Hepatitis C

Definition

Hepatitis C is inflammation of the liver in humans caused by the hepatitis C virus. The virus is primarily transmitted by blood-to-blood contact associated with transfusion and intravenous drug use. The infection is often asymptomatic, but chronic infection can lead to cirrhosis.

Latest Research and Reviews

  • Research | | open

    • Mei-Hsuan Lee
    • , Chung-Feng Huang
    • , Hsueh-Chou Lai
    • , Chun-Yen Lin
    • , Chia-Yen Dai
    • , Chun-Jen Liu
    • , Jing-Houng Wang
    • , Jee-Fu Huang
    • , Wen-Pang Su
    • , Hung-Chih Yang
    • , Kwong-Ming Kee
    • , Ming-Lun Yeh
    • , Po-Heng Chuang
    • , Shih-Jer Hsu
    • , Ching-I Huang
    • , Jung-Ta Kao
    • , Chieh-Chang Chen
    • , Sheng-Hung Chen
    • , Wen-Juei Jeng
    • , Hwai-I Yang
    • , Yong Yuan
    • , Sheng-Nan Lu
    • , I-Shyan Sheen
    • , Chen-Hua Liu
    • , Cheng-Yuan Peng
    • , Jia-Horng Kao
    • , Ming-Lung Yu
    • , Wan-Long Chuang
    •  & Chien-Jen Chen
  • Research | | open

    Lambda interferons (IFNL) are involved in the immune response to viral infection. Here the authors show that zinc can interfere with IFNL signalling, and that in HCV patients the rs12979860 polymorphism regulates blood zinc levels and, subsequently, the hepatic immune response.

    • Scott A. Read
    • , Kate S. O’Connor
    • , Vijay Suppiah
    • , Chantelle L. E. Ahlenstiel
    • , Stephanie Obeid
    • , Kristina M. Cook
    • , Anthony Cunningham
    • , Mark W. Douglas
    • , Philip J. Hogg
    • , David Booth
    • , Jacob George
    •  & Golo Ahlenstiel
  • Reviews |

    Lipid droplets (LDs) are dynamic organelles and many metabolic disorders results in abnormal lipid accumulation in the liver. This Review provides insights into LD biology and lipid homeostasis in the liver, as well as the role of LDs in liver diseases, including NAFLD, NASH and hepatitis C.

    • Nina L. Gluchowski
    • , Michel Becuwe
    • , Tobias C. Walther
    •  & Robert V. Farese Jr
  • Research |

    Chris Spencer, Eleanor Barnes and colleagues use human genotyping arrays and whole-genome viral sequencing to perform a systematic genome-to-genome study of 542 individuals chronically infected with hepatitis C virus (HCV). They show that both HLA alleles and genes encoding factors of the innate immune system drive viral genome polymorphism and that IFNL4 genotypes determine HCV viral load through a mechanism dependent on a specific polymorphism encoded in the HCV polyprotein.

    • M Azim Ansari
    • , Vincent Pedergnana
    • , Camilla L C Ip
    • , Andrea Magri
    • , Annette Von Delft
    • , David Bonsall
    • , Nimisha Chaturvedi
    • , Istvan Bartha
    • , David Smith
    • , George Nicholson
    • , Gilean McVean
    • , Amy Trebes
    • , Paolo Piazza
    • , Jacques Fellay
    • , Graham Cooke
    • , Graham R Foster
    • , STOP-HCV Consortium
    • , Eleanor Barnes
    • , Jonathan Ball
    • , Diana Brainard
    • , Gary Burgess
    • , Graham Cooke
    • , John Dillon
    • , Graham R Foster
    • , Charles Gore
    • , Neil Guha
    • , Rachel Halford
    • , Cham Herath
    • , Chris Holmes
    • , Anita Howe
    • , Emma Hudson
    • , William Irving
    • , Salim Khakoo
    • , Paul Klenerman
    • , Diana Koletzki
    • , Natasha Martin
    • , Benedetta Massetto
    • , Tamyo Mbisa
    • , John McHutchison
    • , Jane McKeating
    • , John McLauchlan
    • , Alec Miners
    • , Andrea Murray
    • , Peter Shaw
    • , Peter Simmonds
    • , Chris C A Spencer
    • , Paul Targett-Adams
    • , Emma Thomson
    • , Peter Vickerman
    • , Nicole Zitzmann
    • , Emma Hudson
    • , John McLauchlan
    • , Peter Simmonds
    • , Rory Bowden
    • , Paul Klenerman
    • , Eleanor Barnes
    •  & Chris C A Spencer
    Nature Genetics 49, 666–673

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