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A new role for PGA1 in inhibiting hepatitis C virus-IRES-mediated translation by targeting viral translation factors.

Abstract：

:Previous studies have demonstrated that cyclopentenone prostaglandins (cyPGs) inhibit the replication of a wide variety of DNA and RNA viruses in different mammalian cell types. We investigated a new role for prostaglandin A1 (PGA1) in the inhibition of hepatitis C virus (HCV)-IRES-mediated translation. PGA1 exhibited dose-dependent inhibitory effects on HCV translation in HCV replicon cells. Furthermore, repetitive PGA1 treatment demonstrated the potential to safely induce the suppression of HCV translation. We also validated a new role for PGA1 in the inhibition of HCV-IRES-mediated translation by targeting cellular translation factors, including the small ribosomal subunit (40S) and eukaryotic initiation factors (eIFs). In pull-down assays, biotinylated PGA1 co-precipitated with the entire HCV IRES RNA/eIF3-40S subunit complex. Moreover, the interactions between PGA1 and the elongation factors and ribosomal subunit were dependent upon HCV IRES RNA binding, and the PGA1/HCV IRES RNA/eIF3-40S subunit complex inhibited HCV-IRES-mediated translation. The novel mechanism revealed in this study may aid in the search for more effective anti-HCV drugs.

journal_name

Antiviral Res

journal_title

Antiviral research

authors

Tsukimoto A,Sugiyama R,Abe M,Nishitsuji H,Shimizu Y,Shimotohno K,Kawai G,Takaku H

doi

10.1016/j.antiviral.2015.01.013

subject

Has Abstract

pub_date

2015-05-01 00:00:00

pages

1-9

eissn

0166-3542

issn

1872-9096

pii

S0166-3542(15)00026-1

journal_volume

117

pub_type

杂志文章

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