Abstract
Bluetongue virus (BTV) is an arthropod-borne virus infecting livestock. Its frequent emergence in Europe and North America had caused significant agricultural and economic loss. BTV is also of scientific interest as a model to understand the mechanisms underlying non-enveloped virus release from mammalian and insect cells. The BTV particle, which is formed of a complex double-layered capsid, was first considered as a lytic virus that needs to lyse the infected cells for cell to cell transmission. In the last decade, however, a more in-depth focus on the role of the non-structural proteins has led to several examples where BTV particles are also released through different budding mechanisms at the plasma membrane. It is now clear that the non-structural protein NS3 is the main driver of BTV release, via different interactions with both viral and cellular proteins of the cell sorting and exocytosis pathway. In this review, we discuss the most recent advances in the molecular biology of BTV egress and compare the mechanisms that lead to lytic or non-lytic BTV release.
Highlights
Bluetongue virus (BTV) is an arthropod-borne virus vectored by biting midges from the Culicoides genus
BTV is known to have a close association with multivesicular bodies (MVBs), via the interaction between NS3 and NEDD4 ubiquitin ligase
Extensive study of the non-structural proteins of BTV, and of the infection of mammalian and insect cells has significantly enhanced our understanding on virus replication processes
Summary
Bluetongue virus (BTV) is an arthropod-borne virus vectored by biting midges from the Culicoides genus. NS1 is necessary for BTV replication and selectively enhances viral protein synthesis [6]. It undergoes polymerisation producing large tubules in infected cells, whose functional consequence is unknown [7]. Rotavirus viroporin induces an increase of cytosolic calcium concentration, that is required for the formation of vesicular puncta surrounding the sites of replication. To form this viroporin, NS3 is likely to form oligomers, possibly through a predicted coiled-coil motif located in its N-terminus. BTV-induced apoptosis and activation of the pro-inflammatory pathways are the main events leading to BTV lytic release from infected mammalian cells. Several studies on NS3 mutant viruses revealed that when non-lytic release of BTV is inhibited, BTV is still able to spread from cell to cell but is highly attenuated, suggesting that lytic release is not the main mode of BTV egress [17,18,32]
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