Search results for: Julie Lucifora

Items from 1 to 19 out of 19 results

article

Hepatic inflammation elicits production of proinflammatory netrin‐1 through exclusive activation of translation

Romain Barnault, Claire Verzeroli, Carole Fournier, Maud Michelet, more

Hepatology > 76 > 5 > 1345 - 1359

Background and Aims Netrin‐1 displays protumoral properties, though the pathological contexts and processes involved in its induction remain understudied. The liver is a major model of inflammation‐associated cancer development, leading to HCC. Approach and Results A panel of cell biology and biochemistry approaches (reverse transcription quantitative polymerase chain reaction, reporter assays,...

article

Hypoxia‐Inducible Factor 1 Alpha–Mediated RelB/APOBEC3B Down‐regulation Allows Hepatitis B Virus Persistence

Tobias Riedl, Suzanne Faure‐Dupuy, Maude Rolland, Svenja Schuehle, more

Hepatology > 74 > 4 > 1766 - 1781

Background and Aims Therapeutic strategies against HBV focus, among others, on the activation of the immune system to enable the infected host to eliminate HBV. Hypoxia‐inducible factor 1 alpha (HIF1α) stabilization has been associated with impaired immune responses. HBV pathogenesis triggers chronic hepatitis‐related scaring, leading inter alia to modulation of liver oxygenation and transient immune...

article

Hepatitis B Virus Evasion From Cyclic Guanosine Monophosphate–Adenosine Monophosphate Synthase Sensing in Human Hepatocytes

Eloi R. Verrier, Seung‐Ae Yim, Laura Heydmann, Houssein El Saghire, more

Hepatology > 68 > 5 > 1695 - 1709

Chronic hepatitis B virus (HBV) infection is a major cause of chronic liver disease and cancer worldwide. The mechanisms of viral genome sensing and the evasion of innate immune responses by HBV infection are still poorly understood. Recently, the cyclic guanosine monophosphate–adenosine monophosphate synthase (cGAS) was identified as a DNA sensor. In this study, we investigated the functional role...

article

Liver macrophages: Friend or foe during hepatitis B infection?

Suzanne Faure‐Dupuy, David Durantel, Julie Lucifora

Liver International > 38 > 10 > 1718 - 1729

The Hepatitis B virus chronically infects the liver of 250 million people worldwide. Over the past decades, major advances have been made in the understanding of Hepatitis B virus life cycle in hepatocytes. Beside these parenchymal cells, the liver also contains resident and infiltrating myeloid cells involved in immune responses to pathogens and much less is known about their interplay with Hepatitis...

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Detection of the hepatitis B virus (HBV) covalently-closed-circular DNA (cccDNA) in mice transduced with a recombinant AAV-HBV vector

Julie Lucifora, Anna Salvetti, Xavier Marniquet, Laurent Mailly, more

Antiviral Research > 2017 > 145 > C > 14-19

Hepatitis B Virus (HBV) persists in infected hepatocytes as an episomal covalently-closed-circular DNA mini-chromosome, called cccDNA. As the main nuclear transcription template, HBV cccDNA is a key replication intermediate in the viral life cycle. Little is known about the mechanisms involved in its formation, maintenance and fate under antiviral therapies. This is mainly due to the lack of small...

article

Autophagy determines efficiency of liver‐directed gene therapy with adeno‐associated viral vectors

Marianna Hösel, Anke Huber, Susanne Bohlen, Julie Lucifora, more

Hepatology > 66 > 1 > 252 - 265

Use of adeno‐associated viral (AAV) vectors for liver‐directed gene therapy has shown considerable success, particularly in patients with severe hemophilia B. However, the high vector doses required to reach therapeutic levels of transgene expression caused liver inflammation in some patients that selectively destroyed transduced hepatocytes. We hypothesized that such detrimental immune responses...

article

HDV RNA replication is associated with HBV repression and interferon-stimulated genes induction in super-infected hepatocytes

Dulce Alfaiate, Julie Lucifora, Natali Abeywickrama-Samarakoon, Maud Michelet, more

Antiviral Research > 2016 > 136 > C > 19-31

Hepatitis D virus (HDV) super-infection of Hepatitis B virus (HBV)-infected patients is the most aggressive form of viral hepatitis. HDV infection is not susceptible to direct anti-HBV drugs, and only suboptimal antiviral responses are obtained with interferon (IFN)-alpha-based therapy. To get insights on HDV replication and interplay with HBV in physiologically relevant hepatocytes, differentiated...

article

Attacking hepatitis B virus cccDNA – The holy grail to hepatitis B cure

Julie Lucifora, Ulrike Protzer

Journal of Hepatology > 2016 > 64 > 1(S) > S41-S48

HBV deposits a covalently closed circular DNA form, called cccDNA, in the nucleus of infected cells. As the central transcription template, the cccDNA minichromosome is a key intermediate in the HBV life cycle. Its location in the nucleus makes cccDNA a difficult target for antivirals and immune response, and therefore it is responsible for chronicity of HBV infection. While little is known about...

article

Interferon-γ and Tumor Necrosis Factor-α Produced by T Cells Reduce the HBV Persistence Form, cccDNA, Without Cytolysis

Yuchen Xia, Daniela Stadler, Julie Lucifora, Florian Reisinger, more

Gastroenterology > 2016 > 150 > 1 > 194-205

Viral clearance involves immune cell cytolysis of infected cells. However, studies of hepatitis B virus (HBV) infection in chimpanzees have indicated that cytokines released by T cells also can promote viral clearance via noncytolytic processes. We investigated the noncytolytic mechanisms by which T cells eliminate HBV from infected hepatocytes.We performed a cytokine enzyme-linked immunosorbent assay...

article

Early inhibition of hepatocyte innate responses by hepatitis B virus

Souphalone Luangsay, Marion Gruffaz, Nathalie Isorce, Barbara Testoni, more

Journal of Hepatology > 2015 > 63 > 6 > 1314-1322

The outcome of hepatitis B virus (HBV) infection may be influenced by early interactions between the virus and hepatocyte innate immune responses. To date, the study of such interactions during the very early step of infection has not been adequately investigated.We used the HepaRG cell line, as well as primary human hepatocytes to analyze, within 24h of exposure to HBV, either delivered by a physiologic...

article

Expression and functionality of Toll- and RIG-like receptors in HepaRG cells

Souphalone Luangsay, Malika Ait-Goughoulte, Maud Michelet, Océane Floriot, more

Journal of Hepatology > 2015 > 63 > 5 > 1077-1085

HepaRG cells are considered as the best surrogate model to primary human hepatocyte (PHH) culture to investigate host-pathogen interactions. Yet their innate immune functions remain unknown. In this study, we explored the expression and functionality of Toll-like (TLR) and retinoic acid-inducible gene-1 (RIG-I)-like receptors (RLR) in these cells.Gene and protein expression levels of TLR-1 to 9 and...

article

Immune-modulators to combat hepatitis B virus infection: From IFN-α to novel investigational immunotherapeutic strategies

Nathalie Isorce, Julie Lucifora, Fabien Zoulim, David Durantel

Antiviral Research > 2015 > 122 > Complete > 69-81

Chronic hepatitis B virus (HBV) infection remains a major challenge for clinicians, as there are only two types of approved therapies: interferon-alpha (IFN-α) or its pegylated form, Peg-IFN-α and nucleoside analogs (e.g. tenofovir, entecavir…). The first are used as finite-duration treatments of around 48–52weeks, while the second must be taken life-long to prevent rebound. Other immune-modulators,...

article

Hepatitis B virus infection enhances susceptibility toward adeno‐associated viral vector transduction in vitro and in vivo

Marianna Hösel, Julie Lucifora, Thomas Michler, Gisela Holz, more

Hepatology > 59 > 6 > 2110 - 2120

Gene therapy has become an accepted concept for the treatment of a variety of different diseases. In contrast to preclinical models, subjects enrolled in clinical trials, including gene therapy, possess a history of infection with microbes that may influence its safety and efficacy. Especially, viruses that establish chronic infections in the liver, one of the main targets for in vivo gene therapy,...

article

Ezetimibe blocks hepatitis B virus infection after virus uptake into hepatocytes

Julie Lucifora, Knud Esser, Ulrike Protzer

Antiviral Research > 2013 > 97 > 2 > 195-197

Current treatment of chronic hepatitis B virus (HBV) infection mainly targets viral replication in hepatocytes and leads to curing only in exceptional cases. Despite their potential to improve therapeutic success, no drugs interfering with early infection steps of the hepatotropic pathogen HBV are available to date. Recently, entry of the hepatitis C virus (HCV) has been shown to occur along hepatic...

article

Hepatitis B virus X protein is essential to initiate and maintain virus replication after infection

Julie Lucifora, Silke Arzberger, David Durantel, Laura Belloni, more

Journal of Hepatology > 2011 > 55 > 5 > 996-1003

The molecular biology of hepatitis B virus (HBV) has been extensively studied but the exact role of the hepatitis B X protein (HBx) in the context of natural HBV infections remains unknown.Primary human hepatocytes and differentiated HepaRG cells allowing conditional trans complementation of HBx were infected with wild type (HBV(wt)) or HBx deficient (HBV(x−)) HBV particles and establishment of HBV...

article

5′ Triphosphorylated Small Interfering RNAs Control Replication of Hepatitis B Virus and Induce an Interferon Response in Human Liver Cells and Mice

Gregor Ebert, Hendrik Poeck, Julie Lucifora, Nikola Baschuk, more

Gastroenterology > 2011 > 141 > 2 > 696-706.e3

Approved therapies for chronic hepatitis B include systemic administration of interferon (IFN)-alfa and inhibitors of hepatitis B virus (HBV) reverse-transcription. Systemic application of IFN-alfa is limited by side effects. Reverse-transcriptase inhibitors effectively control HBV replication, but rarely eliminate the virus and can select drug-resistant variants. We aimed to develop an alternative...

article

Hepatitis B virus replication in primary macaque hepatocytes: Crossing the species barrier toward a new small primate model

Julie Lucifora, Isabelle E. Vincent, Pascale Berthillon, Tatiana Dupinay, more

Hepatology > 51 > 6 > 1954 - 1960

The development of new anti–hepatitis B virus (HBV) therapies, especially immunotherapeutic approaches, has been limited by the lack of a primate model more accessible than chimpanzees. We have previously demonstrated that sylvanus and cynomolgus macaques are susceptible to in vivo HBV infection after intrahepatic HBV DNA inoculation. In this study, we evaluated the susceptibility of primary macaque...

article

Control of hepatitis B virus replication by innate response of HepaRG cells

Julie Lucifora, David Durantel, Barbara Testoni, Olivier Hantz, more

Hepatology > 51 > 1 > 63 - 72

Hepatitis B virus (HBV) is currently viewed as a stealth virus that does not elicit innate immunity in vivo. This assumption has not yet been challenged in vitro because of the lack of a relevant cell culture system. The HepaRG cell line, which is physiologically closer to differentiated hepatocytes and permissive to HBV infection, has opened new perspectives in this respect.HBV baculoviruses were...

article

In Vitro Characterization of Viral Fitness of Therapy-Resistant Hepatitis B Variants

Stéphanie Villet, Gaëtan Billioud, Christian Pichoud, Julie Lucifora, more

Gastroenterology > 2009 > 136 > 1 > 168-176.e2

Because of the overlapping of polymerase and envelope genes in the hepatitis B virus (HBV) genome, nucleoside analog therapy can lead to the emergence of complex HBV variants that harbor mutations in both the reverse transcriptase and the envelope proteins. To understand the selection process of HBV variants during antiviral therapy, we analyzed the in vitro fitness (the ability to produce infectious...

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Keywords

HEPATITIS B VIRUS (9)
CCCDNA (2)
HEPATOCYTES (2)
IFN RESPONSE (2)
ADENO-ASSOCIATED VIRUS (1)
ANTIVIRAL (1)
ANTIVIRAL ACTIVITY (1)
APOLIPOPROTEIN B MRNA EDITING ENZYME (1)
CYTOKINES/CHEMOKINES (1)
DSRNA-MEDIATED INNATE IMMUNITY (1)
EARLY HOST/VIRUS INTERACTION (1)
EZETIMIBE (1)
GENE SILENCING (1)
HBV INFECTION (1)
HBV PERSISTENCE (1)
HBX PROTEIN (1)
HEPARG (1)
HEPATITIS B (1)
HEPATITIS D VIRUS (1)
HEPATOCYTE (1)
IMMUNE REGULATION (1)
IMMUNE-COMPETENT MOUSE (1)
IMMUNE-MODULATORS (1)
IMMUNE-THERAPEUTICS (1)
IMMUNOTHERAPY (1)
INFECTION (1)
INNATE IMMUNITY INHIBITION (1)
INTERFERON (1)
INTERFERON STIMULATED GENES (1)
KUPFFER CELLS (1)
LIVER (1)
NATURAL INFECTION (1)
PATHOGEN RECOGNITION RECEPTOR (1)
PRIMARY HUMAN HEPATOCYTES (1)
T-CELL RECEPTOR (1)
TOLERANCE (1)
TOLL-LIKE RECEPTOR (1)
VIRAL INTERFERENCE (1)
VIROLOGY (1)
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