Division of Clinical Virology, Center for Infectious Diseases, Kobe University Graduate School of Medicine, Kobe, Hyogo 650-0017, Japan.
Viruses. 2021 Apr 25;13(5):754. doi: 10.3390/v13050754.
Herpes simplex virus 1 (HSV-1) replicates its genome and packages it into capsids within the nucleus. HSV-1 has evolved a complex mechanism of nuclear egress whereby nascent capsids bud on the inner nuclear membrane to form perinuclear virions that subsequently fuse with the outer nuclear membrane, releasing capsids into the cytosol. The viral-encoded nuclear egress complex (NEC) plays a crucial role in this vesicle-mediated nucleocytoplasmic transport. Nevertheless, similar system mediates the movement of other cellular macromolecular complexes in normal cells. Therefore, HSV-1 may utilize viral proteins to hijack the cellular machinery in order to facilitate capsid transport. However, little is known about the molecular mechanisms underlying this phenomenon. This review summarizes our current understanding of the cellular and viral factors involved in the nuclear egress of HSV-1 capsids.
单纯疱疹病毒 1（HSV-1）在细胞核内复制其基因组并将其包装成衣壳。HSV-1 已经进化出一种复杂的核出芽机制，新生的衣壳在内核膜上出芽，形成核周病毒颗粒，随后与外核膜融合，将衣壳释放到细胞质中。病毒编码的核出芽复合物（NEC）在这种囊泡介导的核质转运中起着至关重要的作用。然而，类似的系统介导正常细胞中其他细胞大分子复合物的运动。因此，HSV-1 可能利用病毒蛋白劫持细胞机制，以促进衣壳运输。然而，对于这种现象的分子机制知之甚少。本文综述了我们目前对 HSV-1 衣壳核出芽所涉及的细胞和病毒因子的理解。
