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Cellular factors implicated in filovirus entry

Suchita Bhattacharyya1, Thomas J Hope

  • 1University of Mumbai and Department of Atomic Energy-Centre for Excellence in Basic Sciences, Health Centre Building, Vidyanagari, Kalina, Santacruz East, Mumbai 400098, India.

Advances in Virology
|February 1, 2013
PubMed

Insights

Filoviruses cause deadly infections and can be biological weapons, necessitating research into their entry mechanisms. Understanding filoviral entry factors is crucial for developing effective antiviral therapies.

Area of Science:

  • Virology
  • Cell Biology
  • Infectious Diseases

Background:

  • Filoviral infections pose significant global health threats and potential bioweapon risks.
  • Current preventive and treatment strategies against filoviruses are lacking.
  • Filovirus entry is a critical step in their replication cycle, involving numerous cellular factors.

Purpose of the Study:

  • To summarize existing literature on filoviral entry mechanisms.
  • To highlight cellular factors implicated in filovirus entry.
  • To identify fundamental questions for future research in filoviral entry.

Main Methods:

  • Literature review of studies on filoviral entry.
  • Focus on cellular factors, including plasma membrane, cytoskeletal, and endosomal components.
  • Examination of signaling molecules like TAM receptor tyrosine kinases and potential receptors (TIM-1, NPC1).

Main Results:

  • Filovirus entry involves a complex interplay of cellular factors.
  • TAM family receptor tyrosine kinases (Tyro3, Axl, Mer) are implicated as entry factors.
  • T-cell immunoglobulin and mucin domain 1 (TIM-1) and Niemann-Pick C1 (NPC1) are proposed as potential filovirus receptors.

Conclusions:

  • Comprehensive understanding of filoviral entry is essential for developing antiviral therapeutics.
  • Further research into identified cellular factors and receptors can guide novel treatment strategies.
  • Addressing fundamental questions in filoviral entry is key to combating these deadly infections.

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