中文摘要：

皮是占据在 nucleocapsid 和信封之间的空间的 herpesvirion 的唯一的结构。积累的数据显示了在皮蛋白质之中的相互作用在 virion 形态发生起一个关键作用。包括 Kaposis 联系肉瘤的 herpesvirus (KSHV ) 和 Epstein-Barr 病毒(EBV ) 的 gammaherpesviruses 的形态发生糟糕由于有效 de novo 的缺乏被理解在房间文化的 lysin 的复制。鼠科的 gammaherpesvirus-68 (MHV-68 ) 是遗传上与这二人的 herpesviruses 有关并且担任一个有效模型学习 gammaherpesviruses 的 lysin 的复制。我们以前证明 MHV-68 的 ORF33 编码皮蛋白质并且在细胞质在 virion 成熟起一个必要作用。然而， ORF33 怎么参予 virion 形态发生的分子的机制没被阐明。在这研究，我们证明 MHV-68 的 ORF38 也是皮蛋白质并且在短暂 transfection 和病毒的感染期间对细胞质的分隔空间局部性。把试金标记的免疫黄金证明 ORF38 仅仅是进入了细胞质的泡的 virions 上的现在，显示 ORF38 被包装进在第二等的包封期间的 virions。我们进一步证明 ORF38 在病毒的感染期间与 ORF33 共同本地化；因此，在 ORF38 和 ORF33 之间的相互作用在 herpesviruses 之中被保存。尤其是，我们发现尽管由自己的 ORF33 在原子核和细胞质是分布式的，面对 ORF38， ORF33 对 trans-Golgi 网络(TGN )co 局部性，第二等的包封发生的一个地点。

英文摘要：

Tegument is the unique structure of a herpesvirion which occupies the space between nucleocapsid and envelope. Accumulating data have indicated that inter- actions among tegument proteins play a key role in virion morphogenesis. Morphogenesis of gam- maherpesviruses including Kaposi＇s sarcoma-associ- ated herpesvirus （KSHV） and Epstein-Barr virus （EBV） is poorly understood due to the lack of efficient de novo lytic replication in cell culture. Murine gammaherpesvi- rus-68 （MHV-68） is genetically related to these two human herpesviruses and serves as an effective model to study the lytic replication of gammaherpesviruses. We previously showed that ORF33 of MHV-68 encodes a tegument protein and plays an essential role in virion maturation in the cytoplasm. However, the molecular mechanism of how ORF33 participates in virion mor- phogenesis has not been elucidated. In this study we demonstrated that ORF38 of MHV-68 is also a tegument protein and is localized to cytoplasmic compartments during both transient transfection and viral infection. Immuno-gold labeling assay showed that ORF38 is only present on virions that have entered the cytoplasmic vesicles, indicating that ORF38 is packaged into virions during secondary envelopment. We further showed that ORF38 co-localizes with ORF33 during viral infection; therefore, the interaction between ORF38 and ORF33 is conserved among herpesviruses. Notably, we found that although ORF33 by itself is distributed in both the nucleus and the cytoplasm, in the presence of ORF38, ORF33 is co-localized to trans-Golgi network （TGN）, a site where secondary envelopment takes place.