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Title: A role for 3-O-sulfotransferase isoform-4 in assisting HSV-1 entry and spread

Journal Article · · Biochemical and Biophysical Research Communications
DOI:https://doi.org/10.1016/J.BBRC.2005.1· OSTI ID:20793220
 [1];  [1];  [1];  [2];  [3]
  1. Department of Ophthalmology and Visual Sciences, College of Medicine, University of Illinois at Chicago, Chicago, IL 60612 (United States)
  2. Department of Pathology, College of Medicine, University of Illinois at Chicago, Chicago, IL 60612 (United States)
  3. Department of Ophthalmology and Visual Sciences, College of Medicine, University of Illinois at Chicago, Chicago, IL 60612 (United States) and Department of Microbiology and Immunology, College of Medicine, University of Illinois at Chicago, Chicago, IL 60612 (United States)

Many heparan sulfate (HS) 3-O-sulfotransferase (3-OST) isoforms generate cellular receptors for herpes simplex virus type-1 (HSV-1) glycoprotein D (gD). Interestingly, the ability of 3-OST-4 to mediate HSV-1 entry and cell-to-cell fusion has not been determined, although it is predominantly expressed in the brain, a primary target of HSV-1 infections. We report that expression of 3-OST-4 can render Chinese hamster ovary K1 (CHO-K1) cells susceptible to entry of wild-type and a mutant (Rid1) strain of HSV-1. Evidence for generation of gD receptors by 3-OST-4 was suggested by gD-mediated interference assay and the ability of 3-OST-4 expressing CHO-K1 cells to preferentially bind HSV-1 gD, which could be reversed by prior treatment of cells with HS lyases (heparinases-II/III). In addition, 3-OST-4 expressing CHO-K1 cells acquired the ability to fuse with cells-expressing HSV-1 glycoproteins. Demonstrating specificity, the cell fusion was inhibited by soluble 3-O-sulfated forms of HS, but not unmodified HS. Taken together our results suggest a role of 3-OST-4 in HSV-1 pathogenesis.

OSTI ID:
20793220
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 338, Issue 2; Other Information: DOI: 10.1016/j.bbrc.2005.10.056; PII: S0006-291X(05)02268-0; Copyright (c) 2005 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English