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5
B Cells in the Line of Sight of HIV-1
Yolande Richard,* Eric A. Lef Á vre,* Roman Krzysiek,* Christophe
Legendre, y Dominique Dormont, y Pierre Galanaud,* and Gabriel Gras y
* INSERM U 131, Institut Paris-Sud sur les Cytokines, Clamart, France;
y
Service de Neurovirologie, CEA/CRSSA, Institut Paris-Sud sur les
Cytokines, Fontenay aux Roses, France
INTRODUCTION
Infection with human immunode®ciency virus (HIV )-1 results in a wide spec-
trum of clinical manifestations. HIV-1 preferentially infects CD4 cells includ-
ing monocytes, T cells, and cells from the central nervous system (CNS), but
the peripheral B cells of HIV patients have an abnormal phenotype (Amadori
and Chieco-Bianchi, 1990; Lane et al., 1983; Martinez-Maza et al., 1987) and
spontaneously produce high levels of antibodies (Ab) (Amadori et al., 1989).
Forster et al. recently reported a decrease in CXCR5 expression, a chemokine
receptor important for the migration of B cells into lymphoid organs, on periph-
eral B cells from HIV patients ( Forster et al., 1997). Within lymphoid organs,
HIV replication occurs mainly in areas essential for antigen-speci®c T-B inter-
actions, and germinal centers (GC) are required for HIV-1 replication ( Hufert
et al., 1997; Pantaleo et al., 1995). Soon after HIV infection, strong follicular
hyperplasia is detectable within the lymphoid organs of HIV patients and
persists throughout the asymptomatic phase, whereas it rapidly decreases dur-
ing normal immune responses (Cohen et al., 1995; Racz et al., 1986). In addi-
tion to an increase in size and disorganization of the follicular dendritic cells
( FDC) network, we have observed a thin and frequently disrupted mantle zone,
a loss of GC polarization, and a decrease in CD80 expression on GC B cells of
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