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Institut National de la Santé et de la Recherche Médicale Unité 430, Hôpital Broussais; and
Institut National de la Santé et de la Recherche Médicale Unité 255, Institut Curie, Paris, France
We demonstrate that soluble CD16 (sCD16; soluble Fc
RIII), a
natural ligand of CR3, inhibits the infection of monocytes by primary
R5 HIV-1 strain opsonized with serum of seronegative individuals.
Inhibition of monocyte infection by sCD16 was similar to that observed
with anti-CR3 mAbs, indicating that opsonized HIV may use a
CR3-dependent pathway for entry in monocytic cells. Cultured human
monocytes express both CR3 (CD11b/CD18) and CCR5 receptors. RANTES, the
natural ligand of CCR5, inhibited infection of monocytes with
unopsonized HIV particles and partially that of monocytes infected with
HIV particles opsonized with complement-derived fragments. Although
HIV-infected monocytes from homozygous CCR5 
32/ 32 (CCR5-/-)
individuals produce low levels of p24, cells infected with opsonized
particles produced higher levels of p24 than cells infected with
unopsonized particles. Our results thus suggest that CR3 may represent
an alternative coreceptor to CCR5 of opsonized primary R5 virus entry
into monocytes/macrophages. We also observed that the concentration of
sCD16 is greatly decreased in sera of HIV-infected patients with low
lymphocyte CD4+ counts. Taken together, our findings
suggest that sCD16, present in plasma, may play an important role in
controlling HIV-1 spread.
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