Background/aims: To identify the inflammatory damage caused by chronic hepatitis B (CHB) in patients of chronic hepatitis B virus (HBV) infection complicated with non-alcoholic fatty liver disease (NAFLD), then guiding clinicians to carry out antiviral treatment.
Methods: According to the pathological features of liver biopsy, treatment-naïve obese patients of chronic HBV infection complicated with NAFLD who had elevated alanine transaminase (ALT) were divided into CHB group and NASH group. Transcriptome chips were used to analyze the expression profiles of long non-coding RNA (lncRNA) and mRNA in liver puncture tissues from the two groups. The chip data of CHB and NASH groups were analyzed for differential expression analysis, gene function analysis, signal pathway analysis, target gene prediction and competing endogenous RNAs (ceRNA) network analysis.
Results: By comparing CHB group with NASH group, a total of 44 differentially expressed lncRNAs and 567 differentially expressed mRNAs were screened. GO analysis predicted that the differentially expressed mRNAs may affect monooxygenase activity and oxidoreductase activity. KEGG analysis predicted that the differentially expressed mRNAs may be related to signaling pathways involved in oxidative phosphorylation, phagosomes, and NAFLD. Differential analysis of lncRNA shown that the expression of metastasis associated in lung adenocarcinoma transcript 1 (MALAT1) in CHB group was significantly upregulated. Subsequently, through target gene prediction and ceRNA network analysis, we found thioredoxin interacting protein (TXNIP), which was significantly upregulated in the CHB group and had a ceRNA relationship with MALAT1. It is predicted that there may be a ceRNA regulation relationship of MALAT1/hsa-miR- 20b-5p/TXNIP.
Conclusion: The MALAT1/hsa-miR-20b-5p/TXNIP axis may mediate CHB-induced inflammatory damage in chronic HBV infection complicated with NAFLD, and the mechanism may be related to the activation of NLRP3 inflammatory bodies and downstream inflammatory responses.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.virusres.2021.198405 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Intrahepatic CD161CD8+T Cell Recruitment Has a Pathogenetic Potential in Chronic HBV Infection.
Immun Inflamm Dis
January 2025
Department of Clinical Laboratory, the Second Affiliated Hospital of Anhui Medical University, Hefei, China.
Backgrounds And Aims: CD8+T cells are crucially associated with the fight against hepatitis B virus (HBV) infection. CD161 has been shown to express remarkably on HCV-specific CD8+T cells. However, the accurate function of CD161+CD8+T cells in HBV immunity or pathogenesis remains undetermined.
View Article and Find Full Text PDFAssociation between extracellular matrix protein 1 (ECM1) gene polymorphisms (rs3834087 and rs3754217) and Hepatitis B Virus evolution in an African cohort.
Cell Mol Biol (Noisy-le-grand)
January 2025
Université Joseph KI-ZERBO, Laboratoire de Biologie Moléculaire et de Génétique (LABIOGENE), 03 BP 7021 Ouagadougou 03, Burkina Faso.
Article Synopsis
- Hepatitis B virus (HBV) is a major global health concern linked to liver disease and cancer, with research focusing on genetic factors that affect its evolution.
- Recent studies highlighted the ECM1 gene, specifically two polymorphisms (rs3834087 and rs3754217), which may influence HBV pathogenesis, particularly in an African cohort analyzed in this research.
- The study found that the heterozygous genotype of rs3754217 appears to protect against chronic hepatitis, suggesting that certain genetic variations may impact the severity of the disease in infected individuals.
[Advances in the study of viruses inhibiting the production of advanced autophagy or interferon through Rubicon to achieve innate immune escape].
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
January 2025
Department of Pathogen Biology and Immunology, Kunming Medical University, Kunming 650500, China. *Corresponding authors, E-mail:
The innate immune response is the first line of defense for the host against viral infections. Targeted degradation of pathogenic microorganisms through autophagy, in conjunction with pattern recognition receptors synergistically inducing the production of interferon (IFN), constitutes an important pathway for the body to resist viral infections. Rubicon, a Run domain Beclin 1-interacting and cysteine-rich domain protein, has an inhibitory effect on autophagy and IFN production.
View Article and Find Full Text PDFGenome-Wide Association Study to Identify Genetic Factors Linked to HBV Reactivation Following Liver Transplantation in HBV-Infected Patients.
Int J Mol Sci
December 2024
Department of Surgery, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam 13620, Republic of Korea.
This study utilized a genome-wide association study (GWAS) to investigate the genetic variations linked to the risk of hepatitis B virus (HBV) reactivation in patients who have undergone liver transplantation (LT), aiming to enhance understanding and improve clinical outcomes. Genotyping performed on a selected patients from the Korean Organ Transplantation Registry (KOTRY) data using high-throughput platforms with the Axiom Korea Biobank array 1.1.
View Article and Find Full Text PDFEvaluation of the role of unconventional prefoldin RPB5 interactor (URI1) in hepatitis B virus infection.
Virol J
January 2025
Institute of Organic Chemistry and Biochemistry, Czech Academy of Sciences, Prague, Czech Republic.
Hepatitis B virus (HBV) infection can cause liver disease and lead to hepatocellular carcinoma (HCC). To better understand the factors involved in viral infection and pathogenesis and to develop novel therapies, it is crucial to investigate virus-host interactions. HBV infection has been shown to increase the expression of the unconventional prefoldin RPB5 interactor (URI1), a cellular protein that promotes liver tumorigenesis and HCC metastasis.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!