PRIMARY STRUCTURE OF THE ALCELAPHINE HERPESVIRUS-1 GENOME

Citation
A. Ensser et al., PRIMARY STRUCTURE OF THE ALCELAPHINE HERPESVIRUS-1 GENOME, Journal of virology, 71(9), 1997, pp. 6517-6525
Citations number
77
Categorie Soggetti
Virology
Journal title
ISSN journal
0022538X
Volume
71
Issue
9
Year of publication
1997
Pages
6517 - 6525
Database
ISI
SICI code
0022-538X(1997)71:9<6517:PSOTAH>2.0.ZU;2-I
Abstract
Alcelaphine herpesvirus 1 (AHV-1) causes wildebeest-associated maligna nt catarrhal fever, a lymphoproliferative syndrome in ungulate species other than the natural host. Based on biological properties and limit ed structural data, it has been classified as a member of the genus Rh adinovirus of the subfamily Gammaherpes-virinae. Here, we report on cl oning and structural analysis of the complete genome of AHV-1 C500, Th e low GC content DNA (L-DNA) region of the genome consists of 130,608 bp with low (46.17%) GC content and marked suppression of CpG dinucleo tide frequency. Like in herpesvirus saimiri, the prototype of the rhad inoviruses, the L-DNA is banked by approximately 20 to 25 GC-rich (71. 83%) high GC content DNA (H-DNA) repeats of 1,113 to 1,118 nucleotides . The analysis of the L-DNA sequence revealed 70 open reading frames ( ORFs), 61 of which showed homology to other herpesviruses, The conserv ed ORFs are arranged in four blocks collinear to other Rhadinovirus ge nomes, These gene blocks are flanked by nonconserved regions containin g ORFs without similarities to known herpesvirus genes. Notably, a spl iced reading frame with a coding capacity for a 199-amino-acid protein is located in a position homologous to the transforming genes of herp esvirus saimiri at the left end of the L-DNA. A gene with homology to the semaphorin family is located adjacent to this, Despite common biol ogical and epidemiological properties, AHV-1 differs significantly fro m herpesvirus saimiri with regard to cell homologous genes, probably u sing a different set of effector proteins to achieve a similar T-lymph ocyte-transforming phenotype.