ArticlePLoS pathogens2024
Picornavirus security proteins promote the release of extracellular vesicle enclosed viruses via the modulation of host kinases.
Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Therapeutic Poxviruses Induce the Secretion of Immunostimulating and Anti-Tumoral Extracellular Vesicles.Journal of extracellular vesicles · 2026Article
- Extracellular Vesicles Released by Picornavirus-Infected Cells Modify Antiviral Immune Cell Responses.Journal of extracellular vesicles · 2026Article
- Classification and biogenesis of vesicles, and their roles in the transport of viral components.Archives of microbiology · 2026Review
- Interactions between extracellular vesicles and viruses: lessons learned across species and kingdoms.FEMS microbiology reviews · 2026Review
- The leader proteins of Theiler's virus and Boone cardiovirus use a combination of short linear motifs (SLiMs) to target RSK kinases to the nuclear pore complex.Journal of virology · 2025Article
- Unraveling the molecular basis of membrane-associated release of coxsackievirus B3.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The discovery that extracellular vesicles (EVs) serve as carriers of virus particles calls for a reevaluation of the release strategies of non-enveloped viruses. Little is currently known about the molecular mechanisms that determine the release and composition of EVs produced by virus-infected cells, as well as conservation of these mechanisms among viruses. We previously described an important role for the Leader protein of the picornavirus encephalomyocarditis virus (EMCV) in the induction of virus-carrying EV subsets with distinct molecular and physical properties. EMCV L acts as a 'viral security protein' by suppressing host antiviral stress and type-I interferon (IFN) responses. Here, we tested the ability of functionally related picornavirus proteins of Theilers murine encephalitis virus (TMEV L), Saffold virus (SAFV L), and coxsackievirus B3 (CVB3 2Apro), to rescue EV and EV-enclosed virus release when introduced in Leader-deficient EMCV. We show that all viral security proteins tested were able to promote virus packaging in EVs, but that only the expression of EMCV L and CVB3 2Apro increased overall EV production. We provide evidence that one of the main antiviral pathways counteracted by this class of picornaviral proteins, i.e. the inhibition of PKR-mediated stress responses, affected EV and EV-enclosed virus release during infection. Moreover, we show that the enhanced capacity of the viral proteins EMCV L and CVB3 2Apro to promote EV-enclosed virus release is linked to their ability to simultaneously promote the activation of the stress kinase P38 MAPK. Taken together, we demonstrate that cellular stress pathways involving the kinases PKR and P38 are modulated by the activity of non-structural viral proteins to increase the release EV-enclosed viruses during picornavirus infections. These data shed new light on the molecular regulation of EV production in response to virus infection.
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