scholarly journals A Bioinformatic Analysis of Correlations between Polymeric Immunoglobulin Receptor (PIGR) and Liver Fibrosis Progression

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Yuan Zhang ◽  
Wenjun Lu ◽  
Xiaorong Chen ◽  
Yajuan Cao ◽  
Zongguo Yang
Keyword(s):  
Liver Fibrosis ◽  
Virus Infection ◽  
Predictive Value ◽  
Hepatitis Virus ◽  
Enrichment Analysis ◽  
Normal Liver ◽  
Fibrosis Stage ◽  
Polymeric Immunoglobulin Receptor ◽  
Immunoglobulin Receptor ◽  
Hepatitis Virus Infection

Objective. This study is aimed at investigating the enriched functions of polymeric immunoglobulin receptor (PIGR) and its correlations with liver fibrosis stage. Methods. PIGR mRNA expression in normal liver, liver fibrosis, hepatic stellate cells (HSCs), and hepatitis virus infection samples was calculated in Gene Expression Omnibus (GEO) and Oncomine databases. Enrichment analysis of PIGR-related genes was conducted in Metascape and Gene Set Enrichment Analysis (GSEA). Logistic model and ROC curve were performed to evaluate the correlations between pIgR and liver fibrosis. Results. PIGR mRNA was upregulated in advanced liver fibrosis, cirrhosis compared to normal liver (all p < 0.05 ). PIGR mRNA was also overexpressed in activated HSCs compared to senescent HSCs, liver stem/progenitor cells, and reverted HSCs (all p < 0.05 ). Enrichment analysis revealed that PIGR-related genes involved in the defense response to virus and interferon (IFN) signaling. In GEO series, PIGR mRNA was also upregulated by hepatitis virus B, C, D, and E infection (all p < 0.05 ). After adjusting age and gender, multivariate logistic regression models revealed that high PIGR in the liver was a risk factor for liver fibrosis ( OR = 82.2 , p < 0.001 ). The area under curve (AUC), positive predictive value (PPV), negative predictive value (NPV), sensitivity, and specificity of PIGR for liver fibrosis stage >2 were 0.84, 0.86, 0.7, 0.61, and 0.90. Conclusion. PIGR was correlated with liver fibrosis and might involve in hepatitis virus infection and HSC transdifferentiation.

scholarly journals A PREDICTIVE MODEL FOR NON-INVASIVE EVALUATION OF LIVER FIBROSIS IN PATIENTS WITH CHRONIC HEPATITIS VIRUS INFECTION

2014 ◽  
Vol 10 (4-5) ◽  
pp. 405
Author(s):  
A. A. Ostanin ◽  
E. L. Gelfgadt ◽  
M. V. Shipunov ◽  
E. Ya. Shevela ◽  
E. V. Kurganova ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Liver Fibrosis ◽  
Virus Infection ◽  
Predictive Model ◽  
Hepatitis Virus ◽  
Non Invasive ◽  
Hepatitis Virus Infection ◽  
Invasive Evaluation

scholarly journals Discordant Liver Fibrosis Predictors in Virologically Suppressed People Living with HIV without Hepatitis Virus Infection

Diagnostics ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 14
Author(s):  
Barbara Rossetti ◽  
Valentina Borgo ◽  
Arianna Emiliozzi ◽  
Marta Colaneri ◽  
Giacomo Zanelli ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Virus Infection ◽  
Viral Hepatitis ◽  
Hepatitis Virus ◽  
People Living With Hiv ◽  
Non Invasive ◽  
Tenofovir Alafenamide ◽  
Living With Hiv ◽  
Hepatitis Virus Infection ◽  
Hiv 1

Severe liver fibrosis (LF) is associated with poor long-term liver-related outcomes in people living with HIV (PLWH). The study aimed to explore the prevalence and predictors of LF and the concordance between different non-invasive methods for the estimation of LF in HIV-infected individuals without hepatitis virus infection. We enrolled PLWH with HIV-1-RNA <50 copies/mL for >12 months, excluding individuals with viral hepatitis. LF was assessed by transient elastography (TE) (significant >6.65 kPa), fibrosis-4 (FIB-4) (significant >2.67), and AST-to-platelet ratio index (APRI) (significant >1.5). We included 234 individuals (67% males, median age 49 years, median time from HIV diagnosis 11 years, 38% treated with integrase strand transfer inhibitors). In terms of the TE, 13% had ≥F2 stage; FIB-4 score was >1.5 in 7%; and APRI > 0.5 in 4%. Higher body mass index, diabetes mellitus, detectable baseline HIV-1 RNA and longer atazanavir exposure were associated with higher liver stiffness as per TE. Predictors of higher APRI score were CDC C stage and longer exposure to tenofovir alafenamide, while HBcAb positivity and longer exposure to tenofovir alafenamide were associated to higher FIB-4 scores. Qualitative agreement was poor between FIB-4/TE and between APRI/TE by non-parametric Spearman correlation and kappa statistic. In our study, in the group of PLWH without viral hepatitis, different non-invasive methods were discordant in predicting liver fibrosis.

Mouse Hepatitis Virus Infection Suppresses Modulation of Mouse Spleen T- Cell Activation

1988 ◽  
Author(s):  
Joan M. Cook-Mills ◽  
Hidayatulla G. Munshi ◽  
Robert L. Perlman ◽  
Donald A. Chambers
Keyword(s):  
T Cell ◽  
Virus Infection ◽  
T Cell Activation ◽  
Cell Activation ◽  
Hepatitis Virus ◽  
Mouse Hepatitis Virus ◽  
Mouse Spleen ◽  
Hepatitis Virus Infection

scholarly journals Antiviral Activities of Oral 1-O-Hexadecylpropanediol-3-Phosphoacyclovir and Acyclovir in Woodchucks with Chronic Woodchuck Hepatitis Virus Infection

2000 ◽  
Vol 44 (7) ◽  
pp. 1964-1969 ◽  
Author(s):  
Karl Y. Hostetler ◽  
James R. Beadle ◽  
William E. Hornbuckle ◽  
Christine A. Bellezza ◽  
Ilia A. Tochkov ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Virus Infection ◽  
Hepatitis B ◽  
Hepatitis Virus ◽  
Response To Therapy ◽  
Hydroxyl Group ◽  
Woodchuck Hepatitis Virus ◽  
Acyclovir Treatment ◽  
B Virus ◽  
Hepatitis Virus Infection

ABSTRACT Acyclovir triphosphate is a potent inhibitor of hepatitis B virus DNA polymerase, but acyclovir treatment provides no benefit in patients with hepatitis B virus infection. This is due in part to the fact that hepatitis B virus, unlike herpes simplex virus, does not code for a viral thymidine kinase which catalyzes the initial phosphorylation of acyclovir. We synthesized 1-O-octadecyl-sn-glycero-3-phospho (3-P)-acyclovir and found that it was highly active in reducing hepatitis B virus replication in 2.2.15 cells, while acyclovir was inactive. The greater antiviral activity of 1-O-octadecyl-sn-glycero-3-P-acyclovir appeared to be due to liver cell metabolism of the compound to acyclovir monophosphate (K. Y. Hostetler et al., Biochem. Pharmacol. 53:1815–1822, 1997). However, a closely related compound without a hydroxyl group at the sn-2 position of glycerol, 1-O-hexadecylpropanediol-3-P-acyclovir, was more active and selective in 2.2.15 cells in vitro. In this study, we treated woodchucks chronically infected with woodchuck hepatitis virus with increasing oral doses of 1-O-hexadecylpropanediol-3-P-acyclovir and assessed the response to therapy versus acyclovir or a placebo. At a dosage of 10 mg/kg of body weight twice a day, the test compound significantly inhibited viral replication in vivo, as indicated by a 95% reduction in serum woodchuck hepatitis virus DNA levels and by a 54% reduction in levels of woodchuck hepatitis virus replicative intermediates in the liver. Higher doses were somewhat less effective. In contrast, 20 mg of acyclovir/kg twice daily, a 5.3-fold-higher molar dosage, had no demonstrable activity against woodchuck hepatitis virus. Oral 1-O-hexadecylpropanediol-3-P-acyclovir appeared to be safe and effective in chronic woodchuck hepatitis virus infection.

p16 Promoter Hypermethylation in Human Hepatocellular Carcinoma with or without Hepatitis Virus Infection

Intervirology ◽  
2004 ◽  
Vol 47 (1) ◽  
pp. 26-31 ◽  
Author(s):  
Takashi Narimatsu ◽  
Akihiro Tamori ◽  
Noritoshi Koh ◽  
Shoji Kubo ◽  
Kazuhiro Hirohashi ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Virus Infection ◽  
Hepatitis Virus ◽  
Promoter Hypermethylation ◽  
Human Hepatocellular Carcinoma ◽  
Hepatitis Virus Infection
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