The Ebola Virus Matrix Protein VP40 Interacts With Several Host Protein Networks to Facilitate Viral Replication

Cary T. Frick, Robert V. Stahelin

Research output: Contribution to journalReview article

Abstract

The Ebola virus (EBOV) is a lipid-enveloped virus that is filamentous in shape and belongs to the Filoviridae family. EBOV can cause viral hemorrhagic fever in humans and non-human primates with high rates of fatality. Using a negative sense RNA genome that encodes just eight proteins, the lipid-enveloped EBOV can enter mammalian cells and undergo efficient replication to produce more virions to sustain and spread the infection. Throughout the replication cycle, EBOV inhibits or hijacks several host protein networks to suppress the immune response and to enhance the efficiency of assembly and budding from the host cell plasma membrane. Assembly and budding of EBOV is regulated by its matrix protein VP40, which can form different structures with distinct functions in the viral life cycle. VP40 has been shown to interact with several important host proteins, and although the conformational regulation of these interactions is mostly unknown, the sites of interaction have been somewhat resolved and will serve as the basis of this review article.

Original languageEnglish (US)
Pages (from-to)137-141
Number of pages5
JournalCurrent Clinical Microbiology Reports
Volume2
Issue number3
DOIs
StatePublished - Sep 1 2015
Externally publishedYes

Keywords

  • Ebola virus
  • Filovirus
  • Protein-protein interaction
  • VP40
  • Virus budding
  • Virus-host interactions

ASJC Scopus subject areas

  • Microbiology (medical)
  • Infectious Diseases

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