Abstract
The filoviruses Ebolavirus and Marburgvirus are among the deadliest viral pathogens known to infect humans, causing emerging diseases with fatality rates of up to 90% during some outbreaks. The replication cycles of these viruses are comprised of numerous complex molecular processes and interactions with their human host, with one key feature being the means by which nascent virions exit host cells to spread to new cells and ultimately to a new host. This review focuses on our current knowledge of filovirus egress and the viral and host factors and processes that are involved. Within the virus, these factors consist of the major matrix protein, viral protein 40 (VP40), which is necessary and sufficient for viral particle release, and nucleocapsid and glycoprotein that interact with VP40 to promote egress. In the host cell, some proteins are hijacked by filoviruses in order to enhance virion budding capacity that include members of the family of E3 ubiquitin ligase and the endosomal sorting complexes required for transport (ESCRT) pathway, while others such as tetherin inhibit viral egress. An understanding of these molecular interactions that modulate viral particle egress provides an important opportunity to identify new targets for the development of antivirals to prevent and treat filovirus infections.
Highlights
Ebola virus and Marburg virus are among the deadliest viral pathogens known to infect humans, being transmittable primarily through contact with infectious bodily fluids [1]
Both Ebola virus (EBOV) and Marburg virus (MARV) hijack the endosomal sorting complexes required for transport (ESCRT) machinery to drive their egress from the cell surface, with a number of ESCRT proteins shown to be critical for efficient viral budding
ALG-2-interacting protein X (Alix) enhances budding of EBOV virus-like particles (VLPs) only when the PPxY domain of EBOV VP40 (eVP40) is mutated, an enhancement that is increased from 2–3 fold to 4–7 fold when the Alix Bro1-V fragment is used in place of the wild-type molecule [118]
Summary
Ebola virus and Marburg virus are among the deadliest viral pathogens known to infect humans, being transmittable primarily through contact with infectious bodily fluids [1]. These viruses can be transmitted between humans and from non-human hosts. The Ebolavirus genus comprises five species that are named after the regions in which they were first observed These viruses are Bundibugyo virus (BDBV; species Bundibugyo ebolavirus); Ebola virus (EBOV; species Zaire ebolavirus); Sudan virus (SUDV; species Sudan ebolavirus); Tai Forest virus (TAFV; species Tai Forest ebolavirus) and Reston virus (RESTV; species Reston ebolavirus), with the newly discovered Bombali virus (BOMV; species Bombali ebolavirus) currently unclassified but may form a Viruses 2019, 11, 25; doi:10.3390/v11010025 www.mdpi.com/journal/viruses. An understanding of the molecular interactions relevant to viral particle egress is important to identify new targets for the development of antivirals to prevent and treat filovirus infections
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