Open AccessHerpes simplex virus-1 utilizes the host actin cytoskeleton for its release from axonal growth cones
Author(s) -
Kevin Danastas,
Ava Larsen,
Sophie Jobson,
Gerry Guo,
Anthony L. Cunningham,
Monica Miranda-Saksena
Publication year - 2022
Publication title -
plos pathogens
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.719
H-Index - 206
eISSN - 1553-7374
pISSN - 1553-7366
DOI - 10.1371/journal.ppat.1010264
Subject(s) - myosin , growth cone , microbiology and biotechnology , actin , cytoskeleton , actin cytoskeleton , biology , axon , herpes simplex virus , actin remodeling , molecular motor , axoplasmic transport , actin remodeling of neurons , biophysics , virus , biochemistry , cell , virology
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.