Entry of influenza virus into a glycosphingolipid-deficient mouse skin fibroblast cell line

S Ablan1, S S Rawat, R Blumenthal

  • 1LECB, CCR, NCI-Frederick, National Institutes of Health, Frederick, MD 21702-1201, USA.

Archives of Virology
|January 5, 2002
PubMed

Insights

Influenza virus infects and fuses with cells lacking glycosphingolipids (GSLs), indicating GSLs are not essential for these processes. Sialoglycoproteins, not gangliosides, are the primary targets for influenza virus entry.

Area of Science:

  • Virology
  • Cell Biology
  • Biochemistry

Background:

  • Glycosphingolipids (GSLs) are complex lipids found in cell membranes.
  • Their role in viral entry and fusion is not fully understood.
  • Influenza virus is a significant human pathogen.

Purpose of the Study:

  • To investigate the role of GSLs in influenza virus infection and fusion.
  • To determine if GSLs are essential for influenza virus-host cell interactions.

Main Methods:

  • Utilized a GSL-deficient mouse skin fibroblast mutant cell line (GM95).
  • Assessed influenza virus fusion using octadecyl rhodamine labeled virus.
  • Measured influenza virus infection levels.
  • Investigated the effect of neuraminidase pre-treatment on infection and fusion.

Main Results:

  • Influenza virus fused with GM95 cells similarly to parental cell lines.
  • Influenza virus infected GM95 cells at comparable levels to parental cells.
  • Neuraminidase pre-treatment blocked both infection and fusion.

Conclusions:

  • Gangliosides, a type of GSL, are not essential for influenza virus fusion and infection.
  • Influenza virus primarily utilizes sialoglycoproteins for cell entry and fusion.