Abstract
Arenaviruses have a bisegmented negative-strand RNA genome, which encodes four viral proteins: GP and NP by the S segment and L and Z by the L segment. These four viral proteins possess multiple functions in infection, replication and release of progeny viruses from infected cells. The small RING finger protein, Z protein is a matrix protein that plays a central role in viral assembly and budding. Although all arenaviruses encode Z protein, amino acid sequence alignment showed a huge variety among the species, especially at the C-terminus where the L-domain is located. Recent publications have demonstrated the interactions between viral protein and viral protein, and viral protein and host cellular protein, which facilitate transportation and assembly of viral components to sites of virus egress. This review presents a summary of current knowledge regarding arenavirus assembly and budding, in comparison with other enveloped viruses. We also refer to the restriction of arenavirus production by the antiviral cellular factor, Tetherin/BST-2.
Highlights
We previously showed that Tsg101 is important for Marburg virus (MARV) VP40-induced virus-like particles (VLPs) budding and the PPPY motif located in VP40 is crucial for Tsg101-mediated budding and incorporation into VP40-induced VLP [66], it is unlikely that MARV VP40-Tsg101 interaction is direct [103]
We showed previously that ALIX/AIP1 does not contribute to Lassa virus (LASV) Z-mediated budding based on analysis using siRNA specific for ALIX/AIP1 [82], but we did not examine whether ALIX/AIP1 contributes to other processes
This review described current knowledge regarding arenavirus assembly and budding
Summary
Arenaviruses are divided into two groups, Old World (OW) and New World (NW) arenaviruses, based on geographical, serological, and phylogenetic differences (Figure 1). Lassa virus (LASV), Junin virus (JUNV), Machupo virus (MACV), Guanarito virus (GTOV), and Sabia virus (SABV) are the causative agents of Lassa fever (LF), Argentine HF, Bolivian HF, Venezuelan HF and Brazilian HF diseases, respectively [2]. In addition to these arenaviruses, Chapare virus and Lujo virus (LUJV) have been reported to cause HF [3,4,5]. Despite of the complexity of the virus budding mechanism, there is evidence that targeting of viral budding and high-throughput screening (HTS) would be useful to identify specific anti-arenaviral drugs [18]. This review presents a summary of current knowledge regarding arenavirus budding and the current model of arenavirus assembly and budding
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