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

ABSTRACT:

Background

The 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.

Results

In this study, it was found that serine-arginine-rich splicing factor 6 (SRSF6) binds to the splice donor site of the human OAS1 ex

SUBMITTER: Iida K 

PROVIDER: S-EPMC11874701 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature