Gray W L, Yalamanchili R, Raengsakulrach B, Baumann R P, Staczek J, O'Callaghan D J
Department of Microbiology and Immunology, Louisiana State University Medical Center, Shereveport 71130.
Virology. 1989 Sep;172(1):1-10. doi: 10.1016/0042-6822(89)90101-3.
Equine herpesvirus type 1 (EHV-1) preparations enriched in defective interfering particles (DIPs) have previously been demonstrated to mediate the coestablishment of persistent infection and oncogenic transformation in primary hamster embryo fibroblasts. In this study, it was demonstrated that infection of a rabbit kidney (RK) cell line with EHV-1 DIP-enriched preparations also results in the establishment of persistent infection. Viral transcription was characterized in RK cells infected with DIP-enriched stocks and compared to viral transcription in RK cells infected with standard (STD) EHV-1. During the first 8 hr of infection with the DIP-enriched EHV-1 preparation, viral DNA sequences which are conserved in the DIP genome were predominantly expressed. Thus, these transcripts originate from DNA sequences that contain the components of the defective genome which originates from DNA sequences mapping at 0.00-0.04 of the Long region terminus and within two portions of the Short region inverted repeats (IR), 0.78-0.79 and 0.83-0.865 of the internal IRs and 0.99-1.00 and 0.915-0.95 of the terminal IRs. The overwhelming majority of viral transcripts that were synthesized in the DIP-enriched infections appeared to correspond to transcripts expressed in STD infection as assessed by Northern hybridization analysis but the synthesis of transcripts originating from sequences not conserved in the defective genome was significantly delayed. However, some high molecular weight RNA species that were synthesized in STD infections were not detected in DIP-enriched infections. Studies utilizing metabolic inhibitors indicated that viral transcription in DIP-enriched infections, like that of STD cytocidal infection, is regulated in an immediate early, early and late manner.
先前已证明,富含缺陷干扰颗粒(DIPs)的1型马疱疹病毒(EHV-1)制剂可介导原代仓鼠胚胎成纤维细胞中持续性感染的共同建立和致癌转化。在本研究中,已证明用富含EHV-1 DIP的制剂感染兔肾(RK)细胞系也会导致持续性感染的建立。对感染富含DIP的毒株的RK细胞中的病毒转录进行了表征,并与感染标准(STD)EHV-1的RK细胞中的病毒转录进行了比较。在用富含DIP的EHV-1制剂感染的最初8小时内,DIP基因组中保守的病毒DNA序列主要被表达。因此,这些转录本源自包含缺陷基因组成分的DNA序列,该缺陷基因组源自位于长区域末端0.00-0.04以及短区域反向重复序列(IR)的两个部分(内部IR的0.78-0.79和0.83-0.865以及末端IR的0.99-1.00和0.915-0.95)的DNA序列。通过Northern杂交分析评估,在富含DIP的感染中合成的绝大多数病毒转录本似乎与STD感染中表达的转录本相对应,但源自缺陷基因组中不保守序列的转录本的合成明显延迟。然而,在富含DIP的感染中未检测到在STD感染中合成的一些高分子量RNA种类。利用代谢抑制剂的研究表明,富含DIP的感染中的病毒转录,与STD杀细胞感染一样,以立即早期、早期和晚期的方式受到调控。