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Journal of Virology, December 2002, p. 12723-12734, Vol. 76, No. 24
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.24.12723-12734.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Similar Regulation of Cell Surface Human T-Cell Leukemia Virus Type 1 (HTLV-1) Surface Binding Proteins in Cells Highly and Poorly Transduced by HTLV-1-Pseudotyped Virions

Kathryn S. Jones,1 Manisha Nath,2 Cari Petrow-Sadowski,1 Andrea C. Baines,2 Megan Dambach,2 Ying Huang,2 and Francis W. Ruscetti2*

Basic Research Program, SAIC-Frederick,1 Basic Research Laboratory, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, Maryland 217022

Received 30 August 2001/ Accepted 12 September 2002

Little is known about the requirements for human T-cell leukemia virus type 1 (HTLV-1) entry, including the identity of the cellular receptor(s). Previous studies have shown that although the HTLV receptor(s) are widely expressed on cell lines of various cell types from different species, cell lines differ dramatically in their susceptibility to HTLV-Env-mediated fusion. Human cells (293, HeLa, and primary CD4+ T cells) showed higher levels of binding at saturation than rodent (NIH 3T3 and NRK) cells to an HTLV-1 SU immunoadhesin. A direct comparison of the binding of the HTLV-1 surface glycoprotein (SU) immunoadhesin and transduction by HTLV-1 pseudotyped virus revealed parallels between the level of binding and the titer for various cell lines. When cells were treated with phorbol myristate acetate (PMA), which down-modulates a number of cell surface molecules, the level of SU binding was markedly reduced. However, PMA treatment only slightly reduced the titer of murine leukemia virus(HTLV-1) on both highly susceptible and poorly susceptible cells. Treatment of target cells with trypsin greatly reduced binding, indicating that the majority of HTLV SU binding is to proteins. Polycations, which enhance the infectivity of several other retroviruses, inhibited HTLV-1 Env-mediated binding and entry on both human and rodent cells. These results suggest that factors other than the number of primary binding receptors are responsible for the differences in the titers of HTLV-1 pseudotypes between highly susceptible cells and poorly susceptible cells.

* Corresponding author. Mailing address: Basic Research Laboratory, Bldg. 567, Rm. 253, National Cancer Institute at Frederick, Frederick, MD 21702-1201. Phone: (301) 846-5610. Fax: (301) 846-7034. E-mail: ruscettif{at}ncifcrf.gov.

Journal of Virology, December 2002, p. 12723-12734, Vol. 76, No. 24
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.24.12723-12734.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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