Significance of mutations in hepatitis B virus X gene for the pathogenesis of HB-associated glomerulonephritis

Hui, David S.; Yan, Xiaojun; Wei, Jing; Ruixia, M; Guang-ju, Guo

doi:10.4149/av_2014_03_278

Cited by 11 publications

(4 citation statements)

References 13 publications

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“…In addition, acquired missense nucleotide mutations of the HBV x gene in specific locations (C1653T, A1726C, A1727T, C1730G, T1753C, A1762T, and G1764A) were found in 84% of patients with MN and in only 8% of control patients, which may explain the predisposition of certain HBV carriers to develop renal disease (10). Of the eight genotypes of HBV, genotype A appears to have the highest risk of MN or MPGN.…”

Section: Membranous Nephropathymentioning

confidence: 97%

Viral-Associated GN: Hepatitis B and Other Viral Infections

Kupin

2016

CJASN

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By definition, viral-associated GN indicates the direct pathogenic relationship between active viral replication and the development of acute GN. This definition is in sharp contrast to the semantic label and pathophysiologic foundation behind postinfectious GN that uniquely develops only during a period of resolved and absent active infection. The primary example of postinfectious GN are the glomerular lesions described after a pharyngeal or cutaneous streptococcal infection and do not represent the clinical or immunologic pattern seen with viralassociated GN. Hepatitis B (HBV) is the most common chronic viral infection in the world affecting >400 million people which is more than double the prevalence of chronic HIV and hepatitis C carriers combined. In addition, 10%-20% of HBV patients may be coinfected with hepatitis C and 5%-10% will have coinfection with HIV. Being able to distinguish the different types of GN seen with each viral infection is essential for the practicing clinician as each virus requires its own specific antiviral therapy. HBV-induced immune complex disease with renal injury lies on one end of the spectrum of disorders that occurs after a prolonged chronic carrier state. On the opposite end of the spectrum are renal diseases that develop from acute or subacute viral infections. One important glomerular lesion in this category is the association of collapsing FSGS with acute active cytomegalovirus, Epstein-Barr virus, and parvovirus B19 infection. The data supporting or disproving this relationship for each of these viruses will be discussed. A second renal manifestation of acute viral infections often occurs with many different sporadic or epidemic infections such as dengue and hantavirus and can lead to a transient proliferative GN that resolves upon viral clearance. The complex interplay of HBV and all viruses with the immune system provides conceptual lessons on the pathophysiology of immune complex GN that can be applied to all infection-related renal disease and plays an integral role in developing an approach to therapeutic intervention.

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Section: Membranous Nephropathymentioning

confidence: 97%

Viral-Associated GN: Hepatitis B and Other Viral Infections

Kupin

2016

CJASN

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“…We have mentioned the possible relationship between different genotypes of HBV and associated nephropathy. Further studies have found that mutations in HBV genes (C1653T, A1726C, A1727T, C1730G, T1753C, A1762T, and G1764A) are present in 84% of patients with membranous nephropathy (21).…”

Section: Host and Viral Genetic Factorsmentioning

confidence: 99%

HBV Hepatitis and Related Renal Nephropathies: Pathogenesis and Treatment

Salvadori

Tsalouchos²

2020

jrenhep

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The extrahepatic manifestations of hepatitis B virus (HBV) infection include reactive arthritis, vasculitis (panarteritisnodosa), and primary glomer-ulonephritis (membranous nephropathy, membranoproliferative glomerulonephritis, and, less frequently, IgA nephropathy, focal and segmental glomerulosclerosis, and minimal change disease). No specific histomorphological patterns have been reported in association with HBV infection. The treatment of HBV-related glomerulopathies is essentially antiviral. Peginterferon and nucleos(t)ide drugs are the treatment of choice. Cortico-steroids have been proved to be ineffective (except in panarteritisnodosa), while immunosuppressants can lead to exacerbation of HBV infection.

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“…HBx as a multifunctional protein encoded by HBV can modulate multiple signaling pathways such as HBV replication, cellular transcription, cell cycle, DNA repair, etc ( Lei et al, 2019 ; Yang et al, 2018 ). Past studies have shown that mutations at key genetic loci plays an important role in HBV-GN progression ( Hui et al, 2014 ). HBx overexpression could decrease cell viability of podocytes and cause increased podocyte injury ( Lei et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

Bone marrow mesenchymal stem cell-derived exosomes protect podocytes from HBx-induced ferroptosis

Yang

et al. 2023

PeerJ

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Introduction Hepatitis B virus-associated glomerulonephritis (HBV-GN) is a common secondary kidney disease in China, the pathogenesis of which is not completely clear, and there is still a lack of effective treatment. Methods The mechanism of exosomes derived from bone marrow mesenchymal stem cells (BMSCs) was investigated by using HBx-transfected human renal podocytes. Cell viability was detected by CCK8 assay. Iron and malondialdehyde (MDA) contents were detected by using commercial kits. Reactive oxygen species (ROS) levels were measured by flow cytometry analysis. The expression of ferroptosis related molecules was detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. The effect of miR-223-3p transferred by BMSC-derived exosomes on HBx-overexpressing podocytes was proved by using miR-223-3p inhibitor. Results The cell viability of podocytes reduced at 72 h or 96 h after the transfection of lentivirus overexpressing HBx protein (p < 0.05). Ferroptosis-related proteins, including glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) were down-regulated upon HBx overexpression, while acyl-CoA synthetase long-chain family member 4 (ACSL4) was up-regulated (p < 0.05). Intracellular levels of iron, MDA, and ROS were also enhanced (p < 0.05). BMSC-derived exosomes protected against ferroptosis induced by HBx overexpression in podocytes. miR-223-3p was enriched in BMSC-derived exosomes. Application of miR-223-3p inhibitor reversed the protective effect of BMSC-derived exosomes on HBx-induced ferroptosis in podocytes. Conclusion BMSC-derived exosomes inhibit HBx-induced podocyte ferroptosis by transferring miR-223-3p.

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Significance of mutations in hepatitis B virus X gene for the pathogenesis of HB-associated glomerulonephritis

Cited by 11 publications

References 13 publications

Viral-Associated GN: Hepatitis B and Other Viral Infections

Viral-Associated GN: Hepatitis B and Other Viral Infections

HBV Hepatitis and Related Renal Nephropathies: Pathogenesis and Treatment

Bone marrow mesenchymal stem cell-derived exosomes protect podocytes from HBx-induced ferroptosis

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