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Mi R-122 in hepatitis B virus and hepatitis C virus dual infection

World Journal of Hepatology 2015年第3期7卷 498-506页

作者： Kyoungsub Song Chang Han Srikanta Dash luis a balart Tong Wu Department of Pathology and Laboratory Medicine Tulane University School of Medicine Department of Medicine Tulane University School of Medicine

Hepatitis B virus(HBV) and hepatitis C virus(HCV) infections are the most common causes of chronic liver diseases and hepatocelluar carcinomas. Over the past few years, the liver-enriched micro RNA-122(mi R-122) has been shown to differentially regulate viral replication of HBV and HCV. It is notable that thelevel of mi R-122 is positively and negatively regulated by HCV and HBV, respectively. Consistent with the welldocumented phenomenon that mi R-122 promotes HCV accumulation, inhibition of mi R-122 has been shown as an effective therapy for the treatment of HCV infection in both chimpanzees and humans. On the other hand, mi R-122 is also known to block HBV replication, and HBV has recently been shown to inhibit mi R-122 expression; such a reciprocal inhibition between mi R-122 and HBV suggests an intriguing possibility that mi R-122 replacement may represent a potential therapy for treatment of HBV infection. As HBV and HCV have shared transmission routes, dual infection is not an uncommon scenario, which is associated with more advanced liver disease than either HBV or HCV mono-infection. Thus, there is a clear need to further understand the interaction between HBV and HCV and to delineate the role of mi R-122 in HBV/HCV dual infection in order to devise effective therapy. This review summarizes the current understanding of HBV/HCV dual infection, focusing on the pathobiological role and therapeutic potential of mi R-122.

关键词： MiR-122 Hepatitis B virus Hepatitis C virus Hepatitis B virus/hepatitis C virus dual infection

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Hepatocellular carcinoma xenograft supports HCV replication:A mouse model for evaluating antivirals

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World Journal of Gastroenterology 2011年第3期17卷 300-312页

作者： Sidhartha Hazari Henry J Hefler Partha K Chandra Bret Poat Feyza Gunduz Tara Ooms Tong Wu luis a balart Srikanta Dash Department of Pathology and Laboratory Medicine Tulane University Health Sciences Center New Orleans LA 70112 United States Department of Gastroenterology and Hepatology Tulane University Health Sciences Center New Orleans LA 70112 United States Department of Comparative Medicine Tulane University Health Sciences Center New Orleans LA 70112 United States

AIM: To develop a hepatocellular carcinoma (HCC) xenograft model for studying hepatitis C virus (HCV) replication in a mice, and antiviral ***: We developed a stable S3-green fluorescence protein (GFP) cell line that replicated the GFP-tagged HCV sub-genomic RNA derived from a highly efficient JFH1 virus. S3-GFP replicon cell line was injected subcutaneously into γ-irradiated SCID mice. We showed that the S3-GFP replicon cell line formed human HCC xenografts in SCID mice. Cells were isolated from subcutaneous tumors and then serially passaged multiple times in SCID mice by culturing in growth medium supplemented with G-418. The mouse-adapted S3-GFP replicon cells were implanted subcutaneously and also into the liver of SCID mice via intrasplenic infusion to study the replication of HCV in the HCC xenografts. The tumor model was validated for antiviral testing after intraperitoneal injection of interferon-α (IFN-α). RESULTS: A highly tumorigenic S3-GFP replicon cell line was developed that formed subcutaneous tumors within 2 wk and diffuse liver metastasis within 4 wk in SCID mice. Replication of HCV in the subcutaneous and liver tumors was confirmed by cell colony assay, detection of the viral RNA by ribonuclease protection assay and real-time quantitative reverse transcription polymerase chain reaction. High-level replication of HCV sub-genomic RNA in the tumor could be visualized by GFP expression using fluorescence microscopy. IFN-α cleared HCV RNA replication in the subcutaneous tumors within 2 wk and 4 wk in the liver tumor model. CONCLUSION: A non-infectious mouse model allows us to study replication of HCV in subcutaneous and metastatic liver tumors. Clearance of HCV by IFN-α supports use of this model to test other anti-HCV drugs.

关键词： Hepatitis C virus Hepatocellular carcinoma Tumor xenograft SCID mouse Interferon-α Antiviral agent Virus replication

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Mastabol induced acute cholestasis: A case report

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World Journal of Hepatology 2013年第3期5卷 133-136页

作者： Brett M Hymel David W Victor luis Alvarez Nathan J Shores luis a balart Department of Gastroenterology Louisiana State University School of Medicine Department of Gastroenterology and Hepatology Tulane University School of Medicine

A 26-year-old male presented with three weeks of jaundice after the self-initiation of the injectable anabolic steroid, Mastabol [Dromastanolone Di-Propionate (17 beta-Hydroxy-2alpha-methyl-5alpha-androstan-3one propionate)]. He reported dark urine, light stools, and pruritus. He denied abdominal pain, intravenous drug use, intranasal cocaine, blood transfusions, newly placed tattoos, or sexually transmitted diseases. He used alcohol sparingly. Physical exam revealed jaundice with deep scleral icterus. The liver was palpable 2 cm below the right costal margin with no ascites. The peak bilirubin was 23.6 mg/dL, alkaline phosphatase was 441 units/L, and aspartate aminotransferase/alanine aminotransferase were 70 units/L and 117 units/L respectively. A working diagnosis of acute intrahepatic cholestasis was made. Liver biopsy revealed a centrilobular insult with neutrophilic infiltrates and Ito cell hyperplasia consistent with acute drug induced cholestasis. The patient' s clinical symptoms resolved and his liver enzymes, bilirubin, and alkaline phosphatase normalized. Anabolic steroids with 17 alpha carbon substitutions have been associated with a bland variety of cholestatic injury with little hepatocellular injury. Cholestasis, under these circumstances, may be secondary to the binding of drugs to canalicular membrane transporters, accumulation of toxic bile acids from canalicular pump failure, or genetic defects in canalicular transport proteins. Mastabol is an injectable, 17 beta hydroxyl compound with no alpha alkyl groups at the 17 carbon position. As such, it has been reported to have little potential toxic effects on the liver. This is the first known reported case of Mastabolinduced cholestatic liver injury. It highlights the need for physicians to consider such widely available substances when faced with hepatic injury of unclear etiology.

关键词： Cholestatic Mastabol Hepatic Anabolic Steroids

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Portal vein thrombosis in liver transplantation: radiologic evaluation, risk factors, and occult diagnosis

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Hepatoma Research 2016年第1期2卷 36-41页

作者： Adam Hauch Carl Winkler Eric Katz Peter W.Lundberg Mary Killackey Anil S.Paramesh luis A.balart Nathan J.Shores Martin Moehlen Ward Miller Douglas P.Slakey Joseph F.Buell Bob H.Saggi Tulane Transplant Institute Tulane University School of MedicineNew OrleansLA 70112USA Department of Gastroenterology Section of HepatologyTulane University School of MedicineNew OrleansLA 70112USA

Aim:Portal vein thrombosis(PVT)in the liver transplant recipient poses many ***,the risk factors and effects on outcomes of PVT are not ***:This study analyzed the experience with PVT in liver transplant program from 2007 to *** included the effectiveness of PVT diagnostics and its risk factors using logistical *** primary endpoints were Kaplan-Meir patient and graft *** secondary endpoints were the length of stay(LOS),transfusion rate,and overall *** predictors of survival were identified using a Cox’s proportional hazards ***:Two hundred and sixteen consecutive liver transplant recipients were examined,and 30(13.8%)had either a total or partial *** hundred and five patients had imaging within 1 year of liver transplantation with only 7(23.3%)of the 30 PVTs identified *** sensitivity(4.8-50%)and negative predictive values(10.5-22.2%)were ***,age significantly predicted PVT[P=0.037/hazard ratio(HR)=0.95].Ninety-day-patient and graft survival for PVT was similar at 6 months,although 1-year survival was significantly lower.“Occult”PVT was not associated with inferior *** for end-stage liver disease score>25(P=0.001,HR=0.49/P=0.004,HR=0.52)and age>60 years(P=0.017,HR=0.64/P=0.013,HR=0.67)were significant predictors of patient and graft *** the transfusion rate was significantly greater with PVT,LOS,and morbidity were ***:Older recipients had a greater likelihood of *** studies were not effective at excluding PVT,and occult diagnosis did not affect the *** was not an independent predictor of mortality or graft loss,but was associated with greater blood loss but not increased LOS or morbidity.

关键词： Advanced age graft survival patient survival post-transplant outcomes resource utilization

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