Abstract
Herpes simplex virus type-1 (HSV-1) is a common human pathogen that relies heavily on cell-to-cell spread for establishing a lifelong latent infection. Molecular aspects of HSV-1 entry into host cells have been well studied; however, the molecular details of the spread of the virus from cell-to-cell remain poorly understood. In the past, the role of heparan sulfate proteoglycans (HSPG) during HSV-1 infection has focused solely on the role of HS chains as an attachment receptor for the virus, while the core protein has been assumed to perform a passive role of only carrying the HS chains. Likewise, very little is known about the involvement of any specific HSPGs in HSV-1 lifecycle. Here we demonstrate that a HSPG, syndecan-1, plays an important role in HSV-1 induced membrane fusion and cell-to-cell spread. Interestingly, the functions of syndecan-1 in fusion and spread are independent of the presence of HS on the core protein. Using a mutant CHO-K1 cell line that lacks all glycosaminoglycans (GAGs) on its surface (CHO-745) we demonstrate that the core protein of syndecan-1 possesses the ability to modulate membrane fusion and viral spread. Altogether, we identify a new role for syndecan-1 in HSV-1 pathogenesis and demonstrate HS-independent functions of its core protein in viral spread.
Highlights
Herpes simplex virus type-1 (HSV-1) is a worldwide health problem that causes a wide range of diseases
While substantial work has focused on delineating the role of heparan sulfate (HS) as an attachment receptor for HSV-1, far less is known about the contribution of the heparan sulfate proteoglycans (HSPG) core protein in HSV-1 infection
Our study demonstrates a novel role for the core protein of HSPG during HSV-1 infection
Summary
Herpes simplex virus type-1 (HSV-1) is a worldwide health problem that causes a wide range of diseases. It is a leading cause of infectious corneal blindness in the developed world and sporadic, fatal encephalitis worldwide. HSV-1 follows different entry routes depending on the type of the cell it infects [5,6,7]. It can fuse at the plasma membrane, enter via endocytosis, or get captured by cells in a phagocytosis-like manner and fuse with the phagosomal membrane [6,7,8]. Fusion of the viral envelope with the host cell membrane follows with the combined action of HSV-1 gD, gD receptor, gB, gH, gL [14], and possibly gB receptors [17,18] and gH receptors [19]
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