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HIV Induces TRAIL Sensitivity in Hepatocytes  [PDF]
Challagundla K. Babu, Kanitta Suwansrinon, Gary D. Bren, Andrew D. Badley, Stacey A. Rizza
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0004623
Abstract: Background HIV infected patients have an increased susceptibility to liver disease due to Hepatitis B Virus (HBV), Hepatitis C Virus (HCV), alcoholic, and non-alcoholic steatohepatitis. Clinically, this results in limited options for antiretroviral therapy and accelerated rates of liver disease, causing liver disease to be the second leading cause of death for HIV infected patients. The mechanisms causing this propensity for liver dysfunction during HIV remains unknown. Methodology/Principal Findings We demonstrate that HIV and/or the HIV glycoprotein gp120 ligation of CXCR4 on hepatocytes selectively up-regulates TRAIL R2 expression and confers an acquired sensitivity to TRAIL mediated apoptosis which is mediated by JNK II, but not p38 nor G-proteins. Conclusions/Significance These findings suggest that HIV infection renders hepatocytes more susceptible to liver injury during disease states associated with enhanced TRAIL production such as HBV, HCV, or steatohepatitis.
Innate Host Response in Primary Human Hepatocytes with Hepatitis C Virus Infection  [PDF]
Darong Yang, Nianli Liu, Chaohui Zuo, Shoahua Lei, Xinjiao Wu, Fei Zhou, Chen Liu, Haizhen Zhu
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0027552
Abstract: Background and Aim The interaction between hepatitis C virus (HCV) and innate antiviral defense systems in primary human hepatocytes is not well understood. The objective of this study is to examine how primary human hepatocytes response to HCV infection. Methods An infectious HCV isolate JFH1 was used to infect isolated primary human hepatocytes. HCV RNA or NS5A protein in the cells was detected by real-time PCR or immunofluorescence staining respectively. Apoptosis was examined with flow cytometry. Mechanisms of HCV-induced IFN-β expression and apoptosis were determined. Results Primary human hepatocytes were susceptible to JFH1 virus and released infectious virus. IFN-α inhibited viral RNA replication in the cells. IFN-β and interferon-stimulated genes were induced in the cells during acute infection. HCV infection induced apoptosis of primary human hepatocytes through the TRAIL-mediated pathway. Silencing RIG-I expression in primary human hepatocytes inhibited IFN-β and TRAIL expression and blocked apoptosis of the cells, which facilitated viral RNA replication in the cells. Moreover, HCV NS34A protein inhibited viral induced IFN-β expression in primary human hepatocytes. Conclusion Innate host response is intact in HCV-infected primary human hepatocytes. RIG-I plays a key role in the induction of IFN and TRAIL by viruses and apoptosis of primary human hepatocytes via activation of the TRAIL-mediated pathway. HCV NS34A protein appears to be capable of disrupting the innate antiviral host responses in primary human hepatocytes. Our study provides a novel mechanism by which primary human hepatocytes respond to natural HCV infection.
The state of membrane of the hepatocytes and the blood erytrocytes in pations with chronic hepatitis with signs of cholestasis.  [PDF]
Zakharash A.D.
Морфолог?я , 2007,
Abstract: The purpose of work was to give morphological and morphometric characteristic of the hepatocytes and the blood erytrocytes against a background to determine the state of lipid peroxidation and antioxidant system of protection in case chronic cryptogenic hepatitis. Morphological and morphometric liver parameters were measured at the icteris in 5 patients (control – 5 patients). It was found that in patients with chronic hepatitis square of hepatocytes, square of their nuclei have been decreased, their relationship change for the better of cytoplasm. The hepatocytes and their nuclei have been deformed. The modifications of morphological and morphometric characteristic of the hepatocytes and the blood erytrocytes have been determined, drastic increase of the level CD95+ lymphocytes is evidence of the system reaction of apoptosis of the cells were studied in case chronic hepatitis with signs of cholestasis. In same patients with chronic hepatitis of non-virus etiology there were determined changes of area, perimeter and deformity of erythrocytes both on the basis of free radical reactions disorder and antioxidate protection system disorders; it induces us to quest their pathogenetically substantiated treatment.
One step closer to an experimental infection system for Hepatitis B Virus? --- the identification of sodium taurocholate cotransporting peptide as a viral receptor
Pei-Jer Chen, T-C Wu
Cell & Bioscience , 2013, DOI: 10.1186/2045-3701-3-2
Abstract: Among the five hepatotropic hepatitis viruses, only hepatitis B virus (HBV) and its satellite hepatitis D virus (HDV) still wait for the development of an in vitro infection system in cell culture. One hepatocellular carcinoma (HCC) cell line, HepaRG, can be infected at a modest efficiency after weeks of culture and induced differentiation [1]. Even primary human hepatocytes rapidly lose the capacity for HBV infection after brief cell culture. The HBV infection demands both intracellular and cell-surface factors. The intracellular requirements appear less stringent, as after transfection of HBV DNA into many HCC cell lines or mouse liver, which cannot be infected naturally, the viral genome is expressed and replicates actively. Thus, the failure of HBV infection is considered largely to be due to strict restriction on the interaction between HBV virions and the cell membrane.The molecules on the cell membrane needed for HBV infection can be divided into two classes: low affinity and high affinity molecules. Among others, the heparan sulfates in the membrane proteins mediate the broad, but less specific, virus-cell interaction. However, the high affinity membrane partners for HBV remain elusive (the carboxypeptidase D found for duck hepatitis B virus may be the only serious contender [2]).HBV envelope protein, namely the surface antigens, plays an essential role in the infection process. Both genetic and functional examination identified one domain in the N-terminus of HBV preS1 (amino acids 1–47) necessary for infection. This domain has been shown to function as a direct mediator for HBV by binding presumably cellular corresponding receptor(s) [3]. More importantly, the myristoylated peptide is shown to effectively block HBV infection in primary human hepatocytes and in the human hepatocyte-chimera mouse at a nanomolar concentration [4]. In fact, a clinical trial testing the efficacy of this peptide in preventing HBV infection has been ongoing [5]. Clearly, this pre
Purinergic Receptor Functionality Is Necessary for Infection of Human Hepatocytes by Hepatitis Delta Virus and Hepatitis B Virus  [PDF]
John M. Taylor,Ziying Han
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0015784
Abstract: Hepatitis B virus (HBV) and hepatitis delta virus (HDV) are major sources of acute and chronic hepatitis. HDV requires the envelope proteins of HBV for the processes of assembly and infection of new cells. Both viruses are able to infect hepatocytes though previous studies have failed to determine the mechanism of entry into such cells. This study began with evidence that suramin, a symmetrical hexasulfated napthylurea, could block HDV entry into primary human hepatocytes (PHH) and was then extrapolated to incorporate findings of others that suramin is one of many compounds that can block activation of purinergic receptors. Thus other inhibitors, pyridoxal-phosphate-6-azophenyl-2′,4′-di?sulfonate(PPADS) and brilliant blue G (BBG), both structurally unrelated to suramin, were tested and found to inhibit HDV and HBV infections of PHH. BBG, unlike suramin and PPADS, is known to be more specific for just one purinergic receptor, P2X7. These studies provide the first evidence that purinergic receptor functionality is necessary for virus entry. Furthermore, since P2X7 activation is known to be a major component of inflammatory responses, it is proposed that HDV and HBV attachment to susceptible cells, might also contribute to inflammation in the liver, that is, hepatitis.
Proteomic analysis of primary duck hepatocytes infected with duck hepatitis B virus
Yanfeng Zhao, Haijing Ben, Su Qu, Xinwen Zhou, Liang Yan, Bin Xu, Shuangcheng Zhou, Qiang Lou, Rong Ye, Tianlun Zhou, Pengyuan Yang, Di Qu
Proteome Science , 2010, DOI: 10.1186/1477-5956-8-28
Abstract: The effects of hepadnavirus infection on hepatocytes were investigated in DHBV infected PDHs by the 2-DE analysis. Proteomic profile of PDHs infected with DHBV were analyzed at 24, 72 and 120 h post-infection by comparing with uninfected PDHs, and 75 differentially expressed protein spots were revealed by 2-DE analysis. Among the selected protein spots, 51 spots were identified corresponding to 42 proteins by MS/MS analysis; most of them were matched to orthologous proteins of Gallus gallus, Anas platyrhynchos or other avian species, including alpha-enolase, lamin A, aconitase 2, cofilin-2 and annexin A2, etc. The down-regulated expression of beta-actin and annexin A2 was confirmed by Western blot analysis, and potential roles of some differentially expressed proteins in the virus-infected cells have been discussed.Differentially expressed proteins of DHBV infected PDHs revealed by 2-DE, are involved in carbohydrate metabolism, amino acid metabolism, stress responses and cytoskeleton processes etc, providing the insight to understanding of interactions between hepadnavirus and hepatocytes and molecular mechanisms of hepadnavirus pathogenesis.The HBV, prototype of the Hepadnaviridae family, is a noncytopathic hepatotropic DNA virus replicating via reverse transcription [1]. More than 350 million individuals are HBV carriers worldwide and over one-third of them develop serious liver diseases such as chronic hepatitis, cirrhosis and primary hepatocellular carcinoma [2]. Major obstacles in HBV research have been the inability of the virus to infect cells in vitro and lack of adequate animal models for HBV infection, though primary human hepatocytes and HepaRG cell line have been used to study HBV infection [3]. Human primary hepatocytes and HepaRG cells can support HBV life cycle, but have limitations in accessibility, reproducibility and low level of HBV replication, and a large amount of input virus was needed to infect low proportion of cells [4-6]. DHBV and woodchuc
An Implantable Vascularized Protein Gel Construct That Supports Human Fetal Hepatoblast Survival and Infection by Hepatitis C Virus in Mice  [PDF]
Martha J. Harding,Christin M. Lepus,Thomas F. Gibson,Benjamin R. Shepherd,Scott A. Gerber,Morven Graham,Frank X. Paturzo,Christoph Rahner,Joseph A. Madri,Alfred L. M. Bothwell,Brett D. Lindenbach,Jordan S. Pober
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0009987
Abstract: Widely accessible small animal models suitable for the study of hepatitis C virus (HCV) in vivo are lacking, primarily because rodent hepatocytes cannot be productively infected and because human hepatocytes are not easily engrafted in immunodeficient mice.
Pathogenic Mouse Hepatitis Virus or Poly(I:C) Induce IL-33 in Hepatocytes in Murine Models of Hepatitis  [PDF]
Muhammad Imran Arshad, Solène Patrat-Delon, Claire Piquet-Pellorce, Annie L’Helgoualc’h, Michel Rauch, Valentine Genet, Catherine Lucas-Clerc, Christian Bleau, Lucie Lamontagne, Michel Samson
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0074278
Abstract: The IL-33/ST2 axis is known to be involved in liver pathologies. Although, the IL-33 levels increased in sera of viral hepatitis patients in human, the cellular sources of IL-33 in viral hepatitis remained obscure. Therefore, we aimed to investigate the expression of IL-33 in murine fulminant hepatitis induced by a Toll like receptor (TLR3) viral mimetic, poly(I:C) or by pathogenic mouse hepatitis virus (L2-MHV3). The administration of poly(I:C) plus D-galactosamine (D-GalN) in mice led to acute liver injury associated with the induction of IL-33 expression in liver sinusoidal endothelial cells (LSEC) and vascular endothelial cells (VEC), while the administration of poly(I:C) alone led to hepatocyte specific IL-33 expression in addition to vascular IL-33 expression. The hepatocyte-specific IL-33 expression was down-regulated in NK-depleted poly(I:C) treated mice suggesting a partial regulation of IL-33 by NK cells. The CD1d KO (NKT deficient) mice showed hepatoprotection against poly(I:C)-induced hepatitis in association with increased number of IL-33 expressing hepatocytes in CD1d KO mice than WT controls. These results suggest that hepatocyte-specific IL-33 expression in poly(I:C) induced liver injury was partially dependent of NK cells and with limited role of NKT cells. In parallel, the L2-MHV3 infection in mice induced fulminant hepatitis associated with up-regulated IL-33 expression as well as pro-inflammatory cytokine microenvironment in liver. The LSEC and VEC expressed inducible expression of IL-33 following L2-MHV3 infection but the hepatocyte-specific IL-33 expression was only evident between 24 to 32h of post infection. In conclusion, the alarmin cytokine IL-33 was over-expressed during fulminant hepatitis in mice with LSEC, VEC and hepatocytes as potential sources of IL-33.
Infección crónica por el VHB Chronic Hepatitis B Virus infection  [cached]
C. Carretero,M. Herráiz
Anales del Sistema Sanitario de Navarra , 2004,
Abstract: Existen muchos factores implicados en la patogénesis de la infección crónica por el virus de la hepatitis B (VHB), como por ejemplo características del virus, la ingesta de etanol, la coinfección con otros virus (VHC, VIH, VHD), e intervenciones terapéuticas como el uso de fármacos citotóxicos o inmunosupresores, o agentes antivirales específicos. Las características clínicas, patológicas y serológicas de la hepatitis crónica por VHB, además, son muy heterogéneas. Se puede reconocer la infección crónica por VHB ante la persistencia del antígeno Australia (HBsAg) durante más de seis meses. La presencia de HBeAg se suele asociar a la replicación viral activa y puede ser medida por la cantidad de DNA-VHB presente en el suero o bien por la expresión hepática de HBcAg. El da o hepático que se produce en la hepatitis crónica por VHB no es tanto por el efecto del virus sobre los hepatocitos sino por la reacción inmune que éste provoca en el huésped. Por ello puede verse cierta correlación inversamente proporcional entre la intensidad de la replicación viral y el grado de inflamación hepática. La presencia de hepatitis crónica activa en la biopsia inicial no se ha asociado al desarrollo de cirrosis así como tampoco el diagnóstico histológico de hepatitis crónica persistente puede asegurar que se vaya a desarrollar cirrosis en un futuro. Many factors are involved in the pathogenesis of chronic hepatitis B virus infection (HBV), such as, for example, characteristics of the virus, ethanol intake, coinfection with other viruses (HCV, HIV, HDV), and therapeutic interventions such as the use of cytotoxic drugs or immunosuppressors, or specific antiviral agents. The clinical, pathological and serological characteristics of chronic hepatitis B virus infection are besides very heterogeneous. Chronic HBV infection can be recognised facing persistence of the Australia antigen (HBsAg) for more than six months. The presence of HBeAg is usually associated with active viral replication and can be measured by the quantity of DNA-HBV present in the serum or by the hepatic expression of HBcAg. The hepatic damage that is produced in chronic hepatitis due to HBV is not so much due to the effect of the virus on the hepatocytes as to the immune reaction that it provokes in the host. For this reason a certain inversely proportionate correlation can be observed between the intensity of viral replication and the degree of hepatic inflammation. The presence of active chronic hepatitis in the initial biopsy has not been associated with the development of cirrhosis, nor does the histologi
Epidemiology of Occult Hepatitis B Infection Among Thalassemic, Hemophilia, and Hemodialysis Patients
Mohammad Kazemi Arababadi,Behzad Nasiri Ahmadabadi,Hassan Youse? Daredor,Derek Kennedy
Hepatitis Monthly , 2012,
Abstract: Context: Hepatitis B virus (HBV) is the most common disease commuted through blood transfusion. Occult hepatitis B infection (OBI) is a form of the disease which does not present Hepatitis B surface antigens (HBsAg) in the serum of patients; however, HBVDNA is detectable in the serum and hepatocytes of patients. OBI is an important risk factor to induce post transfusion hepatitis (PTH), cirrhosis, hepatocellular carcinoma (HCC) and reactivation of the HBV. Recently, several reports from various regions of the world have been published regarding PTH among blood recipients as well as HCC, and cirrhosis among patients who require permanent blood transfusion, including diseases such as hemophilia, hemodialysis and thalassemia. This form of the hepatitis also creates problems for individuals that are co-infected with other viruses such as HCV and HIV. To determine the prevalence of OBI among hemophilia, hemodialysis and thalassemia patients is important because it is a high risk factor for PTH, HCC and cirrhosis therefore, its detection is a critical strategy for most health care services. This review addresses recent information regarding prevalence of OBI in relation to the mentioned diseases.Evidence Acquisition: The data presented here was collected by searching the key words in Pubmed and Scopous databases.Results: Our searching in the published papers revealed that OBI prevalence is frequent in patients receiving frequent blood transfusions.Conclusions: it seems that one of the main mechanisms for OBI transmission is most likely through infected blood and its component and evaluation of the prevalence of OBI in donors and patients, especially those with hemophilia and thalassemia should be foul considered.
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