4株鸡马立克氏病病毒国内分离株Meq基因的克隆与序列分析

根据鸡马立克氏病病毒(MDV)GA株Meq基因序列,设计并合成一对用于扩增Meq基因的引物,利用这对引物通过PCR方法分别扩增4株东北地区分离的强毒株、国内标准强毒株J-1株、国内疫苗株814株的Meq基因片段,进行克隆测序,对4株MDV分离毒株Meq基因与国内传统毒株Meq基因及GenBank上收录的国内外9株毒株Meq基因序列进行比较分析.序列比较显示,不同的MDV株的Meq基因序列相对比较保守,它们相互间氨基酸序列的同源性在96.5%～99.7%之间.4株MDV分离毒株Meq基因在相关报道中提到的与毒力相关的脯氨酸重复区存在点突变;3株分离毒株Meq基因上相同位置均存在两个定点突变,这两处点突变是国内近几年分离株所特有的,国外已发表的MDV毒株Meq序列中不存在这种变化.分离株Meq基因的这些突变和毒株毒力的关系具有一定的规律性,但是这些规律性还有待进一步研究.     

Involvement of Jun dimerization protein 2 (JDP2) in the maintenance of Epstein-Barr virus latency

Reactivation of the Epstein-Barr virus from latency is dependent on expression of the BZLF1 viral immediate-early protein. The BZLF1 promoter (Zp) normally exhibits only low basal activity but is activated in response to chemical inducers such as 12-O-tetradecanoylphorbol-13-acetate and calcium ionophore. We found that Jun dimerization protein 2 (JDP2) plays a significant role in suppressing Zp activity. Reporter, EMSA, and ChIP assays of a Zp mutant virus revealed JDP2 association with Zp at the ZII cis-element, a binding site for CREB/ATF/AP-1. Suppression of Zp activity by JDP2 correlated with HDAC3 association and reduced levels of histone acetylation. Although introduction of point mutations into the ZII element of the viral genome did not increase the level of BZLF1 production, silencing of endogenous JDP2 gene expression by RNA interference increased the levels of viral early gene products and viral DNA replication. These results indicate that JDP2 plays a role as a repressor of Zp and that its replacement by CREB/ATF/AP-1 at ZII is crucial to triggering reactivation from latency to lytic replication.