Motor Skills: Recruitment of Kinesins, Myosins and Dynein during Assembly and Egress of Alphaherpesviruses

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.

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“…Although speculative at this point, its location between US8 (gE) and US2 may indicate that the removal of US9 could be a bystander deletion. While this deletion does not appear to have any particular advantage or disadvantage with regard to virus growth in epithelial cell cultures, neuronal anterograde transport of a US9null virus is abolished, thereby leading to severe attenuation in vivo (73,74).…”

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“…It is believed that herpesviruses envelope proteins play a vital role in this process. Many envelope proteins have been reported to be closely associated with secondary envelopment through interaction with teguments (i.e., UL11, UL14, UL16, UL36, UL37, UL49, and UL51) and/or capsid proteins (18,(20)(21)(22)(23)(24)(25)(26)(27). However, data con rming the relationship between envelope proteins and secondary envelopment are limited, and the mechanism by which the envelope protein facilitates secondary envelopment is still obscure (15,16).…”