Key result
GB virus B initiates translation via an internal ribosome entry site similar to HCV.
Why the study?
The functional similarity of the GB virus B 5' untranslated region to the hepatitis C virus internal ribosome entry site was unclear and required investigation.
The 5' untranslated region of GB virus B functions as an internal ribosome entry site, demonstrating functional similarity to hepatitis C virus.
GBV-B 5'UTR drives IRES-mediated translation; extends HCV structural models but leaves open in vivo validation and therapeutic relevance.
Since its characterization in 1995, there has been increasing interest in the significance of GB virus B (GBV-B) due to its close phylogenetic relationship to hepatitis C virus (HCV). The genome of GBV-B is similar in length and organization to that of HCV and the two viruses share sequence similarity in their 5' untranslated regions (5'UTR). A secondary structure model of the GBV-B 5'UTR has been proposed by comparative sequence analysis with HCV. The highly conserved secondary structure, present in HCV and the pestiviruses, is also present in the 5'UTR of GBV-B. Translation of the HCV polyprotein initiates via an internal ribosome entry site (IRES) and it is proposed that the GBV-B UTR may function in a similar manner. Dicistronic reporter constructs were made to investigate the function of the GBV-B 5'UTR. Mutational analysis and in vitro translation experiments demonstrate that GBV-B initiates translation via an IRES.
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Grace et al. (1999) studied GB virus B and hepatitis C virus. Dicistronic reporter constructs and mutational analysis was evaluated on Translation initiation mechanism. Mutational analysis and in vitro translation experiments demonstrate that GB virus B initiates translation via an internal ribosome entry site, similar to hepatitis C virus.
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