Abstract
Herpes simplex virus type 1 (HSV-1) has evolved mechanisms to exploit the host cytoskeleton during entry, replication and exit from cells. In this study, we determined the role of actin and the molecular motor proteins, myosin II and myosin V, in the transport and release of HSV-1 from axon termini, or growth cones. Using compartmentalized neuronal devices, we showed that inhibition of actin polymerization, but not actin branching, significantly reduced the release of HSV-1 from axons. Furthermore, we showed that inhibition of myosin V, but not myosin II, also significantly reduced the release of HSV-1 from axons. Using confocal and electron microscopy, we determined that viral components are transported along axons to growth cones, despite actin or myosin inhibition. Overall, our study supports the role of actin in virus release from axonal growth cones and suggests myosin V as a likely candidate involved in this process.
Highlights
Herpes simplex virus-1 (HSV-1) is a human trophic virus capable of establishing lifelong latent infections in neurons of the peripheral nervous system of human hosts
Herpes simplex virus type 1 (HSV-1) is transported along axons via microtubules; how the virus is released from axon termini, where actin predominates, is unknown
We show that an intact actin cytoskeleton is required for efficient virus release from axon termini
Summary
Herpes simplex virus-1 (HSV-1) is a human trophic virus capable of establishing lifelong latent infections in neurons of the peripheral nervous system of human hosts. HSV-1 infects its host via the mucosa and skin where it replicates in epithelial cells Following this initial infection, the virus enters and infects the sensory nerves of the dorsal root ganglia (DRG) or trigeminal ganglia neurons innervating the site of infection [1,2]. The virus is transported via retrograde axonal transport to the neuronal cell body where the viral genome is deposited in the nucleus, establishing a lifelong latent infection [1,2]. Viral reactivation leads to virus replication in the neuronal cell body and virus transport along nerves to the nerve termini for subsequent virus spread into the skin, resulting in either recurrent disease or asymptomatic virus shedding [1,2].
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