Key result
The synthesis of full-length infectious RNA of Saffold virus type 3 by T7 RNA polymerase was prematurely terminated by a PTH signal motif, which was overcome by using a variant T7 RNA polymerase.
The generation of an infectious cDNA clone of Saffold virus type 3 requires bypassing a PTH signal motif that causes premature transcription termination by standard T7 RNA polymerase.
May aid Saffold virus research models; leaves open any clinical relevance or applications.
The pathogenicity of Saffold virus (SAFV) among humans still remains unclear, although it was identified as a novel human cardiovirus in 2007. In order to encourage the molecular pathogenetic studies of SAFV, we generated an infectious cDNA clone of SAFV type 3 (SAFV-3). The present study demonstrated that the synthesis of the full-length infectious RNA by T7 RNA polymerase was terminated by a homologous sequence motif with the human preproparathyroid hormone (PTH) signal in the SAFV-3 genome. To obtain the infectious RNA using T7 promoter, a variant of T7 RNA polymerase, which fails to recognize the PTH signal, was useful. This study will provide a valuable technical insight into the reverse genetics of SAFV.
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Himeda et al. (2011) studied Saffold virus infection (in vitro). Infectious full-length cDNA clone of Saffold virus (pSAF404) was evaluated on Synthesis of full-length infectious RNA and generation of infectious virus particles. The synthesis of full-length infectious RNA of Saffold virus type 3 by T7 RNA polymerase was prematurely terminated by a PTH signal motif, which was overcome by using a variant T7 RNA polymerase.
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