Abstract:
:Hepatitis C virus (HCV) often establishes a persistent infection that leads to chronic liver diseases. The viral core protein modulates various cellular activities involved in this process. We found two mutations, K23E and V31A, in the core gene of the transfected HCV JFH-1 genome, which had been replicated for a prolonged period. The mutant viruses escaped immunochemical detection by a core-specific antibody and demonstrated enhanced RNA replication and protein expression, compared to the parental virus. The mutant core proteins bound less tightly than the parental type core to the DEAD-box RNA helicase DDX3 and attenuated the TBK1-mediated activation of interferon-related promoters. These results suggest a mechanism by which the viruses adapt to attenuate cellular antiviral activity and to establish persistent infection.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Kang JI,Kwon YC,Ahn BYdoi
10.1016/j.febslet.2012.03.062subject
Has Abstractpub_date
2012-05-07 00:00:00pages
1272-8issue
9eissn
0014-5793issn
1873-3468pii
S0014-5793(12)00272-4journal_volume
586pub_type
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