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Zinc is a negative regulator of hepatitis C virus RNA replication
Author(s) -
Yuasa Kazuhisa,
Naganuma Atsushi,
Sato Ken,
Ikeda Masanori,
Kato Nobuyuki,
Takagi Hitoshi,
Mori Masatomo
Publication year - 2006
Publication title -
liver international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.873
H-Index - 110
eISSN - 1478-3231
pISSN - 1478-3223
DOI - 10.1111/j.1478-3231.2006.01352.x
Subject(s) - replicon , subgenomic mrna , viral replication , hepatitis c virus , biology , rna , virology , interferon , virus , genome , gene , genetics
Abstract: Background/Aims: Hepatitis C virus (HCV) infection is a significant global public health problem. In clinical studies, zinc has been closely related to the pathogenesis of chronic hepatitis C. However, the role of zinc in both viral replication and the expression of viral proteins remains unclear. We aimed to clarify the effect of zinc on the replication of HCV in vitro . Methods: We incubated subgenomic HCV replicon cells (sO) and genome‐length HCV RNA‐replicating cells (O) treated with several chemicals including trace elements. Total RNAs were collected and subjected to real‐time reverse‐transcriptase polymerase chain reaction in order to examine the level of HCV RNA replication, and Western blotting was performed to confirm the expression of viral proteins. Results: Iron salts and interferon‐α suppressed HCV RNA replication and protein expression in both sO and O cells. Zinc salts effectively reduced the viral replication in the genome‐length HCV RNA replication system but not in the subgenomic HCV replicon system. Conclusions: We demonstrated that zinc may play an important role as a negative regulator of HCV replication in genome‐length HCV RNA‐replicating cells. Zinc supplementation thus appears to offer a novel approach to the development of future strategies for the treatment of intractable chronic hepatitis C.