Research Progress of Splicing Factor SART1 in Viral Infection and Immune Regulation

Corresponding author: Gao Guosheng, 495926922@qq.com

DOI: 10.12201/bmr.202605.00065

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  Abstract: SART1 (squamous cell carcinoma antigen recognized by T cells 1) was initially discovered as a tumor rejection antigen and later confirmed to be a crucial component of the U4/U6.U5 tri-snRNP complex, playing a key role in precursor mRNA (pre-mRNA) splicing. Recent studies indicate that SART1 is not only involved in canonical RNA splicing regulation but also broadly mediates diverse biological processes, including viral infection, host antiviral immunity, hypoxia response, DNA damage repair, and tumor immune regulation, demonstrating significant functional versatility. In the context of viral infection, SART1 acts as an important host restriction factor and an interferon effector gene (IEG), capable of inhibiting the replication of hepatitis B virus (HBV) and hepatitis C virus (HCV) by regulating the expression of interferon-stimulated genes (ISGs) and the host transcriptional network. Specifically, SART1 can significantly suppress HBV replication by inhibiting hepatocyte nuclear factor 4α (HNF4α) transcription, thereby downregulating the activity of HBV covalently closed circular DNA (cccDNA). Its baseline expression level is also closely associated with the interferon-α (IFN-α) treatment response in chronic HBV patients, suggesting its potential value for predicting therapeutic efficacy. Regarding tumor immunity, antigenic peptides encoded by SART1 can induce HLA-A24/A26-restricted cytotoxic T lymphocyte (CTL) responses and have been applied in dendritic cell (DC) vaccine and mRNA vaccine research. Additionally, SART1 is involved in reshaping the immune microenvironment and the progression from metabolic dysfunction-associated steatohepatitis (MASH) to hepatocellular carcinoma (HCC) by regulating macrophage polarization and the NF-κB signaling pathway. This article systematically reviews the structural characteristics, molecular functions, mechanisms of action in viral infection, roles in tumor immunity, and clinical translational prospects of SART1. It also explores its pivotal role within the splicing–metabolism–immunity interaction network, aiming to provide a new theoretical basis and potential therapeutic targets for the combined intervention of chronic persistent infections and associated malignant tumors.

  Key words: SART1; virus; interferon; tumor rejection antigen; immune regulation

  Submit time: 18 May 2026

  Copyright: The copyright holder for this preprint is the author/funder, who has granted biomedRxiv a license to display the preprint in perpetuity.
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