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Our data suggest, however, that GBV-B domain III might be involved in regulating a switch between translation and replication when both activities are coupled, since a chimeric IIGB-IIIHC segment ensuring both translation and replication (in GBneoD/IIIHC) provides parental-type translational activity, but not full replication capacity.
However, it is important to note that the genomes of positive-strand RNA viruses functions for both translation and replication, hence any interference with one step will have a concomitant effect on the other.
Two other sequences are located between stem-loops I and II of the 5′-UTR and thus reside in a region involved in the regulation of both translation and replication.
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In summary, we identified RBM24 as a host factor involved in both translation and RNA replication in HCV life cycle.
The secondary structures of hepatitis C virus (HCV RNAandnd the cellular proteins that bind to them are important for modulating both translation and RNA replication.
In this study, we identified RBM24 as a host factor involved in both translation and RNA replication in HCV life cycle.
Open image in new window Figure 2 The involvement of RBM24 in HCV translation and replication.
Thus the control of translation and replication during the initial period post-infection is essential for viral proliferation.
Here, we identified RNA binding motif protein 24 (RBM24) as a host factor participated in HCV translation and replication.
It has been proposed that the TYMV TLS acts as a molecular switch between translation and replication.
Thus it is possible that RBM24 participates in translation and replication by enhancing the interaction of the HCV 5′-UTR and 3′-UTRs.
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