Genetic and phenotypic changes to Venezuelan equine encephalitis virus following treatment with β-D-N4-hydroxycytidine, an RNA mutagen.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
25 Oct 2024
Historique:
received: 27 08 2024
accepted: 16 10 2024
medline: 25 10 2024
pubmed: 25 10 2024
entrez: 25 10 2024
Statut: epublish

Résumé

The high mutation rate of RNA viruses provides viral populations with the ability to adapt to new environments but also makes them vulnerable to extinction due to the deleterious effects of mutations, which is the conceptual basis for the antiviral activity of RNA mutagens. However, there are still gaps in the quantitative understanding of the dynamics between the mutations induced by an RNA mutagen and its effects on viral fitness. To address this, we used Venezuelan Equine Encephalitis Virus (VEEV) and the potent RNA mutagen β-d-N4-hydroxycytidine (NHC) as a model to analyze virus replication competency and mutation frequency following treatment in the total and replication-competent viral populations separately. We found that NHC induced transition mutations in a concentration dependent manner in the total population, while the replication-competent population maintained itself within an increased, yet narrow, mutation spectrum. The incorporation of NHC mainly happened during the positive sense RNA synthesis of VEEV. A growth kinetic analysis of VEEV population treated with NHC pointed to a lower but more diverse distribution in mutational fitness, demonstrating that NHC-induced mutations negatively and broadly affect the fitness of the virus. Together, our study provides mechanistic insight into how RNA mutagens affect viral population landscape and the potential of RNA mutagens as an antiviral strategy for alphaviruses.

Identifiants

pubmed: 39448734
doi: 10.1038/s41598-024-76788-x
pii: 10.1038/s41598-024-76788-x
doi:

Substances chimiques

Cytidine 5CSZ8459RP
Mutagens 0
N(4)-hydroxycytidine C3D11PV2O4
RNA, Viral 0
Antiviral Agents 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

25265

Subventions

Organisme : NIH HHS
ID : 1U19AI142762
Pays : United States
Organisme : NIH HHS
ID : 1U19AI142762
Pays : United States
Organisme : NIH HHS
ID : 1U19AI142762
Pays : United States
Organisme : NIH HHS
ID : P20GM103436
Pays : United States
Organisme : NIH HHS
ID : P20GM103436
Pays : United States
Organisme : NIH HHS
ID : P30ES030283
Pays : United States

Informations de copyright

© 2024. The Author(s).

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Auteurs

Brian Alejandro (B)

Center for Predictive Medicine, University of Louisville, Louisville, KY, USA.

Eun Jung Kim (EJ)

Center for Predictive Medicine, University of Louisville, Louisville, KY, USA.

Jae Yeon Hwang (JY)

Department of Medicine, University of Louisville, Louisville, KY, USA.
Brown Cancer Center Bioinformatics Core, University of Louisville, Louisville, KY, USA.

Juw Won Park (JW)

Department of Medicine, University of Louisville, Louisville, KY, USA.
Brown Cancer Center Bioinformatics Core, University of Louisville, Louisville, KY, USA.

Melissa Smith (M)

Department of Biochemistry and Molecular Genetics, School of Medicine, University of Louisville, Louisville, KY, USA.

Donghoon Chung (D)

Center for Predictive Medicine, University of Louisville, Louisville, KY, USA. hoon.chung@louisville.edu.
Department of Microbiology and Immunology, School of Medicine, University of Louisville, Louisville, KY, USA. hoon.chung@louisville.edu.

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