Abstract
Ebola Virus Disease (EVD) is one of the most lethal transmissible infections, characterized by a high fatality rate, and caused by a member of the Filoviridae family. The recent large outbreak of EVD in Western Africa (2013–2016) highlighted the worldwide threat represented by the disease and its impact on global public health and the economy. The development of highly needed anti-Ebola virus antivirals has been so far hampered by the shortage of tools to study their life cycle in vitro, allowing to screen for potential active compounds outside a biosafety level-4 (BSL-4) containment. Importantly, the development of surrogate models to study Ebola virus entry in a BSL-2 setting, such as viral pseudotypes and Ebola virus-like particles, tremendously boosted both our knowledge of the viral life cycle and the identification of promising antiviral compounds interfering with viral entry. In this context, the combination of such surrogate systems with large-scale small molecule compounds and haploid genetic screenings, as well as rational drug design and drug repurposing approaches will prove priceless in our quest for the development of a treatment for EVD.
Highlights
The genus Ebolavirus of the Filoviridae family includes five species: Bundibugyo ebolavirus, Reston ebolavirus, Sudan ebolavirus, Tai Forest ebolavirus, and Zaire ebolavirus
Such viral models can be handled under BSL-2 conditions, representing safe systems to identify host factors. Both systems have been extensively used as surrogates of the authentic virus. Such viral models can be handled under BSL-2 conditions, representing safe systems to identify host factors involved in viral entry as well as to identify and validate new therapeutic approaches aimed at blocking viral entry
One of the most suitable VLP models to study Ebola virus (EBOV) entry and its inhibition is represented by EBOV-like particles (eVLPs) obtained by expressing VP40 fused in frame with the beta-lactamase enzyme
Summary
The genus Ebolavirus of the Filoviridae family includes five species: Bundibugyo ebolavirus, Reston ebolavirus, Sudan ebolavirus, Tai Forest ebolavirus, and Zaire ebolavirus. The Zaire ebolavirus, usually called Ebola virus (EBOV), is the main causative agent of human outbreaks, causing the Ebola virus disease (EVD) [1]. EVD is a disease of human and non-human primates that is characterized by a high fatality rate (30–90%). EBOV can be transmitted to non-human primates and duikers in an epizootic cycle causing outbreaks with high mortality [1]. The recent large outbreak of EVD (Western Africa, 2013–2016) characterized by 28,616 cases and 11,310 deaths, highlighted the worldwide danger of this disease and its impact on global public health and economy [5]. We summarize the current knowledge of a specific step of the EBOV life cycle, the entry process, and the compounds identified so far capable of interfering with it, as well as the molecular models used to these purposes
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