Abstract
Viroplasms are cytoplasmic, membraneless structures assembled in rotavirus (RV)-infected cells, which are intricately involved in viral replication. Two virus-encoded, non-structural proteins, NSP2 and NSP5, are the main drivers of viroplasm formation. The structures (as far as is known) and functions of these proteins are described. Recent studies using plasmid-only-based reverse genetics have significantly contributed to elucidation of the crucial roles of these proteins in RV replication. Thus, it has been recognized that viroplasms resemble liquid-like protein–RNA condensates that may be formed via liquid–liquid phase separation (LLPS) of NSP2 and NSP5 at the early stages of infection. Interactions between the RNA chaperone NSP2 and the multivalent, intrinsically disordered protein NSP5 result in their condensation (protein droplet formation), which plays a central role in viroplasm assembly. These droplets may provide a unique molecular environment for the establishment of inter-molecular contacts between the RV (+)ssRNA transcripts, followed by their assortment and equimolar packaging. Future efforts to improve our understanding of RV replication and genome assortment in viroplasms should focus on their complex molecular composition, which changes dynamically throughout the RV replication cycle, to support distinct stages of virion assembly.
Highlights
Species A rotaviruses (RVs) are a major cause of acute gastroenteritis in infants and young children worldwide [1]
Rotavirus is a non-enveloped RNA virus whose genome is composed of 11 segments of double-stranded RNA encoding six structural proteins (VP1-VP4, VP6, VP7) and 5-6 non-structural proteins (NSP1-NonStructural Protein 5 (NSP5)/NSP6)
The interaction between the virus-encoded Non-Structural Protein 2 (NSP2) and NonStructural Protein 5 (NSP5) results in the formation of 0.1–5 μm cytoplasmic inclusions, termed viroplasms, which appear to concentrate the viral components required for genome assortment and replication, and the assembly of subviral particles, acting as ‘viral factories’
Summary
Species A rotaviruses (RVs) are a major cause of acute gastroenteritis in infants and young children worldwide [1]. Despite the effectiveness and availability of several RVvaccines [2], RV-associated deaths in children < 5 years of age are still a problem, in countries in sub-Saharan Africa and SE Asia [3]. Despite extensive investigations that haven taken place over 50 years, and the significant progress made during the last decade, there are still aspects of the molecular biology, pathogenesis and immunology of these viruses that are poorly understood. This review will concentrate on cytoplasmic sites of RV replication, or viroplasms, known as RV replication factories
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