Potential factors induced by filoviruses that lead to immune supression

Research output: Contribution to journalReview articlepeer-review

18 Scopus citations

Abstract

The filoviruses, Ebola (EBOV) and Marburg (MARV), are among the deadliest of human pathogens, causing acute diseases typified by rapidly fatal hemorrhagic fevers. Upon filoviral infection, innate immune cells become paralyzed and lose the capacity to properly co-stimulate and activate filovirus-specific, T-cell responses. Deleterious inflammation and upregulation of co-inhibitory molecules expressed by monocytic lineage cells (e.g., dendritic cells) and their co-inhibitory receptors on T- and B-cells may lead to incomplete humoral and T-cell immunity, anergy, exhaustion, apoptosis, and subsequent immune subversion. Hence, the dysregulation of inflammatory and co-inhibitory molecules may be exploited by filoviruses to further deteriorate host immune responses, ultimately leading to fulminant infections in susceptible species. Thus, in light of accumulating scientific observations, the challenge is now to characterize the molecular mechanisms that may result in rational strategies leading to new therapeutics and vaccines.

Original languageEnglish (US)
Pages (from-to)174-185
Number of pages12
JournalCurrent Molecular Medicine
Volume9
Issue number2
DOIs
StatePublished - 2009
Externally publishedYes

Keywords

  • Anergy
  • Co-inhibition
  • Dendritic cells
  • Filovirus
  • Inflammation
  • Programmed death

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Medicine
  • Molecular Biology

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