Chen S Y, Matsuoka Y, Compans R W
Department of Microbiology, University of Alabama, Birmingham 35294.
J Virol. 1991 Mar;65(3):1427-39. doi: 10.1128/JVI.65.3.1427-1439.1991.
Punta Toro virus (PTV), a member of the sandfly fever group of bunyaviruses, is assembled by budding at intracellular membranes of the Golgi complex. We have examined PTV glycoprotein transport, assembly, and release and the effects of brefeldin A (BFA) on these processes. Both the G1 and G2 proteins were transported out of the endoplasmic reticulum (ER) and retained in the Golgi complex in a stable structure, either during PTV infection or when expressed from a vaccinia virus recombinant. BFA treatment causes a rapid and dramatic change in the distribution of the G1 and G2 proteins, from a Golgi pattern to an ER pattern. The G1 and G2 proteins were found to be modified by medial but not trans Golgi network enzymes, in the presence or absence of BFA. We found that BFA blocks PTV release from cells but does not interfere with the intracellular assembly of infectious virions. Further, the BFA block of virus release is fully reversible, with high levels of virus release occurring upon removal of the inhibitor. It was also found that the release of PTV virions is polarized, occurring exclusively from the basolateral surfaces of the polarized Vero C1008 epithelial cell line.
蓬塔托罗病毒(PTV)是白蛉热组布尼亚病毒的成员,通过在高尔基体复合物的细胞内膜出芽进行组装。我们研究了PTV糖蛋白的运输、组装和释放以及布雷菲德菌素A(BFA)对这些过程的影响。在PTV感染期间或从痘苗病毒重组体表达时,G1和G2蛋白均从内质网(ER)转运出来并以稳定结构保留在高尔基体复合物中。BFA处理导致G1和G2蛋白的分布迅速发生显著变化,从高尔基体模式转变为内质网模式。无论有无BFA,G1和G2蛋白都被中间高尔基体网络酶修饰,但未被反式高尔基体网络酶修饰。我们发现BFA阻断PTV从细胞中释放,但不干扰感染性病毒粒子的细胞内组装。此外,BFA对病毒释放的阻断是完全可逆的,去除抑制剂后会有高水平的病毒释放。还发现PTV病毒粒子的释放是极化的,仅从极化的Vero C1008上皮细胞系的基底外侧表面发生。