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Related Experiment Videos

Cell entry by human pathogenic arenaviruses.

Jillian M Rojek1, Stefan Kunz

  • 1Viral Immunobiology Laboratory, Molecular and Integrative Neurosciences Department, The Scripps Research Institute, La Jolla, CA 92037, USA.

Cellular Microbiology
|January 10, 2008
PubMed
Summary
This summary is machine-generated.

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Human pathogenic arenaviruses like Lassa virus (LASV) cause severe hemorrhagic fevers. This review details their cellular receptor interactions and entry mechanisms, highlighting differences between Old World and New World viruses.

Area of Science:

  • Virology
  • Cell Biology
  • Infectious Diseases

Background:

  • Arenaviruses, including Lassa virus (LASV), cause severe hemorrhagic fevers with high fatality rates.
  • Pathogenic Old World and New World arenaviruses share genomic and structural similarities but differ in host cell entry mechanisms.

Purpose of the Study:

  • To review the initial steps of human pathogenic arenavirus infection.
  • To elucidate the interaction of arenaviruses with cellular receptors and their subsequent entry into host cells.

Main Methods:

  • Review of existing literature on arenavirus-host interactions.
  • Analysis of viral entry pathways, including receptor usage and endocytosis mechanisms.

Main Results:

  • Old World arenaviruses utilize alpha-dystroglycan, while New World arenaviruses use transferrin receptor 1 as primary receptors.

Related Experiment Videos

  • Junin virus (JUNV) enters via clathrin-dependent endocytosis; lymphocytic choriomeningitis virus (LCMV) entry appears clathrin-independent.
  • pH-dependent membrane fusion mediated by the envelope glycoprotein (GP) occurs in the endosome.

    • Conclusions:

    • Distinct cellular receptors are employed by Old World and New World arenaviruses.
    • Arenavirus entry mechanisms, including endocytosis and GP-mediated fusion, exhibit unique features with implications for viral pathogenesis.