Intracellular events and cell fate in filovirus infection

Judith Olejnik1, Elena Ryabchikova, Ronald B Corley

  • 1Department of Microbiology, School of Medicine, Boston University, Boston, MA 02118, USA. jolejnik@bu.edu

Viruses
|September 20, 2011
PubMed

Insights

Marburg and Ebola viruses cause severe hemorrhagic fevers by infecting immune cells. This review explores how these filoviruses damage cells and spread, impacting disease progression.

Area of Science:

  • Virology
  • Immunology
  • Pathogenesis

Background:

  • Marburg and Ebola viruses cause severe hemorrhagic diseases with high fatality rates.
  • Filoviruses initially target monocytes, macrophages, and dendritic cells, spreading via blood and lymph.
  • Bystander lymphocyte apoptosis is a hallmark, but its mechanisms and the fate of infected cells remain unclear.

Purpose of the Study:

  • To review intracellular events in filovirus infection.
  • To explore virus amplification and cell damage mechanisms.
  • To discuss the correlation between cellular dysfunction, cell death, and disease pathogenesis.

Main Methods:

  • Literature review of intracellular events in filovirus infection.
  • Analysis of cellular mechanisms of virus amplification and damage.
  • Discussion of pathogenesis based on cellular dysfunction and death.

Main Results:

  • Filovirus infection leads to immune cell targeting and systemic spread.
  • Cellular dysfunction and death are key features of filovirus disease.
  • Mechanisms of bystander lymphocyte apoptosis require further investigation.

Conclusions:

  • Understanding intracellular events is crucial for filovirus disease pathogenesis.
  • Cellular damage and death pathways are central to disease progression.
  • Further research is needed on bystander lymphocyte apoptosis and infected cell fate.

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