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The active compound of Molnupiravir, N4-hydroxycytidine, promotes SARS-CoV-2 mutagenesis

ABSTRACT: The active compound of Molnupiravir, N4-hydroxycytidine, promotes SARS-CoV-2 mutagenesis

PROVIDER: PRJEB65430 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR11895000_1.fastq.gz	Fastqsanger.gz
	ERR11895000_2.fastq.gz	Fastqsanger.gz
	ERR11895001_1.fastq.gz	Fastqsanger.gz
	ERR11895001_2.fastq.gz	Fastqsanger.gz
	ERR11895002_1.fastq.gz	Fastqsanger.gz

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N4-hydroxycytidine, the active compound of Molnupiravir, promotes SARS-CoV-2 mutagenesis and escape from a neutralizing nanobody.

Project description:N4-hydroxycytidine (NHC), the active compound of the drug Molnupiravir, is incorporated into SARS-CoV-2 RNA, causing false base pairing. The desired result is an "error catastrophe," but this bears the risk of mutated virus progeny. To address this experimentally, we propagated the initial SARS-CoV-2 strain in the presence of NHC. Deep sequencing revealed numerous NHC-induced mutations and host-cell-adapted virus variants. The presence of the neutralizing nanobody Re5D06 selected for immune escape mutations, in particular p.E484K and p.F490S, which are key mutations of the Beta/Gamma and Omicron-XBB strains, respectively. With NHC treatment, nanobody resistance occurred two passages earlier than without. Thus, within the limitations of this purely in vitro study, we conclude that the combined action of Molnupiravir and a spike-neutralizing antagonist leads to the rapid emergence of escape mutants. We propose caution use and supervision when using Molnupiravir, especially when patients are still at risk of spreading virus.

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Project description:Identification of Antibody-Resistant SARS-CoV-2 Mutants via N4-Hydroxycytidine Mutagenesis

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Base-resolution detection of N4-methylcytosine in genomic DNA using 4mC-TAB-seq

Project description:N4-methylcytosine is a major DNA modification integral to restriction-modification (R-M) systems in bacterial genomes. Here we describe 4mC-Tet-Assisted Bisulfite-sequencing (4mC-TAB-seq), a method that accurately and rapidly reveals the genome-wide locations of N4-methylcytosines at single-base resolution. By coupling Tet-mediated oxidation with a modified sodium bisulfite conversion reaction, unmodified cytosines and 5-methylcytosines are read out as thymines, whereas N4-methylcytosines are read out as cytosines revealing their positions throughout the genome. 4mC-TAB-seq

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Spheroid active compound

Project description:Transcriptional expression data for a bioactive small molecule for mechanism identification. MCF7 cells were treated with either the compound NSC620358 or DMSO (control) for 6h prior to RNA isolation, to identify drug specific gene expression changes.

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β-D-N(4)-hydroxycytidine is a potent anti-alphavirus compound that induces high level of mutations in viral genome

Project description:The goal of this project was the analysis of virus variants resistant to β-D-N(4)-hydroxycytidine.

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Project description:Germline mutagenicity of molnupiravir and its active form, beta-d-N4 hydroxycytidine, in Caenorhabitis elegans evaluated using shole genome sequencing

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Pseudomonas sp. N4

Project description:Whole genome sequencing of Pseudomonas sp. N4

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Base-resolution detection of N4-methylcytosine in genomic DNA using 4mC-TAB-seq

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Streptomyces sp. N4-1

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NAT10 and N4-Acetylcytidine restrain R-loop levels and related inflammatory responses

Project description:N4-acetylcytidine (ac4C) is an evolutionarily conserved RNA modification that is deposited on diverse RNAs by N-acetyltransferase 10 (NAT10), a protein with high biological significance for aging and cancer. Here, we performed a comprehensive survey of ac4C using metabolic labeling, sodium cyanoborohydride chemical treatment coupled to next generation sequencing (NGS) and ac4C antibody-based cell and molecular biology techniques. Our NGS analysis confirms robust ac4C modification of rRNA and specific tRNA species in a NAT10-dependent manner, but suggests low or spurious ac4C acetylation in mRNA. Analysis of RNA-seq data also revealed an induction of inflammatory responses as well as mutagenesis at transcriptionally active sites in NAT10-KO cells. This finding led us to further explore the role of NAT10 in R-loops, which have recently been shown to induce APOBEC3B-mediated mutagenesis. Our analysis revealed that R-loops are modified with ac4C in a NAT10-dependent manner. Furthermore, NAT10 restrains the levels of R-loops at a subset of differentially expressed genes in a manner dependent on its catalytic activity. Together with cellular biology data showing ac4C containing RNA in endosomal structures, we propose that increased levels of ac4C-unmodified RNAs, likely derived from R-loops, in endosomal structures induce inflammatory responses.

2025-03-26 | GSE274993 | GEO

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