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Deepak Shukla, Vaibhav Tiwari; Non-professional Phagocytosis Can Play A Role In Herpesvirus Entry Into Ocular Cells. Invest. Ophthalmol. Vis. Sci. 2012;53(14):6161.
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Herpesviruses cause myriads of eye diseases. The goal of the present study was to determine some common features of herpes simplex virus-1 (HSV-1), cytomegalovirus (CMV) and human herpesvirus-8 (HHV-8) entry into ocular cells.
High resolution laser scanning confocal microscopy, transmission electron microscopy (TEM), and fluorescence microscopy were used to monitor cytoskeletal changes associated with herpesvirus infection of ocular cells. HSV-1 infection was studied in human corneal fibroblasts, CMV in human retinal pigment epithelial cells, and human conjunctiva epithelial cells were used to study HHV-8 infection. To assess the effects of phagocytosis and related changes in the cytoskeleton, cells were also exposed to herpesvirus glycoproteins (gB, gH and gL) and analyzed by microscopy. Live cell imaging was performed to study the role of phagocytosis in virus entry and cell-to-cell spread. Biochemical assays and F-actin inhibitors were used to probe the significance of non-professional phagocytosis in viral entry.
Ocular cells respond to herpesvirus infection by inducing filopodia formation. Filopodia assist with virus entry and this phenomenon is common for the herpesviruses tested including HSV-1, CMV and HHV-8. The virus internalization may occur by a mechanism that involves non-professional phagocytosis. In all cases viral entry can be inhibited by F-actin depolymerizers such as Cytochalasin D and Latrunculin B. Small Rho GTPases and PI3 Kinases were implicated as important regulators of this process.
Non-professional phagocytosis may play an important role in herpesvirus entry into ocular cells.
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