Gene end-like sequences within the 3′ non-coding region of the Nipah virus genome attenuate viral gene transcription

- Regulation of downstream gene expression at NiV gene junctions is not constant.
- The 3′ non-coding regions are responsible for reducing of downstream gene expression.
- Uridine-rich tracts within the L 3′ NCR signal transcription termination.

The regulation of transcription during Nipah virus (NiV) replication is poorly understood. Using a bicistronic minigenome system, we investigated the involvement of non-coding regions (NCRs) in the transcriptional re-initiation efficiency of NiV RNA polymerase. Reporter assays revealed that attenuation of NiV gene expression was not constant at each gene junction, and that the attenuating property was controlled by the 3′ NCR. However, this regulation was independent of the gene-end, gene-start and intergenic regions. Northern blot analysis indicated that regulation of viral gene expression by the phosphoprotein (P) and large protein (L) 3′ NCRs occurred at the transcription level. We identified uridine-rich tracts within the L 3′ NCR that are similar to gene-end signals. These gene-end-like sequences were recognized as weak transcription termination signals by the viral RNA polymerase, thereby reducing downstream gene transcription. Thus, we suggest that NiV has a unique mechanism of transcriptional regulation.