Alternate receptor usage of neuropilin-1 and glucose transporter protein 1 by the human T cell leukemia virus type 1

Journal Article · Wed Jan 20 04:00:00 EST 2010 · Virology

OSTI ID:21357582

Qingwen, Jin ^[1]; Alkhatib, Bashar ^[2]; Cornetta, Kenneth ^[3]; Alkhatib, Ghalib ^[1]

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1. Department of Microbiology and Immunology, Indiana University School of Medicine, 635 Barnhill Drive, Rm420, Indianapolis, IN (United States)
2. Department of Biology, IUPUI School of Science (United States)
3. Department of Medical and Molecular Genetics, Indiana University School of Medicine, 635 Barnhill Drive, Rm420, Indianapolis, IN (United States)

Recent studies have demonstrated that neuropilin 1 (NP-1) is involved in HTLV-1 entry; however, the role NP-1 plays in this process is not understood. We demonstrated that ectopic expression of human NP-1 but not NP-2 cDNA increased susceptibility to HTLV-1. SiRNA-mediated inhibition of NP-1 expression correlated with significant reduction of HTLV-1 Env-mediated fusion. The vascular endothelial growth factor (VEGF{sub 165}) caused downmodulation of surface NP-1 and inhibited HTLV-1 infection of U87 cells. In contrast, VEGF{sub 165} partially inhibited infection of primary astrocytes and had no significant effect on infection of HeLa cells. VEGF{sub 165} and antibodies to the glucose transporter protein 1 (anti-GLUT-1) were both needed to block infection of primary astrocytes, however, only anti-GLUT-1 antibodies were sufficient to block infection of HeLa cells. HTLV-1 Env forms complexes with both NP-1 and GLUT-1 in primary human astrocytes. The alternate usage of these two cellular receptors may have important implications regarding HTLV-1 neuro-tropism.

• OSTI ID: 21357582
• Journal Information: Virology, Journal Name: Virology Journal Issue: 2 Vol. 396; ISSN VIRLAX; ISSN 0042-6822
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
ALDEHYDES
ANIMAL CELLS
ANTIBODIES
CARBOHYDRATES
GLUCOSE
GLYCOPROTEINS
GROWTH FACTORS
HELA CELLS
HEXOSES
INHIBITION
LEUKEMIA VIRUSES
MEMBRANE PROTEINS
MICROORGANISMS
MITOGENS
MONOSACCHARIDES
ONCOGENIC VIRUSES
ORGANIC COMPOUNDS
PARASITES
PROTEINS
RECEPTORS
SACCHARIDES
TUMOR CELLS
VIRUSES