scispace - formally typeset
H

Hervé Lerat

Researcher at University of Texas Medical Branch

Publications -  5
Citations -  656

Hervé Lerat is an academic researcher from University of Texas Medical Branch. The author has contributed to research in topics: Hepatitis C virus & Transgene. The author has an hindex of 5, co-authored 5 publications receiving 645 citations. Previous affiliations of Hervé Lerat include Centre national de la recherche scientifique & University of Montpellier.

Papers
More filters
Journal ArticleDOI

Steatosis and liver cancer in transgenic mice expressing the structural and nonstructural proteins of hepatitis C virus.

TL;DR: Constitutive expression of viral proteins leads to common pathologic features of hepatitis C in the absence of specific anti-viral immune responses, while additional low level expression of nonstructural proteins increases the risk of cancer.
Journal ArticleDOI

Impaired Clearance of Virus-Infected Hepatocytes in Transgenic Mice Expressing the Hepatitis C Virus Polyprotein

TL;DR: The results suggest that viral evasion of cell-mediated immune responses leading to apoptotic death of hepatocytes may contribute to viral persistence and might also contribute to the development of liver cancer in HCV.
Journal ArticleDOI

Cell Type-Specific Enhancement of Hepatitis C Virus Internal Ribosome Entry Site-Directed Translation due to 5′ Nontranslated Region Substitutions Selected during Passage of Virus in Lymphoblastoid Cells

TL;DR: The 2- to 2.5-fold increase in translation observed with the modified IRES sequence may facilitate the replication of HCV, possibly accounting for differences in quasispecies variants recovered from liver tissue and peripheral blood mononuclear cells of the same patient.
Journal Article

A transgenic mouse model of steatosis and hepatocellular carcinoma associated with chronic hepatitis C virus infection in humans.

TL;DR: Existing therapies for chronic hepatitis C include recombinant human interferon, either alone or in combination with ribavirin, which are only partially effective, leading to the belief that most if not all of the pathologic consequences of hepatitis C arise as a result of the cellular immune response to the infection.