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Role of clathrin-mediated endocytosis during vesicular stomatitis virus entry into host cells

Xiangjie Sun1, Vivian K Yau, Benjamin J Briggs

  • 1Department of Microbiology and Immunology, Cornell University, C4127 Veterinary Medical Center, Ithaca, NY 14853, USA.

Virology
|June 7, 2005
PubMed

Insights

Clathrin is essential for Vesicular Stomatitis Virus (VSV) entry into cells. Blocking clathrin function, using genetic or chemical methods, significantly inhibits VSV infection, confirming its critical role in viral internalization.

Area of Science:

  • Cell Biology
  • Virology
  • Molecular Biology

Background:

  • Vesicular Stomatitis Virus (VSV) enters cells via pH-dependent endocytosis.
  • The precise mechanisms of VSV internalization, particularly the role of specific cellular machinery, remain incompletely understood.

Purpose of the Study:

  • To elucidate the functional role of clathrin in the cellular entry of Vesicular Stomatitis Virus (VSV).
  • To determine if clathrin-mediated endocytosis is a necessary pathway for VSV infection.

Main Methods:

  • Expression of a dominant-negative mutant of Eps15 (GFP-Eps15Delta95/295), a key protein in clathrin-mediated endocytosis.
  • Treatment of cells with chlorpromazine to inhibit clathrin-mediated endocytosis.
  • Utilizing small interfering RNA (siRNA) to knock down clathrin heavy chain expression.

Main Results:

  • Expression of GFP-Eps15Delta95/295 significantly reduced VSV infection.
  • Chlorpromazine treatment effectively inhibited VSV entry into cells.
  • Clathrin heavy chain knock-down using siRNA also prevented VSV infection.

Conclusions:

  • Clathrin-mediated endocytosis is an essential pathway for Vesicular Stomatitis Virus (VSV) entry into host cells.
  • These findings establish clathrin as a critical component required for VSV internalization.

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