Theophilos M B, Huang J A, Holmes I H
Department of Microbiology, University of Melbourne, Parkville, Victoria, Australia.
Virology. 1995 Apr 20;208(2):678-84. doi: 10.1006/viro.1995.1199.
The biological functions of the structural protein sigma C, from avian reovirus strain RAM-1, were investigated in this study. A putative fusion peptide in sigma C was recognized in the deduced amino acid sequence by homology with Pneumovirus fusion sequences, and it was thus postulated that this protein may be involved in the formation of syncytia in cells infected with RAM-1. The sigma C gene was cloned and expressed in mammalian (COS7) cells and the sigma C protein was found to induce syncytia. It was therefore concluded that this protein is indeed responsible for avian reovirus-induced cell fusion. It was also found that sigma C caused condensation of the nuclei within a syncytium, as observed in RAM-1-infected cells. On the basis that this represented condensation of the chromatin, the inhibition of cellular DNA synthesis by the virus and by the sigma C protein was measured. It was found that the virus caused a 50% reduction in cellular DNA synthesis, but the sigma C protein did not inhibit DNA synthesis. Therefore pyknosis of the nuclei and inhibition of cellular DNA synthesis by RAM-1 are likely to be separate events.
本研究对禽呼肠孤病毒株RAM - 1的结构蛋白σC的生物学功能进行了研究。通过与肺病毒融合序列的同源性，在推导的氨基酸序列中识别出σC中的一个假定融合肽，因此推测该蛋白可能参与了感染RAM - 1的细胞中多核巨细胞的形成。σC基因被克隆并在哺乳动物（COS7）细胞中表达，发现σC蛋白可诱导多核巨细胞形成。因此得出结论，该蛋白确实是禽呼肠孤病毒诱导细胞融合的原因。还发现，如在感染RAM - 1的细胞中观察到的那样，σC会导致多核巨细胞内的细胞核浓缩。基于此代表染色质浓缩，测定了病毒和σC蛋白对细胞DNA合成的抑制作用。发现病毒导致细胞DNA合成减少50%，但σC蛋白不抑制DNA合成。因此，RAM - 1导致的细胞核固缩和细胞DNA合成抑制可能是独立事件。
