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Journal of Virology, September 2000, p. 8550-8557, Vol. 74, No. 18
Department of Immunology/Microbiology, Rush
University, Chicago, Illinois 60612
Received 22 February 2000/Accepted 21 June 2000
The ability of human immunodeficiency virus strain MN
(HIVMN), a T-cell line-adapted strain of HIV, and X4 and R5
primary isolates to bind to various cell types was investigated. In
general, HIVMN bound to cells at higher levels than did the
primary isolates. Virus bound to both CD4-positive (CD4+)
and CD4-negative (CD4
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
CD4-Negative Cells Bind Human Immunodeficiency
Virus Type 1 and Efficiently Transfer Virus to T Cells
) cells, including neutrophils, Raji
cells, tonsil mononuclear cells, erythrocytes, platelets, and
peripheral blood mononuclear cells (PBMC), although virus bound at
significantly higher levels to PBMC. However, there was no difference
in the amount of HIV that bound to CD4-enriched or CD4-depleted PBMC.
Virus bound to CD4
cells was up to 17 times more
infectious for T cells in cocultures than was the same amount of
cell-free virus. Virus bound to nucleated cells was significantly more
infectious than virus bound to erythrocytes or platelets. The enhanced
infection of T cells by virus bound to CD4
cells was not
due to stimulatory signals provided by CD4
cells or
infection of CD4
cells. However, anti-CD18 antibody
substantially reduced the enhanced virus replication in T cells,
suggesting that virus that bound to the surface of CD4
cells is efficiently passed to CD4+ T cells during
cell-cell adhesion. These studies show that HIV binds at relatively
high levels to CD4
cells and, once bound, is highly
infectious for T cells. This suggests that virus binding to the surface
of CD4
cells is an important route for infection of T
cells in vivo.
*
Corresponding author. Mailing address: Department of
Immunology/Microbiology, Rush University, 1653 West Congress Pkwy.,
Chicago, IL 60612. Phone: (312) 942-2083. Fax: (312) 942-2808. E-mail: gspear{at}rush.edu.
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