Hepatitis C virus infection and tight junction proteins: The ties that bind

Mailly, Laurent; Baumert, Thomas F.

doi:10.1016/j.bbamem.2020.183296

Cited by 18 publications

(13 citation statements)

References 160 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For DMGs, the functional analysis revealed that the development of NAFLD was primarily related to tight junction, pathogenic Escherichia coli infection, and GTPase-related activity. Tight junctions are intercellular adhesion complexes in the epithelia and endothelia that control paracellular permeability, playing a vital role in architecture and homeostasis in the liver [ 22 , 23 ]. The disruption of tight junctions can impair intestinal permeability, and the subsequent increased gut microbial translocation can lead to the inflammatory pathway involved in NASH development [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

Transcriptional and Epigenetic Alterations in the Progression of Non-Alcoholic Fatty Liver Disease and Biomarkers Helping to Diagnose Non-Alcoholic Steatohepatitis

et al. 2023

View full text Add to dashboard Cite

Non-alcoholic fatty liver disease (NAFLD) encompasses a broad spectrum of conditions from simple steatosis (non-alcoholic fatty liver (NAFL)) to non-alcoholic steatohepatitis (NASH), and its global prevalence continues to rise. NASH, the progressive form of NAFLD, has higher risks of liver and non-liver related adverse outcomes compared with those patients with NAFL alone. Therefore, the present study aimed to explore the mechanisms in the progression of NAFLD and to develop a model to diagnose NASH based on the transcriptome and epigenome. Differentially expressed genes (DEGs) and differentially methylated genes (DMGs) among the three groups (normal, NAFL, and NASH) were identified, and the functional analysis revealed that the development of NAFLD was primarily related to the oxidoreductase-related activity, PPAR signaling pathway, tight junction, and pathogenic Escherichia coli infection. The logistic regression (LR) model, consisting of ApoF, THOP1, and BICC1, outperformed the other five models. With the highest AUC (0.8819, 95%CI: 0.8128–0.9511) and a sensitivity of 97.87%, as well as a specificity of 64.71%, the LR model was determined as the diagnostic model, which can differentiate NASH from NAFL. In conclusion, several potential mechanisms were screened out based on the transcriptome and epigenome, and a diagnostic model was built to help patient stratification for NAFLD populations.

show abstract

Section: Discussionmentioning

confidence: 99%

Transcriptional and Epigenetic Alterations in the Progression of Non-Alcoholic Fatty Liver Disease and Biomarkers Helping to Diagnose Non-Alcoholic Steatohepatitis

et al. 2023

View full text Add to dashboard Cite

show abstract

“…Retroviruses modify the distribution of the tight-junction proteins occludin and claudin-1 and destroy tight junctions via the RhoA/ROCK /MLC signaling pathways [ 103 – 105 ]. Hepatitis C virus also affects occludin and claudin-1, and these proteins may also promote endocytosis of the virus [ 103 , 106 , 107 ]. HPV enters through adherens junctions.…”

Section: Virus Interaction With the Cellular Junctionsmentioning

confidence: 99%

Virus interactions with the actin cytoskeleton—what we know and do not know about SARS-CoV-2

et al. 2022

View full text Add to dashboard Cite

The actin cytoskeleton and actin-dependent molecular and cellular events are responsible for the organization of eukaryotic cells and their functions. Viruses, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), depend on host cell organelles and molecular components for cell entry and propagation. Thus, it is not surprising that they also interact at many levels with the actin cytoskeleton of the host. There have been many studies on how different viruses reconfigure and manipulate the actin cytoskeleton of the host during successive steps of their life cycle. However, we know relatively little about the interactions of SARS-CoV-2 with the actin cytoskeleton. Here, we describe how the actin cytoskeleton is involved in the strategies used by different viruses for entry, assembly, and egress from the host cell. We emphasize what is known and unknown about SARS-CoV-2 in this regard. This review should encourage further investigation of the interactions of SARS-CoV-2 with cellular components, which will eventually be helpful for developing novel antiviral therapies for mitigating the severity of COVID-19.

show abstract

“…The first 18 residues of the cytoplasmic structural domain of OCLN can mediate HCV infection [ 36 ]. Two amino acid sites were found in the EC2 and C-termini of OCLN, involved in HCV infection [ 37 ].…”

Section: Tjs and Virusmentioning

confidence: 99%

Tight Junctions, the Key Factor in Virus-Related Disease

Ding

Shao

et al. 2022

Pathogens

View full text Add to dashboard Cite

Tight junctions (TJs) are highly specialized membrane structural domains that hold cells together and form a continuous intercellular barrier in epithelial cells. TJs regulate paracellular permeability and participate in various cellular signaling pathways. As physical barriers, TJs can block viral entry into host cells; however, viruses use a variety of strategies to circumvent this barrier to facilitate their infection. This paper summarizes how viruses evade various barriers during infection by regulating the expression of TJs to facilitate their own entry into the organism causing infection, which will help to develop drugs targeting TJs to contain virus-related disease.

show abstract

Hepatitis C virus infection and tight junction proteins: The ties that bind

Cited by 18 publications

References 160 publications

Transcriptional and Epigenetic Alterations in the Progression of Non-Alcoholic Fatty Liver Disease and Biomarkers Helping to Diagnose Non-Alcoholic Steatohepatitis

Transcriptional and Epigenetic Alterations in the Progression of Non-Alcoholic Fatty Liver Disease and Biomarkers Helping to Diagnose Non-Alcoholic Steatohepatitis

Virus interactions with the actin cytoskeleton—what we know and do not know about SARS-CoV-2

Tight Junctions, the Key Factor in Virus-Related Disease

Contact Info

Product

Resources

About