Transactivation of Hdv Rna Replication by the SHDAgs of Genotypes I and II

Casey reported that there is genotype-specific complementation of HDV RNA replication by HDAg [39]. The S-HDAg of the genotype III is unable to transac-tivate viral RNA replication of genotype I HDV, and vice versa [39]. However, the transactivation activity of the S-HDAgs from different genotype I and II isolates on a HDAg synthesis-defective genotype I mutant varied from 6% to 172% as compared to that of the cognate S-HDAg, and there appears to be no apparent universal genotypic restriction on the transactivation of genotype I HDV RNA replication by S-HDAg of genotype II [38]. In general, genotype I S-HDAgs are more likely to be stronger supporters of HDV RNA replication of the same genotype [38]. With regard to HDAg synthesis-defective genotype II HDV, the transactivation activities of S-HDAgs from various isolates of the same genotype range from 22% to 250% as compared to that of the cognate S-HDAg. In contrast, there appears to be more genotypic restriction for genotype I S-HDAgs to transactivate genotype II HDV RNA replication. The greater divergence between genotypes I and III HDV sequences than between genotypes I and II may account for the stricter genotype-specific complementation between genotypes I and III. However, genotype per se could only partly predict the degree of the S-HDAgs of different isolates of the same or different genotypes in transactivating the replication of a second HDV isolate [38]. A minimum of 56 residues from the N-terminal portion of the S-HDAg, which covers the CCS responsible for oligomerization, determines the strength of transactivation of HDV RNA replication [38].

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