Zebrafish encoded 3-O-sulfotransferase-2 serves as receptor during HSV-1 entry and spread
- Authors
- Baldwin, J., Antoine, T.E., Shukla, D., and Tiwari, V.
- ID
- ZDB-PUB-130308-16
- Date
- 2013
- Source
- Biochemical and Biophysical Research Communications 432(4): 672-6 (Journal)
- Registered Authors
- Tiwari, Vaibhav
- Keywords
- zebrafish, heparan sulfate, herpes simplex virus type-1, 3-O-Sulfotransferase-2, virus-cell interaction
- MeSH Terms
-
- Animals
- CHO Cells
- Cell Fusion
- Cricetinae
- Heparitin Sulfate/physiology*
- Herpesvirus 1, Human/physiology*
- Receptors, Virus/metabolism*
- Sulfotransferases/genetics
- Sulfotransferases/metabolism*
- Viral Envelope Proteins/genetics
- Viral Envelope Proteins/metabolism
- Virus Internalization*
- Zebrafish/genetics
- Zebrafish/metabolism*
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 23416072 Full text @ Biochem. Biophys. Res. Commun.
Previously we reported the role of zebrafish (ZF) encoded glucosaminyl 3-O-sulfotransferase-3 (3-OST-3) isoform in assisting herpes simplex virus type-1 (HSV-1) entry and spread by generating an entry receptor to HSV-1 envelope glycoprotein D (gD). However, the ability of ZF encoded 3-OST-2 isoform to participate in HSV-1 entry has not been determined although it is predominantly expressed in ZF brain, a prime target for HSV-1 to infect and establish lifelong latency. Here we report the expression cloning of ZF encoded 3-OST-2 isoform and demonstrate HSV-1 entry into resistant Chinese hamster ovary (CHO-K1) cells expressing the clone. Additional significance of ZF encoded 3-OST-2 receptor was demonstrated using medically important isolates of HSV-1. In addition, interference to HSV-1 entry was observed upon co-expression of HSV-1 gD and ZF 3-OST-2. Similarly HSV-1 entry was significantly inhibited by the pre-treatment of cells with enzyme HS lyases (heparinase II/III). Finally, ZF-3-OST-2 expressing CHO-K1 was able to fuse with HSV-1 glycoprotein expressing cells suggesting their role in HSV-1 spread. Taken together our result demonstrates a role for ZF 3-OST-2 in HSV-1 pathogenesis.