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Keeping Siblings Together: Enterovirus Collective Dispersal through Extracellular Vesicles Involves Genetically Related Viral Particles

ABSTRACT: Viruses can disperse collectively using extracellular vesicles and other types of multi-virion structures. It has been hypothesized that, by increasing the cellular multiplicity of infection, this dispersal mode may favor cooperation among viral genomes. However, the spread of defective variants that function as social cheaters could also be promoted. To better understand the nature of virions present in vesicles, here we examine the genetic diversity harboured by vesicles of coxsackievirus B3 (CVB3), a model enterovirus. Our results confirm that CVB3 vesicles contain multiple infectious particles. However, we also find that virus variants coinfecting a cell typically allocate their progenies into different vesicles, precluding long-term interactions among them. Furthermore, Illumina sequencing indicates that dispersal through vesicles does not increase viral population genetic diversity appreciably. We conclude that vesicles enable the co-dispersal of groups of virions, but that these groups are highly related since they share the same parental genome. This should restrict the evolution of defective viruses, but also makes cooperation among different viral genetic variants unlikely. Our results are in line with a fundamental tenet of social evolution theory, according to which the evolution of cooperation typically requires that the interacting partners are genetically related.

ORGANISM(S): Coxsackievirus B3 (strain Nancy)

PROVIDER: GSE124469 | GEO | 2018/12/29

REPOSITORIES: GEO

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Project description:Marine viral concentrates (VCs) contains a substantial amount of non-cellular biological particles, e.g. viruses, gene transfer agents (GTAs) and membrane vesicles that are ecological significant. Metagenomic sequencing of VCs has been extensively applied to study the diversity and function potential of natural virions whereas information of nonn-viral components are often excluded for investigation. Here we apply a shotgun proteomic approach to characterize the origin and function of proteins in the VCs collected from the deep chlorophyll maximum (DCM) of the South China Sea. Using a custom database, we identified 636 non-redundant proteins represented by a total of 7220 spectra from the two VC samples. Cyanophages, pelagiphages, Phycodnaviridae and a group of uncultured viruses (previouly collected from DCM of Mediterranean Sea) contributed the most in the viral proteome. Seldom proteins related to RNA viruses and known GTAs were found despites of the presence of their sequences in the protein-searching database, suggested that these particles might be low abundant in the samples. Over 60% of identified spectra could not be assigned to viruses. The non-viral spectra were dominated by microbial groups of SAR324, SAR11, Actinobacteria and picoeukaryotic algae such as prasinophytes.Interestingly, we found that periplasmic proteins such as diverse ABC and TRAP transporters, and 56 kDa selenium-binding proteins, were enriched in this fraction.Together with other detected non-viral proteins,we could identify significant microbial functions, such as the utilization of glycine betaine, 3-dimethylsulphoniopropionate,and taurine by SAR11,and urea by prochlorococcus, nitrous oxide production by ammonia-oxidizing archaea and peroxide detoxification by unkonwn gammaproteobacteria. Our study of marine VCs demonstrates the potential application of metaproteomics to link the nano-size materials to the diversity of virions and interesting microbial functions in the ocean.

Project description:ABSTRACT Background: Viral myocarditis is a life-threatening illness that may lead to heart failure or cardiac arrhythmias. This study examined whether human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) could be used to model the pathogenic processes of coxsackievirus-induced viral myocarditis and to screen antiviral therapeutics for efficacy. Methods and Results: Human iPSC-CMs were infected with a luciferase-expressing mutant of the coxsackievirus B3 strain (CVB3-Luc). Brightfield microscopy, immunofluorescence, and calcium imaging were used to characterize virally infected hiPSC-CMs. Viral proliferation on hiPSC-CMs was subsequently quantified using bioluminescence imaging. For drug screening, select antiviral compounds including interferon beta 1 (IFNβ1), ribavirin, pyrrolidine dithiocarbamate (PDTC), and fluoxetine were tested for their capacity to abrogate CVB3-Luc proliferation in hiPSC-CMs in vitro. The ability of some of these compounds to reduce CVB3-Luc proliferation in hiPSC-CMs was consistent with the reported drug effects in previous studies. Finally, mechanistic analyses via gene expression profiling of hiPSC-CMs infected with CVB3-Luc revealed an activation of viral RNA and protein clearance pathways within these hiPSC-CMs after IFNβ1 treatment. Conclusions: This study demonstrates that hiPSC-CMs express the coxsackievirus and adenovirus receptor, are susceptible to coxsackievirus infection, and can be used to confirm antiviral drug efficacy. Our results suggest that the hiPSC-CM/CVB3-Luc assay is a sensitive platform that could be used to screen novel antiviral therapeutics for their effectiveness in a high-throughput fashion. For this experiment, human induced pluripotent stem cell derived cardiomyocytes were infected with coxsackievirus at multiplicity of infection (MOI) of 5 for 8 hours. Cells were treated with and without interferon beta 1 in order to determine if treatment activates antiviral response genes and/or viral clearance pathways. 4 total samples (2 for each condition) were analyzed

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Keeping Siblings Together: Enterovirus Collective Dispersal through Extracellular Vesicles Involves Genetically Related Viral Particles

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