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Switching of OAS1 splicing isoforms mitigates SARS-CoV-2 infection [Caco-2]

ABSTRACT: We aimed to study impact of CDC-like kinase (CLK) inhibitor CaNDY on OAS1 splicing manipulation. Our data indicates CaNDY treatment induces switching of OAS1 splice isoforms to provide an increased resistance to SARS-CoV-2 infection.

ORGANISM(S): Homo sapiens

PROVIDER: GSE207270 | GEO | 2025/03/12

REPOSITORIES: GEO

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Switching of OAS1 splicing isoforms mitigates SARS-CoV-2 infection

Project description:We aimed to study impact of CDC-like kinase (CLK) inhibitor CaNDY on OAS1 splicing manipulation. Our data indicates CaNDY treatment induces switching of OAS1 splice isoforms to provide an increased resistance to SARS-CoV-2 infection.

2025-03-12 | GSE244026 | GEO

Switching of OAS1 splicing isoforms mitigates SARS-CoV-2 infection

2021-08-02 | GSE174398 | GEO

Switching of OAS1 splicing isoforms mitigates SARS-CoV-2 infection [Caco-2]

Project description:Switching of OAS1 splicing isoforms mitigates SARS-CoV-2 infection [Caco-2]

| PRJNA854598 | ENA

Switching of OAS1 splicing isoforms mitigates SARS-CoV-2 infection

Project description:Switching of OAS1 splicing isoforms mitigates SARS-CoV-2 infection

| PRJNA729748 | ENA

Switching of OAS1 splicing isoforms mitigates SARS-CoV-2 infection

Project description:Switching of OAS1 splicing isoforms mitigates SARS-CoV-2 infection

| PRJNA1021066 | ENA

Switching of OAS1 splicing isoforms overcomes SNP-derived vulnerability to SARS-CoV-2 infection.

Project description:BackgroundThe SARS-CoV-2 pandemic provided important insights into the relationship between infectious diseases and the human genome. A genomic region encoding the 2'-5'-oligoadenylate synthetase (OAS) family proteins that sense viral genomic RNAs and trigger an antiviral response contains single nucleotide polymorphisms (SNPs) associated with SARS-CoV-2 infection susceptibility. A high-risk SNP identified at the splice acceptor site of OAS1 exon 6-a terminal exon-alters the proportion of various splicing isoforms of OAS1 and its activity. However, the actual causality of this SNP or splicing to infection susceptibility remains unknown.ResultsIn this study, it was found that serine-arginine-rich splicing factor 6 (SRSF6) binds to the splice donor site of the human OAS1 exon 5. SRSF6 determines the selected alternative terminal exon when the risk allele disrupts the splice acceptor site. Subsequently, an inhibitor for CDC-like kinase was rationally selected as a candidate splicing modulator. RNA-Seq and RT-PCR analyses revealed that this inhibitor can induce splice switching of OAS1 mRNAs in the human lung adenocarcinoma cell line Calu-3. Under the inhibitor treatment, the cells exhibited reduced SARS-CoV-2 infection rates. Meanwhile, the colonic epithelial cell line Caco-2 expressed non-risk type OAS1 mRNA isoforms that did not undergo splice-switching or demonstrate altered SARS-CoV-2 sensitivity following treatment with the inhibitor.ConclusionsThese results indicate that a high-risk SNP in OAS1 influences cell susceptibility to SARS-CoV-2 infection by inducing splice-switching at its terminal exon. Additionally, chemical splicing modifiers may prove beneficial in overcoming this genomic vulnerability.

| S-EPMC11874701 | biostudies-literature

Heterozygous OAS1 Gain-of-Function Variants Cause a Polymorphic Autoinflammatory and Immunodeficiency Syndrome

Project description:Oligoadenylate synthase 1 (OAS1) is a type-1 interferon-inducible, intracellular double-stranded RNA (dsRNA) sensor that generates 2'-5'-oligoadenylate (2-5A) to activate RNaseL as a means of antiviral defense. We report four de novo heterozygous OAS1 variants in five patients. Variant OAS1 proteins show dsRNA-independent gain-of-function 2-5A synthetase activity that results in RNaseL-mediated RNA-cleavage, transcriptomic downregulation, and functional impairment and/or apoptosis of monocytes, iPSC-derived macrophages, and B-cells. This leads to a polymorphic syndrome of monocyte, macrophage, and B-cell deficiency characterized by autoinflammation, pulmonary alveolar proteinosis, and hypogammaglobulinemia. RNase-L-inhibition in vitro mitigates, and hematopoietic cell transplantation in vivo corrects the autoinflammatory and immunodeficiency phenotype.

2021-06-18 | GSE173667 | GEO

RNA-Sequencing of EndoC-BH1 cells Overexpressing OAS1, OAS2, or OAS3

Project description:EndoC-BH1 cells were plated in normal media and forward transfected with lipofectamine 3000 (2ug cDNA) of empty, OAS1, OAS2, or OAS3 plasmids from Vector builder

2024-01-01 | GSE244273 | GEO

OAS1 and OAS3 negatively regulate the expression of chemokines and interferon-responsive genes in human macrophages

Project description:We report analysis of mRNA profiles from wild-type and OAS1 and OAS3-KO human cell lines stimulated with PolyI:C.

2021-04-19 | GSE113363 | GEO

OAS1

Project description:Sus scrofa OAS1, 2'-5'-oligoadenylate synthetase 1 [Source:HGNC Symbol;Acc:HGNC:8086], is expressed in 2 baseline experiment(s);

| ENSSSCG00000046640 | ExpressionAtlas

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