Ebola virus uses clathrin-mediated endocytosis as an entry pathway

Suchita Bhattacharyya, Kelly L. Warfield, Gordon Ruthel, Sina Bavari, M. Javad Aman, Thomas J. Hope*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

90 Scopus citations


Ebola virus (EBOV) infects several cell types and while viral entry is known to be pH-dependent, the exact entry pathway(s) remains unknown. To gain insights into EBOV entry, the role of several inhibitors of clathrin-mediated endocytosis in blocking infection mediated by HIV pseudotyped with the EBOV envelope glycoprotein (EbGP) was examined. Wild type HIV and envelope-minus HIV pseudotyped with Vesicular Stomatitis Virus glycoprotein (VSVg) were used as controls to assess cell viability after inhibiting clathrin pathway. Inhibition of clathrin pathway using dominant-negative Eps15, siRNA-mediated knockdown of clathrin heavy chain, chlorpromazine and sucrose blocked EbGP pseudotyped HIV infection. Also, both chlorpromazine and Bafilomycin A1 inhibited entry of infectious EBOV. Sensitivity of EbGP pseudotyped HIV as well as infectious EBOV to inhibitors of clathrin suggests that EBOV uses clathrin-mediated endocytosis as an entry pathway. Furthermore, since chlorpromazine inhibits EBOV infection, novel therapeutic modalities could be designed based on this lead compound.

Original languageEnglish (US)
Pages (from-to)18-28
Number of pages11
Issue number1
StatePublished - May 2010


  • Chlorpromazine
  • Clathrin endocytic pathway
  • Ebola virus
  • Entry
  • Eps15
  • Sucrose

ASJC Scopus subject areas

  • Virology

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