A role for heparan sulfate 3-O-sulfotransferase isoform 2 in herpes simplex virus type 1 entry and spread

Heparan sulfate (HS) 3-O-sulfotransferase isoform-2 (3-OST-2), which belongs to a family of enzymes capable of generating herpes simplex virus type-1 (HSV-1) entry and spread receptors, is predominantly expressed in human brain. Despite its unique expression pattern, the ability of 3-OST-2 to mediat...

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Published inVirology (New York, N.Y.) Vol. 346; no. 2; pp. 452 - 459
Main Authors O'Donnell, Christopher D., Tiwari, Vaibhav, Oh, Myung-Jin, Shukla, Deepak
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 15.03.2006
Subjects
Animals
Cell Fusion
CHO Cells
Cricetinae
Entry
Genes, Reporter
Heparan sulfate
Heparitin Sulfate - metabolism
Herpes simplex virus 1
Herpesvirus 1, Human - physiology
HSV-1
Humans
Isoenzymes - physiology
Luciferases - analysis
Membrane fusion
Receptors, Virus - physiology
Sulfotransferases - physiology
Viral Envelope Proteins - genetics
Viral Envelope Proteins - metabolism
Heparan sulfate
Membrane fusion
HSV-1
Entry
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Summary:Heparan sulfate (HS) 3-O-sulfotransferase isoform-2 (3-OST-2), which belongs to a family of enzymes capable of generating herpes simplex virus type-1 (HSV-1) entry and spread receptors, is predominantly expressed in human brain. Despite its unique expression pattern, the ability of 3-OST-2 to mediate HSV-1 entry and cell-to-cell fusion is not known. Our results demonstrate that expression of 3-OST-2 can render Chinese hamster ovary K1 (CHO-K1) cells susceptible to entry of wild-type and mutant strains of HSV-1. Evidence for generation of gD receptors by 3-OST-2 were suggested by gD-mediated interference assay and the ability of 3-OST-2-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-2-expressing CHO-K1 cells acquired the ability to fuse with cells-expressing HSV-1 glycoproteins, a phenomenon that mimics a way of viral spread in vivo. Demonstrating specificity, the cell fusion was inhibited by soluble 3-O-sulfated forms of HS, but not unmodified HS. Taken together, our results raise the possibility of a role of 3-OST-2 in the spread of HSV-1 infection in the brain.
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ISSN:0042-6822
1096-0341
DOI:10.1016/j.virol.2005.11.003