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Blood, 1 November 2000, Vol. 96, No. 9, pp. 3109-3117
IMMUNOBIOLOGY
Interferon  and interleukin 6 modulate the susceptibility of
macrophages to human immunodeficiency virus type 1 infection
Marina Zaitseva,
Shirley Lee,
Cheryl Lapham,
Rolf Taffs,
Lisa King,
Tatiana Romantseva,
Jody Manischewitz, and
Hana Golding
From the Division of Viral Products, Center for
Biologics Evaluation and Research, Food and Drug Administration,
Bethesda, MD.
The effect of interferon  (IFN-) and interleukin 6 (IL-6) on
infection of macrophages with human immunodeficiency virus type 1 (HIV-1) was investigated. By using a polymerase chain reaction-based viral entry assay and viral infectivity assay, it was demonstrated that
IL-6 and IFN- augmented susceptibility of monocyte-derived macrophages (MDMs) to infection with T-cell tropic CXCR4-utilizing (X4)
HIV-1 strains. Consistent with this finding, IFN- and IL-6 augmented
fusion of MDMs with T-tropic envelope-expressing cells. The enhanced
fusion of cytokine-treated MDMs with T-tropic envelopes was
inhibited by the CXCR4 ligand, SDF-1, and by T22 peptide. IFN- and
IL-6 did not affect expression of surface CXCR4 or SDF-1-induced Ca++ flux in MDMs. In contrast to the effect of IFN- on
the infection of MDMs with X4 strains, IFN- inhibited viral entry
and productive infection of MDMs with macrophage-tropic (M-tropic)
HIV-1. Consistent with this finding, IFN- induced a decrease in
fusion with M-tropic envelopes that correlated with a modest reduction
in surface CCR5 and CD4 on MDMs. It was further demonstrated that
macrophage inflammatory protein (MIP)-1 and MIP- secreted by
cytokine-treated MDMs augmented their fusion with T-tropic-expressing
cells and inhibited their fusion with M-tropic envelope-expressing
cells. These data indicate that proinflammatory cytokines, which are
produced during opportunistic infections or sexually transmitted
diseases, may predispose macrophages to infection with X4 strains
that, in turn, could accelerate disease progression.
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