Microtubules, part of the cytoskeleton, are indispensable for intracellular movement, cell division, and maintaining cell shape and polarity. In addition, microtubules play an important role in viral infection. In this review, we summarize the role of the microtubules' network during polyomavirus infection. Polyomaviruses usurp microtubules and their motors to travel via early and late acidic endosomes to the endoplasmic reticulum. As shown for SV40, kinesin-1 and microtubules are engaged in the release of partially disassembled virus from the endoplasmic reticulum to the cytosol, and dynein apparently assists in the further disassembly of virions prior to their translocation to the cell nucleus-the place of their replication. Polyomavirus gene products affect the regulation of microtubule dynamics. Early T antigens destabilize microtubules and cause aberrant mitosis. The role of these activities in tumorigenesis has been documented. However, its importance for productive infection remains elusive. On the other hand, in the late phase of infection, the major capsid protein, VP1, of the mouse polyomavirus, counteracts T-antigen-induced destabilization. It physically binds microtubules and stabilizes them. The interaction results in the G2/M block of the cell cycle and prolonged S phase, which is apparently required for successful completion of the viral replication cycle.

中文翻译：

---

多瘤病毒感染中的微管。


微管是细胞骨架的一部分，对于细胞内运动、细胞分裂以及维持细胞形状和极性是不可或缺的。此外，微管在病毒感染中发挥着重要作用。在这篇综述中，我们总结了微管网络在多瘤病毒感染过程中的作用。多瘤病毒侵占微管及其马达，通过早期和晚期酸性内体到达内质网。如 SV40 所示，驱动蛋白-1 和微管参与将部分分解的病毒从内质网释放到胞质溶胶，动力蛋白显然有助于病毒粒子在转位到细胞核（病毒粒子的位置）之前进一步分解。复制。多瘤病毒基因产物影响微管动力学的调节。早期 T 抗原会破坏微管的稳定性并导致异常的有丝分裂。这些活性在肿瘤发生中的作用已被记录。然而，它对于生产性感染的重要性仍然难以捉摸。另一方面，在感染后期，小鼠多瘤病毒的主要衣壳蛋白 VP1 会抵消 T 抗原诱导的不稳定。它以物理方式结合微管并稳定它们。这种相互作用导致细胞周期的 G2/M 阻断和 S 期延长，这显然是成功完成病毒复制周期所必需的。