Abstract
A novel role for phagocytosis-like uptake in herpes simplex virus entry
Highlights
Mammalian cells have evolved multiple mechanisms for internalizing fluids, surface-bound ligands, and plasma membrane components
Cultured corneal fibroblasts (CF) are susceptible to herpes simplex virus type-1 (HSV-1) entry and replication
Monolayer cultures of CF and nectin-1-CHO or HVEMexpressing CHO cells (HVEM-CHO) were infected with a recombinant β-galactosidase (β-gal)–expressing reporter virus, HSV-1(KOS)gL86, abbreviated here as KOS-gL86 and interchangeably used in this manuscript for HSV-1. β-gal activity indicates that virus has entered the cell, released its genome into the nucleus, and activated the constitutive promoter for the enzyme production and activity (Shukla et al, 2000)
Summary
Mammalian cells have evolved multiple mechanisms for internalizing fluids, surface-bound ligands, and plasma membrane components. In the case of herpes simplex virus type-1 (HSV-1), endocytosis plays a dominant role in infection of many cell types (Nicola et al, 2003; Nicola and Straus, 2004). This process, appears to be unique because it is likely not mediated by formation of clathrincoated pits or caveolae and it may not always be pH dependent (Gianni et al, 2004; Milne et al, 2005; Nicola et al, 2005)
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