Malur Achut G, Hoffman Michael A, Banerjee Amiya K
Department of Virology NN-10, The Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA.
Virus Res. 2004 Feb;99(2):199-204. doi: 10.1016/j.virusres.2003.11.009.
The C protein of human parainfluenza virus type 3 (HPIV 3), like other paramyxovirus C proteins, is synthesized from an alternate open reading frame (ORF) encoded within the phosphoprotein (P) mRNA, in addition, to two other proteins, namely D and V, which arise from the same mRNA by a process of transcriptional editing. The precise role of the C, D, and V proteins in viral transcription and replication, and their interaction, if any, with other viral proteins remains unknown. To ascertain the role of the C protein, we have examined its effect on transcription using an HPIV 3 minigenome construct and monitoring the luciferase reporter gene expression. Our results demonstrate that the HPIV 3 C protein effectively inhibits minigenome transcription in a dose-dependent manner. Interestingly, the Sendai virus (Se-V) C protein was also capable of inducing an inhibitory effect on the HPIV 3 minigenome transcription, thus demonstrating a heterologous interaction. A coiled-coil motif within the C protein has been identified, and a deletion mutant within this motif abrogated the inhibitory effect significantly thereby implying that oligomerization of the C protein may be involved in inhibition of transcription.
人副流感病毒3型(HPIV 3)的C蛋白与其他副粘病毒的C蛋白一样,是由磷蛋白(P)mRNA内编码的一个交替开放阅读框(ORF)合成的,此外,还有另外两种蛋白,即D蛋白和V蛋白,它们通过转录编辑过程从同一mRNA产生。C、D和V蛋白在病毒转录和复制中的精确作用,以及它们与其他病毒蛋白的相互作用(如果有的话)仍然未知。为了确定C蛋白的作用,我们使用HPIV 3微型基因组构建体并监测荧光素酶报告基因表达来研究其对转录的影响。我们的结果表明,HPIV 3 C蛋白以剂量依赖的方式有效抑制微型基因组转录。有趣的是,仙台病毒(Se-V)C蛋白也能够对HPIV 3微型基因组转录产生抑制作用,从而证明了一种异源相互作用。已在C蛋白内鉴定出一个卷曲螺旋基序,该基序内的一个缺失突变体显著消除了抑制作用,从而暗示C蛋白的寡聚化可能参与转录抑制。