Dep. Experimental Medicine University of Rome "La Sapienza", Laboratory Affiliated to Istituto Pasteur Italia fondazione Cenci-Bolognetti, Italy.
Boston University School of Medicine, Boston, MA, USA.
Microbes Infect. 2020 Nov-Dec;22(10):585-591. doi: 10.1016/j.micinf.2020.08.002. Epub 2020 Sep 1.
Viral egress and autophagy are two mechanisms that seem to be strictly connected in Herpesviruses's biology. Several data suggest that the autophagic machinery facilitates the egress of viral capsids and thus the production of new infectious particles. In the Herpesvirus family, viral nuclear egress is controlled and organized by a well conserved group of proteins named Nuclear Egress Complex (NEC). In the case of EBV, NEC is composed by BFRF1 and BFLF2 proteins, although the alterations of the nuclear host cell architecture are mainly driven by BFRF1, a multifunctional viral protein anchored to the inner nuclear membrane of the host cell. BFRF1 shares a peculiar distribution with several nuclear components and with them it strictly interacts. In this study, we investigated the possible role of BFRF1 in manipulating autophagy, pathway that possibly originates from nucleus, regulating the interplay between autophagy and viral egress.
病毒出芽和自噬是两种似乎在疱疹病毒生物学中紧密相连的机制。有几项数据表明，自噬机制有助于病毒衣壳的出芽，从而产生新的感染性颗粒。在疱疹病毒家族中，病毒核出芽由一组被称为核出芽复合物（NEC）的高度保守蛋白控制和组织。在 EBV 的情况下，NEC 由 BFRF1 和 BFLF2 蛋白组成，尽管核宿主细胞结构的改变主要由 BFRF1 驱动，BFRF1 是一种锚定在宿主细胞内核膜上的多功能病毒蛋白。BFRF1 与几种核成分具有特殊的分布，并与它们严格相互作用。在这项研究中，我们研究了 BFRF1 可能在操纵自噬途径方面的作用，该途径可能起源于细胞核，调节自噬与病毒出芽之间的相互作用。
