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D. Shukla; Dendritic Morphology of Herpetic Ulcers in the Cornea May Mark a Viral Spread Strategy. Invest. Ophthalmol. Vis. Sci. 2010;51(13):3873.
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Herpesviruses cause myriads of eye problems including dendritic ulcers in the infected corneas. The goal of the present study was to study the cytoskeletal changes induced by Herpes Simplex Virus type 1 (HSV-1) and their relevance to viral spread.
High resolution laser confocal microscopy and fluorescent microscopy were used to monitor cytoskeletal changes associated with HSV-1 infection of the cells of the corneal origin including corneal epithelial and corneal fibroblasts. To assess the effect on cytoskeleton cells were also exposed to HSV-1 glycoproteins (gB, gD, gH and gL) in trans or made to transiently express individual glycoproteins. Live cell imaging was performed to study virus spread on cytoskeleton elements. Biochemical assays and F-actin inhibitors were used to probe the significance of the cytoskeletal elements in viral spread.
Ocular cells respond to HSV-1 infection by inducing cytoskeletal changes. Often, depending on the viral dosages, the cells acquire dendritic morphology mimicking herpetic ulcers of the cornea. The dendritic morphology arises mostly due to excessive filopodia formation. The same changes can be induced by exposing cells to purified preparations of the glycoprotein gB. Interestingly, cells over-expressing gB also show an increase in average filopodia numbers. We also demonstrate that HSV-1 virions can use filopodia and filopodial bridges to spread from cell to cell. The spread and the alterations in the cytoskeleton can be inhibited by F-actin depolymerizers such as Cytochalasin D and Latrunculin B. Small Rho GTPases were implicated as important regulators of this process.
Cytoskeletal elements may play an important role in HSV-1 spread. Induction of dendritic morphology may be relevant to the spread of HSV-1 virions both in vitro and in vivo.
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