As obligate intracellular parasites, viruses entirely rely on the resources of the cell for their replication. These pathogens have evolved to produce the optimal concentration of viral proteins which drive their life cycle, notably by hijacking the post-translational machinery of the infected cell. Such regulation is mediated at multiple levels, such as RNA modification, transport, stability and/or translation, through interactions between viral RNAs and host RNA-binding proteins. This is especially true for some RNA viruses which must coordinate in time and space the mutually exclusive steps of their life cycle such as RNA synthesis, translation and encapsidation into assembling viral particles. The molecular mechanisms underlying such equilibrium remains poorly understood and most likely relies on the dynamic interactions between viral RNAs and host and viral proteins as well as on RNA modifications.
Beyond their main role as template for viral genome synthesis and amplification, viral RNAs can also contribute to viral pathogenesis. Notably, they can modulate cellular processes which are potentially detrimental for RNA replication such as early innate immunity or virus-induced cell death. For instance, in the case of some viruses, the methylation of the viral RNA allows it to escape from the innate immunity sensors. There are also reported examples of viruses generating non-coding viral RNAs which inhibit interferon induction as well as virus-induced apoptosis in order to maximize replication efficiency. Finally, viruses can regulate the metabolism of cellular RNAs at the level of splicing, stability and translation.
This Article Collection will focus on the intricate interplays between viruses and RNA metabolism. A better understanding of these virus/host interactions is relevant not only for identifying therapeutic targets and pathogenesis determinants but also for shedding light on the basic principles of RNA molecular biology.
All manuscripts submitted to this Article Collection will undergo desk assessment and peer-review as part of our standard editorial process. Guest Advisors will not be involved in peer-reviewing manuscripts unless they are an existing member of the Editorial Board.
Please review the journal scope and author submission instructions prior to submitting a manuscript.
The deadline for submitting manuscripts is 30 November 2023.
Please contact Ashley Ambros at [email protected] with any queries regarding this Article Collection.
Dr. Laurent Chatel-Chaix obtained in 2007 his PhD of Biochemistry from the University of Montreal (Canada) which focused on the relationship between HIV-1 and a cellular RNA-binding protein. During his two postdoctoral trainings at University of Montreal and University of Heidelberg (Germany), he extended his research to Flaviviridae, namely hepatitis C virus, dengue virus and Zika virus and continued to work on the role of RNA-binding proteins in the viral replication cycle. In 2016, he joined the faculty at the Armand-Frappier Research Centre of the National Institute of Scientific Research (Laval, Quebec, Canada). With the aim to better understand flavivirus pathogenesis and to identify new promising antiviral targets, his research team focuses on the identification of flavivirus/host interactions engaged in the viral hijacking of cellular machineries important for the infection. Since the COVID-19 pandemic, he also works on the impact of SARS-CoV-2 on cell and tissue functions.
Disclosure Statement: Dr. Chatel-Chaix declares no conflict of interest regarding this work.
