Abstract:
:Hepatitis A virus (HAV) infection is still an important issue worldwide. A distinct set of viruses encode proteins that enhance viral cap-independent translation initiation driven by an internal ribosome entry site (IRES) and suppress cap-dependent host translation. Unlike cytolytic picornaviruses, replication of HAV does not cause host cell shut off, and it has been questioned whether HAV proteins interfere with its own and/or host translation. HAV proteins were coexpressed in Huh-7 cells with reporter genes whose translation was initiated by either cap-dependent or cap-independent mechanisms. Among the proteins tested, HAV proteinase 3C suppressed viral IRES-dependent translation. Furthermore, 3C cleaved the polypyrimidine tract-binding protein (PTB) whose interaction with the HAV IRES had been demonstrated previously. The combined results suggest that 3C-mediated cleavage of PTB might be involved in down-regulation of viral translation to give way to subsequent viral genome replication.
journal_name
J Viral Hepatjournal_title
Journal of viral hepatitisauthors
Kanda T,Gauss-Müller V,Cordes S,Tamura R,Okitsu K,Shuang W,Nakamoto S,Fujiwara K,Imazeki F,Yokosuka Odoi
10.1111/j.1365-2893.2009.01221.xsubject
Has Abstractpub_date
2010-09-01 00:00:00pages
618-23issue
9eissn
1352-0504issn
1365-2893pii
JVH1221journal_volume
17pub_type
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