Functional characterization of EUL47 in productive replication, morphogenesis and infectivity of equine herpesvirus 1

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• 作者：Mi Htay Htay Yu^a ; Samy Kasem^a ; ^e ; Norio Yoshizaki^b ; Ochir Pagamjav^a ; Tsuyoshi Yamaguchi^c ; Kenji Ohya^d ; Hideto Fukushi^a ; ^d ; ^{hfukushi@gifu-u.ac.jp}
• 关键词：Equine herpesvirus 1 ; EUL47-null mutant ; Pathogenicity ; Morphogenesis
• 刊名：Virus Research
• 出版年：2012
• 出版时间：January 2012
• 年：2012
• 卷：163
• 期：1
• 页码：310-319
• 全文大小：816 K

文摘

EUL47 is a major component of the tegument of equine herpesvirus 1 (EHV-1). To determine its function, we used Red/ET cloning to delete its gene (gene 13) from EHV-1 strain Ab4p inserted into a bacterial artificial chromosome (BAC), yielding Ab4pattB¦¤13. We also examined the reverted virus (Ab4pattB13R). Ab4pattB¦¤13 replicated in rabbit kidney (RK)-13 cells, indicating that ORF13 is dispensable for virus replication in cell culture. Its intracellular and extracellular titers were about 10- and 100-fold lower than those of the revertant and parent strains, respectively. In addition, the plaque size was half the plaque sizes of the other two strains. The particle-to-plaque forming unit ratio of Ab4pattB¦¤13 was 21-fold greater than the ratios of the revertant and parent strains. No enveloped virions were detected in the cytoplasm of Ab4pattB¦¤13-infected cells by transmission electron microscopy. In hamster, Ab4pattB¦¤13 caused clinical signs and weight loss after only 1 day, but induced less severe neurological signs than did the revertant and parent strains. These results indicate that EUL47 is structurally required for normal virus replication, viral morphogenesis and viral infectivity, and that loss of EUL47 moderately attenuates the neuropathogenicity of EHV-1 in the hamster model.