Hervé Lerat

ORCID: 0000-0002-8505-378X
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About
Contact & Profiles
Research Areas
  • Hepatitis C virus research
  • Liver Disease Diagnosis and Treatment
  • Hepatitis B Virus Studies
  • Viral Infections and Immunology Research
  • Cell Adhesion Molecules Research
  • interferon and immune responses
  • Cancer, Hypoxia, and Metabolism
  • Hepatocellular Carcinoma Treatment and Prognosis
  • Cancer, Lipids, and Metabolism
  • Zoonotic diseases and public health
  • PI3K/AKT/mTOR signaling in cancer
  • Cancer Mechanisms and Therapy
  • Animal Virus Infections Studies
  • HIV Research and Treatment
  • RNA modifications and cancer
  • SARS-CoV-2 and COVID-19 Research
  • Ferroptosis and cancer prognosis
  • Cholesterol and Lipid Metabolism
  • Peptidase Inhibition and Analysis
  • Immunotherapy and Immune Responses
  • Immune Response and Inflammation
  • Endoplasmic Reticulum Stress and Disease
  • Animal testing and alternatives
  • Liver physiology and pathology
  • Epigenetics and DNA Methylation

Inserm
2011-2023

Institut National de Recherche en Santé Publique
2023

Université Grenoble Alpes
2019-2022

Centre National de la Recherche Scientifique
2002-2022

Institut de Biosciences et Biotechnologies
2019

Université Paris-Est Créteil
2008-2017

Biotherapy of Genetic Diseases, Inflammatory Disorders and Cancers
2017

Institut Mondor de Recherche Biomédicale
2010-2015

Department of Virology
2008-2013

Assistance Publique – Hôpitaux de Paris
2013

Background and Aims: The aim of this study was to determine whether expression hepatitis C virus proteins alters hepatic morphology or function in the absence inflammation. Methods: Transgenic C57BL/6 mice with liver-specific RNA encoding complete viral polyprotein (FL-N transgene) structural (S-N were compared nontransgenic littermates for altered liver function. Results: FL-N transcripts detectable only by reverse-transcription polymerase chain reaction, S-N identified Northern blots....

10.1053/gast.2002.31001 article EN cc-by Gastroenterology 2002-02-01

The presence of hepatitis C virus (HCV) negative strand RNA in extrahepatic compartments based on PCR detection assays has been suggested many reports with a very heterologous rate (from 0 to 100%). In this study, we have analyzed the HCV hepatic (liver biopsies, n = 20) and (sera, 32; PBMC, 26 fresh bone marrow cells, 8) from infected patients three different reverse transcriptase (RT)-PCR-based using primers located 5' noncoding region, or without tag selected display viral loads (10(5)-3...

10.1172/jci118485 article EN Journal of Clinical Investigation 1996-02-01

Chronic hepatitis C virus (HCV) infection frequently leads to liver cancer. To determine the viral factor(s) potentially involved in persistence, we focused our work on NS2, a protein of unknown function. assign role for searched cellular proteins that interact with NS2. Performing two-hybrid screen human cDNA library, found NS2 interacted liver-specific pro-apoptotic CIDE-B protein. Binding specificity was confirmed by cell-free assays associated colocalization studies and coprecipitation...

10.1074/jbc.m209732200 article EN cc-by Journal of Biological Chemistry 2003-05-01

Chronic hepatitis C virus (HCV) infection is associated with altered lipid metabolism and hepatocellular steatosis. Virus-induced steatosis a cytopathic effect of HCV replication. The goal this study was to examine the mechanisms underlying HCV-induced metabolic defects in transgenic mouse model expressing full protein repertoire at levels corresponding natural human infection. In model, expression full-length open reading frame reduced plasma triglyceride levels. Triglyceride secretion...

10.1074/jbc.m109.019810 article EN cc-by Journal of Biological Chemistry 2009-10-07

Hepatocellular carcinoma (HCC) is the most common type of liver cancer. The majority HCC cases are associated with fibrosis or cirrhosis developing from chronic injuries. immune system contributes to severity tissue damage, establishment and disease's progression towards HCC. Herein, we provide a detailed characterization DEN-induced rat model during development special focus on liver's inflammatory microenvironment. Fischer 344 male rats were treated weekly for 14 weeks intra-peritoneal...

10.3390/cancers13194981 article EN Cancers 2021-10-04

Hepatocellular steatosis is common in patients with chronic hepatitis C. Steatosis can be considered as a true cytopathic lesion induced by C virus (HCV) genotype 3, suggesting that one or more viral proteins produced during 3 infection are involved the steatogenic process, while same other genotypes not. We examined vitro interactions between lipid droplets and full-length core protein isolated from HCV 3a infection, without steatosis, steatosis-free infected 1b. also morphological changes...

10.1002/hep.22288 article EN Hepatology 2008-06-20

Abstract Members of the Gadd45 family play central roles in cellular response to genotoxic stress and have been implicated several human cancers, including hepatocellular carcinomas. Chronic infection by hepatitis C virus (HCV) is a major risk factor for onset development primary tumors, although underlying mechanisms are unclear. Here, we show novel link between diminished Gadd45β expression HCV infection. Inhibited was observed both nontumoral tumoral tissues from infected individuals,...

10.1158/0008-5472.can-09-4554 article EN Cancer Research 2010-06-09

Objective Infection of human hepatocytes by the hepatitis C virus (HCV) is a multistep process involving both viral and host factors. microRNAs (miRNAs) are small non-coding RNAs that post-transcriptionally regulate gene expression. Given miRNAs were indicated to between 30% 75% all genes, we aimed investigate functional regulatory role for HCV life cycle. Design To systematically reveal affecting cycle, performed two-step high-throughput miRNA mimic screen in Huh7.5.1 cells infected with...

10.1136/gutjnl-2018-317423 article EN Gut 2019-05-10

ABSTRACT Low-level replication of hepatitis C virus (HCV) in cultured lymphoblastoid cells inoculated with H77 serum inoculum led to the appearance new variants containing identical substitutions at three sites within viral 5′ nontranslated RNA (5′NTR): G 107 →A, 204 and 243 →A (N. Nakajima, M. Hijikata, H. Yoshikura, Y. K. Shimizu, J. Virol. 70:3325–3329, 1996). These results suggest that this 5′NTR sequence may have a greater capacity for such cells, possibly due more efficient...

10.1128/jvi.74.15.7024-7031.2000 article EN Journal of Virology 2000-08-01

An unresolved question regarding the physiopathology of hepatitis C virus (HCV) infection is remarkable efficiency with which host defenses are neutralized to establish chronic infection. Modulation an apoptotic response one strategy used by viruses escape immune surveillance. We previously showed that HCV proteins down-regulate expression BH3-only Bcl2 interacting domain (Bid) in hepatocytes transgenic mice. As a consequence, cells acquire resistance Fas-mediated apoptosis, turn leads...

10.1002/hep.23169 article EN Hepatology 2009-07-20

Mice respond to a cage change (CC) with altered activity, disrupted sleep and increased anxiety. A bi-weekly is, therefore, preferred over shorter CC interval is currently the prevailing routine for Individually ventilated cages (IVCs). However, build-up of ammonia (NH 3 ) during this period potential threat animal health literature holds conflicting reports leaving issue unresolved. We have therefor examined longitudinally in-cage across floor female male C57BL/6 mice housed four per IVC...

10.1371/journal.pone.0267281 article EN cc-by PLoS ONE 2022-05-25

The high levels of interleukin 10 (IL-10) present in chronic hepatitis C virus (HCV) infection have been suggested as responsible for the poor antiviral cellular immune responses found these patients. To overcome immunosuppressive effect IL-10 on antigen-presenting cells such dendritic (DCs), we developed peptide inhibitors to restore DC functions and concomitantly induce efficient responses. Two IL-10-binding peptides (p9 p13) were selected using a phage-displayed library their capacity...

10.1002/hep.23980 article EN Hepatology 2010-09-14

Virus-related type 2 diabetes is commonly observed in individuals infected with the hepatitis C virus (HCV); however, underlying molecular mechanisms remain unknown. Our aim was to unravel these using FL-N/35 transgenic mice expressing full HCV ORF. We that displayed glucose intolerance and insulin resistance. also found Glut-2 membrane expression reduced hepatocyte uptake perturbed, partly accounting for HCV-induced mice. Early steps of hepatic signaling pathway, from IRS2 PDK1...

10.1074/jbc.m117.785030 article EN cc-by Journal of Biological Chemistry 2017-05-31

Hepatitis C virus (HCV) nonstructural protein 5A (NS5A) is involved in regulating viral replication through its direct interaction with the HCV RNA-dependent RNA polymerase. NS5A also alters infected cell metabolism complex interactions numerous host proteins. has furthermore been suggested to act as a transcriptional activator, although impact on unclear. To study this, variants were amplified from hepatic tissue an HCV-infected patient, and their abilities activate gene transcription...

10.1128/jvi.00585-12 article EN Journal of Virology 2013-03-07
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