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Published on: February 1, 2017
Type-III interferon stimulated gene TRIM31 mutation in an HBV patient blocks its ability in promoting HBx degradation
Fengchao Xu1, Hongxiao Song1, Qingfei Xiao2
1Department of Immunology, Institute of Translational Medicine, the First Hospital of Jilin University, Changchun, Jilin 130061, China.
Abstract:
TRIM5γ, together with TRIM31, has been shown to promote HBx ubiquitination and degradation. This study aimed to explore whether a patient with HCC (hepatic cell carcinoma) having a small nucleotide inserted into the TRIM31 gene, which made a shorter transcript stop at 768 bp, would result in blocking the activity of TRIM31 in promoting HBx degradation. Besides, this study aimed to determine the binding region of the TRIM31-TRIM5γ-HBx complex. HBV (Hepatitis B virus) infection was reported to induce type-III IFN but not type-I or type-II IFNs, here TRIM31 was found to be a type III rather than a type I stimulated gene, which was indispensable in inhibiting the hepatitis B virus replication by the interferon families. Thus, this study further identified the critical role of TRIM31 in the host-hepatitis B virus interaction.
Insights
TRIM31 gene mutations in hepatocellular carcinoma (HCC) patients may block TRIM31's ability to degrade Hepatitis B virus (HBV) X protein (HBx). This research clarifies TRIM31's role in host-HBV interactions.
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- Hepatitis B virus (HBV) infection is a major cause of hepatocellular carcinoma (HCC).
- The HBV X protein (HBx) plays a crucial role in HBV pathogenesis.
- TRIM proteins, including TRIM5γ and TRIM31, are involved in ubiquitination and degradation of viral proteins.
Observation:
- A specific mutation in the TRIM31 gene (a small nucleotide insertion leading to a premature stop codon) was identified in an HCC patient.
- This mutation resulted in a truncated TRIM31 transcript (768 bp).
- TRIM31 was identified as a type III interferon-stimulated gene, crucial for inhibiting HBV replication.
Findings:
- The study investigated whether the mutated TRIM31 could still promote HBx ubiquitination and degradation.
- The binding regions within the TRIM31-TRIM5γ-HBx complex were determined.
- TRIM31 was confirmed to be indispensable for type III interferon-mediated inhibition of HBV replication.
Implications:
- Understanding the impact of TRIM31 mutations on HBx degradation is vital for HCC treatment strategies.
- This research highlights TRIM31's critical role in the host-pathogen interaction between humans and HBV.
- The findings contribute to the understanding of interferon-based antiviral mechanisms against HBV.
