A guide to viral inclusions, membrane rearrangements, factories, and viroplasm produced during virus replication.
ABSTRACT Virus replication can cause extensive rearrangement of host cell cytoskeletal and membrane compartments leading to the "cytopathic effect" that has been the hallmark of virus infection in tissue culture for many years. Recent studies are beginning to redefine these signs of viral infection in terms of specific effects of viruses on cellular processes. In this chapter, these concepts have been illustrated by describing the replication sites produced by many different viruses. In many cases, the cellular rearrangements caused during virus infection lead to the construction of sophisticated platforms in the cell that concentrate replicase proteins, virus genomes, and host proteins required for replication, and thereby increase the efficiency of replication. Interestingly, these same structures, called virus factories, virus inclusions, or virosomes, can recruit host components that are associated with cellular defences against infection and cell stress. It is possible that cellular defence pathways can be subverted by viruses to generate sites of replication. The recruitment of cellular membranes and cytoskeleton to generate virus replication sites can also benefit viruses in other ways. Disruption of cellular membranes can, for example, slow the transport of immunomodulatory proteins to the surface of infected cells and protect against innate and acquired immune responses, and rearrangements to cytoskeleton can facilitate virus release.
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ABSTRACT: P6 of southern rice black-streaked dwarf virus (SRBSDV) is a multifunctional protein that is involved in the formation of viroplasms by interacting with P5-1. Here, we used yeast two-hybrid and bimolecular fluorescence complementation assays to show that there were homologous and heterologous interactions between SRBSDV P6 and P9-1 in yeast and plant cells. Mutational analysis showed that the N-terminal region (residues 1-93) of P6 was necessary for the interaction between P6 and P9-1. Self-interactions only occurred between the full-length P6 or P9-1. P9-1 was able to form viroplasm-like inclusion structures alone in the absence of other viral proteins.Archives of Virology 10/2014; DOI:10.1007/s00705-014-2268-z · 2.28 Impact Factor
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ABSTRACT: Positive-stranded RNA viruses induce new membranous structures and promote membrane proliferation in infected cells to facilitate viral replication. In this paper, the authors show that a plant-infecting tombusvirus upregulates transcription of phospholipid biosynthesis genes, such as INO1, OPI3 and CHO1, and increases phospholipid levels in yeast model host. This is accomplished by the viral p33 replication protein, which interacts with Opi1p FFAT domain protein and Scs2p VAP protein. Opi1p and Scs2p are phospholipid sensor proteins and they repress the expression of phospholipid genes. Accordingly, deletion of OPI1 transcription repressor in yeast has a stimulatory effect on TBSV RNA accumulation and enhanced tombusvirus replicase activity in an in vitro assay. Altogether, the presented data convincingly demonstrate that de novo lipid biosynthesis is required for optimal TBSV replication. Overall, this work reveals that a (+)RNA virus reprograms the phospholipid biosynthesis pathway in a unique way to facilitate its replication in yeast cells.Virology 12/2014; 471:72-80. DOI:10.1016/j.virol.2014.10.005 · 3.28 Impact Factor