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Journal of Virology, February 2007, p. 1506-1510, Vol. 81, No. 3
0022-538X/07/$08.00+0     doi:10.1128/JVI.01522-06

GLUT1 Is Not the Primary Binding Receptor but Is Associated with Cell-to-Cell Transmission of Human T-Cell Leukemia Virus Type 1

Norihiro Takenouchi,^1, Kathryn S. Jones,^2, Ivonne Lisinski,^3, Kazunori Fugo,¹ Karen Yao,¹ Samuel W. Cushman,³ Francis W. Ruscetti,⁴ and Steven Jacobson^1,*

Viral Immunology Section, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892,¹ Basic Research Program, SAIC-Frederick, Frederick, Maryland 21702,² Experimental Diabetes, Metabolism, and Nutrition Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892,³ Laboratory of Experimental Immunology, Center for Cancer Research, National Cancer Institute-Frederick, Frederick, Maryland 21702⁴

Received 17 July 2006/ Accepted 5 November 2006

GLUT1 has recently been suggested to be a binding receptor for human T-cell leukemia virus type 1 (HTLV-1). We used a novel, short-term assay to define the role of GLUT1 in cell-to-cell transmission. Although increasing cell surface levels of GLUT1 enhanced HTLV-I transfer, efficient virus spread correlated largely with heparan sulfate proteoglycan (HSPG) expression on target cells. Moreover, since activated CD4⁺ T cells and cord blood lymphocytes that are susceptible to HTLV-1 infection expressed undetectable levels of surface GLUT1, these results indicate that GLUT1 and HSPGs are important for efficient cell-to-cell transmission of HTLV-1 but raise concerns on the role of GLUT1 as the HTLV-1 primary binding receptor.

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* Corresponding author. Mailing address: Viral Immunology Section, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20982. Phone: (301) 496-0519. Fax: (301) 402-0373. E-mail: jacobsons{at}ninds.nih.gov.

Published ahead of print on 15 November 2006.

N.T., K.S.J., I.L., and S.J. have contributed equally to this report.

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Journal of Virology, February 2007, p. 1506-1510, Vol. 81, No. 3
0022-538X/07/$08.00+0     doi:10.1128/JVI.01522-06

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