Abstract
The alphaherpesviruses are pathogens of the mammalian nervous system. Initial infection is commonly at mucosal epithelia, followed by spread to, and establishment of latency in, the peripheral nervous system. During productive infection, viral gene expression, replication of the dsDNA genome, capsid assembly and genome packaging take place in the infected cell nucleus, after which mature nucleocapsids emerge into the cytoplasm. Capsids must then travel to their site of envelopment at cytoplasmic organelles, and enveloped virions need to reach the cell surface for release and spread. Transport at each of these steps requires movement of alphaherpesvirus particles through a crowded and viscous cytoplasm, and for distances ranging from several microns in epithelial cells, to millimeters or even meters during egress from neurons. To solve this challenging problem alphaherpesviruses, and their assembly intermediates, exploit microtubule- and actin-dependent cellular motors. This review focuses upon the mechanisms used by alphaherpesviruses to recruit kinesin, myosin and dynein motors during assembly and egress.
Highlights
This review focuses upon the ways in which alphaherpesvirus particles recruit the cellular motors kinesin, dynein and myosin during viral maturation and exit from the infected cell
As we describe in this review, isoforms of nonmuscle form of myosin-II (NM-II) and myosin-V have been implicated in traffic of alphaherpesvirus viral particles within and between infected cells (Sections 2 and 5)
Alphaherpesvirus trafficking within and between cells is critical for viral replication and the spread of disease, and is accomplished by the conscription and exploitation of a variety of cellular motors
Summary
The Alphaherpesvirinae include pathogens of the nervous system such as herpes simplex virus types 1 and 2 (HSV-1 and HSV-2), varicella zoster virus (VZV) and the swine virus pseudorabies virus (PRV) [1,2,3,4]. 40 structural proteins distributed between three distinct layers: (i) An icosahedral capsid packaged with the dsDNA genome, which is ~150 kb in size in the case of HSV-1, HSV-2 and PRV, (ii) A complex multi-subunit protein layer termed tegument, that is anchored to the capsid surface, (iii) An envelope, derived from the lipid bilayer of a host cell cytoplasmic organelle, which contains numerous virally encoded membrane proteins. The structure and composition of HSV-1 particles have recently been reviewed in detail [12,13,14,15,16,17]. This review focuses upon the ways in which alphaherpesvirus particles recruit the cellular motors kinesin, dynein and myosin during viral maturation and exit from the infected cell
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