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Complement and virus-specific antibody-dependent infection of normal B
lymphocytes by human immunodeficiency virus type 1
G Gras, Y Richard, P Roques, R Olivier and D Dormont
Laboratoire de Neuropathologie Experimentale et Neurovirologie,
Commissariat a l'Energie Atomique, Fontenay aux Roses, France.
We tested the susceptibility of human purified, normal B lymphocytes to
human immunodeficiency virus type 1 (HIV-1) infection, in the presence or
absence of complement-sufficient serum and of virus-specific antibodies.
Virus replication was detected when cells were infected in the presence of
both complement and anti-HIV antibodies (C'-ADE conditions), by day 2
postinfection. Similar results were obtained when B lymphocytes were
purified either from peripheral blood (three healthy donors) or from
tonsils (four individuals with chronic tonsillitis). HIV infection was
shown by polymerase chain reaction (PCR) detection of proviral sequences
(gag and pol genes), by p24 antigen synthesis, and by cocultivation assay
with MT2 cells. The higher p24 production was obtained when B cells were
preactivated for 2 days by phorbol 12- myristate 13-acetate (PMA) before
infection and then cultured in the presence of low-molecular weight B-cell
growth factor (LMW-BCGF). Expression of virus envelope glycoprotein (gp)
120 could also be detected on a subpopulation of B cells (CD19+, CD22+) by
flow cytometry. Blocking experiments with monoclonal antibodies (MoAbs)
against CD4, CD21 (complement receptor 2 [CR2]), CD35 (CR1), CD19, and CD5
surface molecules indicated that infection of B cells involves CD4, CD21,
and CD35 antigens. Indeed, blocking of CD4 receptor inhibited 10% of p24
production, and blocking of both CD21 and CD35 led to extinction of p24
signal. CR-dependent pathway is thus a major route for C'-ADE of HIV
infection in normal B cells. Our results emphasize the importance of
studying interactions between HIV and the complement system for better
understanding infection mechanisms and the major dysfunctions of B cells in
HIV-infected individuals.
Volume 81,
Issue 7,
pp. 1808-1818,
04/01/1993
Copyright © 1993 by The American Society of Hematology
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