Proft Alexandra, Spiesschaert Bart, Izume Satoko, Taferner Selina, Lehmann Maik J, Azab Walid
Institut für Virologie, Robert von Ostertag-Haus, Zentrum für Infektionsmedizin, Freie Universität Berlin, Robert-von-Ostertag-Str. 7-13, 14163 Berlin, Germany.
Department of Applied Veterinary Sciences, United Graduate School of Veterinary Sciences, Gifu University, 501-1193 Gifu, Japan.
Viruses. 2016 Oct 12;8(10):275. doi: 10.3390/v8100275.
The serine-threonine protein kinase encoded by gene (pUS3) of alphaherpesviruses was shown to modulate actin reorganization, cell-to-cell spread, and virus egress in a number of virus species. However, the role of the US3 orthologues of equine herpesvirus type 1 and 4 (EHV-1 and EHV-4) has not yet been studied. Here, we show that is not essential for virus replication in vitro. However, growth rates and plaque diameters of a -deleted EHV-1 and a mutant in which the catalytic active site was destroyed were significantly reduced when compared with parental and revertant viruses or a virus in which EHV-1 was replaced with the corresponding EHV-4 gene. The reduced plaque sizes were consistent with accumulation of primarily enveloped virions in the perinuclear space of the -negative EHV-1, a phenotype that was also rescued by the EHV-4 orthologue. Furthermore, actin stress fiber disassembly was significantly more pronounced in cells infected with parental EHV-1, revertant, or the recombinant EHV-1 expressing EHV-4 . Finally, we observed that deletion of in EHV-1 did not affect the expression of adhesion molecules on the surface of infected cells.
α疱疹病毒基因(pUS3)编码的丝氨酸 - 苏氨酸蛋白激酶已被证明可调节多种病毒种类中的肌动蛋白重组、细胞间传播和病毒释放。然而,1型和4型马疱疹病毒(EHV - 1和EHV - 4)的US3同源物的作用尚未得到研究。在此,我们表明其对于体外病毒复制并非必需。然而,与亲本病毒、回复病毒或用相应EHV - 4基因替换EHV - 1的病毒相比,缺失EHV - 1的病毒和催化活性位点被破坏的突变体的生长速率和蚀斑直径显著降低。蚀斑尺寸减小与主要包膜病毒粒子在缺失EHV - 1的病毒的核周空间中积累一致,这种表型也可被EHV - 4同源物挽救。此外,在用亲本EHV - 1、回复病毒或表达EHV - 4的重组EHV - 1感染的细胞中,肌动蛋白应激纤维的解体明显更显著。最后,我们观察到EHV - 1中该基因的缺失不影响感染细胞表面粘附分子的表达。