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Review

Structures and Functions of Viral 5′ Non-Coding Genomic RNA Domain-I in Group-B Enterovirus Infections

1
EA-4684 CardioVir, Faculty of Medicine, University of Reims Champagne-Ardenne (URCA), 51097 Reims, France
2
Laboratoire de Biopathologie, Centre Hospitalier Universitaire Reims, 51097 Reims, France
3
Service de Médecine Interne, Immunologie clinique et maladies infectieuses, Centre Hospitalier Universitaire Reims, 51097 Reims, France
4
Laboratoire de Virologie Médicale et Moléculaire, Centre Hospitalier Universitaire Reims, 51097 Reims, France
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Viruses 2020, 12(9), 919; https://doi.org/10.3390/v12090919
Received: 29 July 2020 / Revised: 17 August 2020 / Accepted: 19 August 2020 / Published: 21 August 2020
(This article belongs to the Special Issue Function and Structure of Viral Ribonucleoproteins Complexes)
Group-B enteroviruses (EV-B) are ubiquitous naked single-stranded positive RNA viral pathogens that are responsible for common acute or persistent human infections. Their genome is composed in the 5′ end by a non-coding region, which is crucial for the initiation of the viral replication and translation processes. RNA domain-I secondary structures can interact with viral or cellular proteins to form viral ribonucleoprotein (RNP) complexes regulating viral genomic replication, whereas RNA domains-II to -VII (internal ribosome entry site, IRES) are known to interact with cellular ribosomal subunits to initiate the viral translation process. Natural 5′ terminally deleted viral forms lacking some genomic RNA domain-I secondary structures have been described in EV-B induced murine or human infections. Recent in vitro studies have evidenced that the loss of some viral RNP complexes in the RNA domain-I can modulate the viral replication and infectivity levels in EV-B infections. Moreover, the disruption of secondary structures of RNA domain-I could impair viral RNA sensing by RIG-I (Retinoic acid inducible gene I) or MDA5 (melanoma differentiation-associated protein 5) receptors, a way to overcome antiviral innate immune response. Overall, natural 5′ terminally deleted viral genomes resulting in the loss of various structures in the RNA domain-I could be major key players of host–cell interactions driving the development of acute or persistent EV-B infections. View Full-Text
Keywords: group-B enterovirus; RNA domain-I; viral ribonucleoprotein complexes; enterovirus replication; 5′ terminally deleted viral forms; antiviral innate immune response; type I interferon group-B enterovirus; RNA domain-I; viral ribonucleoprotein complexes; enterovirus replication; 5′ terminally deleted viral forms; antiviral innate immune response; type I interferon
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MDPI and ACS Style

Glenet, M.; Heng, L.; Callon, D.; Lebreil, A.-L.; Gretteau, P.-A.; Nguyen, Y.; Berri, F.; Andreoletti, L. Structures and Functions of Viral 5′ Non-Coding Genomic RNA Domain-I in Group-B Enterovirus Infections. Viruses 2020, 12, 919. https://doi.org/10.3390/v12090919

AMA Style

Glenet M, Heng L, Callon D, Lebreil A-L, Gretteau P-A, Nguyen Y, Berri F, Andreoletti L. Structures and Functions of Viral 5′ Non-Coding Genomic RNA Domain-I in Group-B Enterovirus Infections. Viruses. 2020; 12(9):919. https://doi.org/10.3390/v12090919

Chicago/Turabian Style

Glenet, Marie, Laetitia Heng, Domitille Callon, Anne-Laure Lebreil, Paul-Antoine Gretteau, Yohan Nguyen, Fatma Berri, and Laurent Andreoletti. 2020. "Structures and Functions of Viral 5′ Non-Coding Genomic RNA Domain-I in Group-B Enterovirus Infections" Viruses 12, no. 9: 919. https://doi.org/10.3390/v12090919

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