Schulze P, Olechnowitz A F
Arch Exp Veterinarmed. 1975 Jun;29(3):441-57.
The previous parts have been concerned with the participation of the cell nucleus in the formation of the RNA of FMD virus. However, the actual morphogenesis of the virus takes place in cytoplasm. In BHK cells, changes attributable to virus infection were visible by the second hour, with the formation of threads and large polysome complexes near the nucleus. Viral particles soon appeared between these structures. There were no pronounced foci of viroplasma, and it seemed that they were not necessary. Simultaneously new membranes formed in the cell. Clumps of viral particles were next visible in the cxtoplasma. The clumps became enveloped and were transported in this way to the periphery of the cell. Elsewhere there was uptake of particles in autophagic vacuoles, an expression of cellular defensive processes. In ultra-thin sections the virions measured 21-25 nm. Within vacuoles the inner part of the virus, the nucleoid, showed greater contrast than the periphery, the capsid. At first there were only slight changes in mitochondria. Liberation of virus by cell rupture occurred only after severe damage to the cell, particularly the lysosome membranes.
前面的部分关注的是细胞核在口蹄疫病毒RNA形成过程中的参与情况。然而，病毒的实际形态发生是在细胞质中进行的。在BHK细胞中，到第二小时就可见到因病毒感染而产生的变化，在细胞核附近形成了细丝和大型多聚核糖体复合物。病毒颗粒很快出现在这些结构之间。没有明显的病毒质病灶，似乎它们并非必需。与此同时，细胞中形成了新的膜。接下来在细胞质中可见病毒颗粒团块。这些团块被包裹起来并以这种方式被转运到细胞周边。在其他地方，自噬泡中有颗粒摄取，这是细胞防御过程的一种表现。在超薄切片中，病毒粒子大小为21 - 25纳米。在液泡内，病毒的内部部分，即核衣壳，比周边的衣壳显示出更大的反差。起初线粒体只有轻微变化。只有在细胞受到严重损伤，特别是溶酶体膜受损后，才会通过细胞破裂释放病毒。
