Ebner Paul D, O'Callaghan Dennis J
Department of Microbiology and Immunology and Center for Molecular and Tumor Virology, Louisiana State University Health Sciences Center, 1501 Kings Hwy, Shreveport, LA 71130-3932, USA.
Virus Genes. 2006 Jun;32(3):313-20. doi: 10.1007/s11262-005-6916-y.
This study examined the genetic complexity of three equine herpesvirus 1 (EHV-1) defective interfering particles (DIP) and found the DIP genomes to range from 5.9 kbp to 7.3 kbp in total size. Each DIP contains an identical 5' end ( approximately 1.9 kb) that harbors UL3 and UL4 genes that are 100% identical to those of the infectious virus. DIP2 and DIP3 contain a previously described unique IR4/UL5 (EICP22/EICP27) hybrid gene (Hyb1.0). The DIP1 genome, however, appears to be generated from a different recombination event which results in the formation of a new distinct hybrid ORF. The new ORF (Hyb2.0) is comprised of 684 bp from the 5' end of IR4 fused to 45 bp from the 3' terminus of UL5. In contrast to Hyb1.0, the UL5 sequences present in Hyb2.0 are not in-frame. Thus, the Hyb2.0 protein is comprised of 228 residues from IR4 linked to a sequence of 15 amino acids that result from a frameshifted reading of UL5 sequences. Western blot analysis confirmed that the Hyb2.0 ORF is expressed during persistent infection to produce a family of proteins that migrate at 36-42 kDa. Fluorescence microscopy revealed that both Hyb proteins display diffuse cytoplasmic localization patterns dissimilar to the nuclear localization patterns of both IR4 and UL5. Neither Hyb protein, however, disrupts the nuclear entry of the EHV-1 immediate-early, IR4, or UL5 proteins or cellular TATA box binding protein (TBP) previously shown to interact with both IR4 or UL5 in productive infection. DIP genomic segments ( approximately 3.5-5.0 kbp) downstream of the 100% conserved origin of replication are highly variable among the three DIP genomes and contain large areas of repetitive sequences. The possibility that the non-coding sequences play a role in viral interference and/or persistent infection remains to be determined.
本研究检测了三种马疱疹病毒1型(EHV-1)缺陷干扰颗粒(DIP)的遗传复杂性,发现DIP基因组的总大小在5.9千碱基对(kbp)至7.3 kbp之间。每个DIP都含有一个相同的5'端(约1.9 kb),其中包含与感染性病毒的UL3和UL4基因100%相同的基因。DIP2和DIP3含有一个先前描述的独特IR4/UL5(EICP22/EICP27)杂交基因(Hyb1.0)。然而,DIP1基因组似乎是由不同的重组事件产生的,这导致形成了一个新的独特杂交开放阅读框(ORF)。新的ORF(Hyb2.0)由来自IR4 5'端的684 bp与来自UL5 3'端的45 bp融合而成。与Hyb1.0不同,Hyb2.0中存在的UL5序列不在读框内。因此,Hyb2.0蛋白由来自IR4的228个残基与由UL5序列移码阅读产生的15个氨基酸序列相连组成。蛋白质印迹分析证实,Hyb2.0 ORF在持续感染期间表达,产生一系列迁移率在36 - 42 kDa的蛋白质。荧光显微镜检查显示,两种Hyb蛋白均呈现弥漫性细胞质定位模式,与IR4和UL5的核定位模式不同。然而,两种Hyb蛋白均未破坏EHV-1立即早期蛋白、IR4或UL5蛋白或细胞TATA盒结合蛋白(TBP)的核进入,先前已证明TBP在 productive感染中与IR4或UL5相互作用。在三个DIP基因组中,100%保守的复制起点下游的DIP基因组片段(约3.5 - 5.0 kbp)高度可变,并且包含大片重复序列。非编码序列在病毒干扰和/或持续感染中发挥作用的可能性仍有待确定。