F
Fabien Zoulim
Researcher at French Institute of Health and Medical Research
Publications - 716
Citations - 40988
Fabien Zoulim is an academic researcher from French Institute of Health and Medical Research. The author has contributed to research in topics: Hepatitis B virus & Hepatitis B. The author has an hindex of 96, co-authored 641 publications receiving 35807 citations. Previous affiliations of Fabien Zoulim include Hotel Dieu Hospital & University of Orléans.
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Response-guided and -unguided treatment of chronic hepatitis C
TL;DR: Several population groups have done better with extended duration therapy as opposed to response guided therapy despite early viral clearance, and these include the Black population, and those with cirrhosis, decreased interferon sensitivity, and unfavorable IL28B genotypes.
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Hepatitis C virus infection in special groups
TL;DR: It is especially important to protect patients at risk for HCV infection, using universal precautionary procedures.
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Decreased infectivity of nucleoside analogs-resistant hepatitis B virus mutants.
Gaëtan Billioud,Christian Pichoud,Christian Pichoud,Romain Parent,Romain Parent,Fabien Zoulim,Fabien Zoulim +6 more
TL;DR: It is found that envelope substitutions modulate viral protein expression, HDV coating, and viral infectivity and suggest that resistant mutants are less prone to transmission than their WT counterpart.
Treatment of chronic viral hepatitis
TL;DR: In this paper, the authors used recombinant interferon (IFN) alpha to treat chronic hepatitis B and chronic hepatitis C. They found that IFN-alpha induces a sustained interruption of hepatitis B virus (HBV) replication, with a HBeAg to anti-HBe seroconversion in about 30%.
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Effect of mutating the two cysteines required for HBe antigenicity on hepatitis B virus DNA replication and virion secretion.
Genie Bang,Kyun-Hwan Kim,Michael T. Guarnieri,Fabien Zoulim,Shigenobu Kawai,Jisu Li,Jack R. Wands,Shuping Tong +7 more
TL;DR: Point mutations of the C61 codon may generate viable HBeAg-negative variants and secretion block of theC61R mutant could be overcome by co-expression of wild-type core protein.