- Meeting abstract
- Open Access
Xylosyltransferase 2, a protein encoded on chromosome 17q, is involved in HTLV entry
© Jensen et al; licensee BioMed Central Ltd. 2011
- Published: 6 June 2011
- Hybrid Cell
- Molecular Evidence
- Hybrid Cell Line
- HTLV Infection
- Pseudotyped Virus
Early studies mapped the entry receptor for HTLV-1 and HTLV-2 to the long arm of chromosome 17. However, later observations that the titer of HTLV Env-pseudotyped viruses was low on some mouse-human hybrid cell lines containing human chromosome 17q led to the belief that this gene was not involved in HTLV infection. Recent studies showing that efficient HTLV-I infection requires three molecules (GLUT-1, NRP-1, and HSPGs), prompted us to examine whether a gene on chromosome 17 is related to this receptor complex.
Since NRP-1 or GLUT-1 map to other chromosomes, we examined chromosome 17q for genes involved in the synthesis of HSPGs. A gene at 17q21.33, XYLT2, encodes Xylosyltransferase 2 (XT-II), one of two isoforms of an enzyme involved in glycosaminoglycan-chain modifications on proteoglycans. Studies revealed that both the titer of HTLV-1 pseudotyped virus and the level of binding of soluble HTLV-1 SU proteins were dramatically lower on a cell line lacking functional xylosyltransferase (CHOK1-745) than on the parental line (CHOK1). Expression of transgenic XT-II in CHOK1-745 cells increased the levels of HTLV-1 SU binding and the titer of HTLV-1 Env pseudotypes to levels similar to those in wild-type cells. The role of XT-II in HTLV-2 and HTLV-3 Env-mediated entry is being investigated, as well as the role of xylosyltransferases in the infection of T and dendritic cells by HTLVs. These data provide molecular evidence for the previously reported association of a chromosome 17-encoded product in HTLV-1 entry and confirm the critical role of proteoglycans in this process.
This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.