisms to evade immune destruction. We postulated that immune evasion could be due to the ability of EBOV and MARV to interfere with dendritic cells (DCs), which link innate and adaptive immune responses. We demonstrate that EBOV and MARV infected and replicated in primary human DCs without inducing cytokine secretion. Infected DC cultures supported exponential viral growth without releasing interferon (IFN)-α and were impaired in IFN-α production if treated with double-stranded RNA. Moreover, EBOV and MARV impaired the ability of DCs to support T cell proliferation, and infected, immature DCs underwent an anomalous maturation. These findings may explain the profound virulence of EBOV and MARV - DCs are disabled, and an effective early host response is delayed by the necessary reliance on less-efficient secondary mechanisms.

Original languageEnglish (US)
Pages (from-to)1630-1638
Number of pages9
JournalJournal of Infectious Diseases
Volume188
Issue number11
DOIs
StatePublished - Dec 1 2003
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases

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