Abstract
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.
Highlights
The nuclear membrane (NM) consists of an inner nuclear membrane (INM) and an outer nuclear membrane (ONM), which separate nuclear and cytoplasmic activities in the eukaryotic cell (Figure 1A)
The ONM and the INM are separated by the perinuclear space and connected at annular junctions, where nuclear pore complexes (NPCs) are found
These observations indicate that the nuclear egress complex (NEC) does not directly play a role in the fusion process related PRV protein, gB or gH are not present in the perinuclear vesicles or the NMs and and that other components of the cellular fusion machinery are involved in de-envelopment
Summary
The nuclear membrane (NM) consists of an inner nuclear membrane (INM) and an outer nuclear membrane (ONM), which separate nuclear and cytoplasmic activities in the eukaryotic cell (Figure 1A). Vesicle-mediated nucleocytoplasmic transport is a mechanism for the nuclear export of macromolecular complexes [4] In this system, a macromolecular complex in the nucleus buds through the INM to form a vesicle in the perinuclear space (‘primary envelopment’). A macromolecular complex in the nucleus buds through the INM to form a vesicle in the perinuclear space (‘primary envelopment’) This vesicle fuses with the ONM to release the complex into the cytoplasm in a process called ‘de-envelopment’ [4] (Figure 1B). This type of transport is observed in herpesvirus-infected mammalian cells and is required for the nuclear export of viral capsids that assemble in the nucleus [5].
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