, and MCP-3, and enhancement by MCP-1
* AIDS Immunopathogenesis Unit, and
Division of Infectious Diseases, San Raffaele Scientific Institute, Milan;
Institute for Scientific Interchange Foundation, Torms, Italy;
Department of Immunology and Cell Biology, "Mario Negri" Institute for Pharmacological Research, Milan; and
Department of Biomedical Sciences and Biotechnology, University of Brescia, Italy
Correspondence: Dr. Guido Poli, P2/P3 Laboratories, DIBIT, Via Olgettina no. 58, 20132, Milano, Italy. E-mail: poli.guido{at}hsr.it
We investigated the role of different CC chemokines, including
regulated upon activation normal T cell expressed and secreted
(RANTES), macrophage inflammatory protein-1
(MIP-1), monocyte
chemotactic protein-1 (MCP-1), and MCP-3 on virus replication in
cultures established from CD8+ T cell-depleted peripheral
blood mononuclear cells (PBMC) of HIV-infected individuals that were
either cocultivated with allogeneic T cell blasts (ATCB) of uninfected
individuals or directly stimulated by mitogen plus interleukin-2.
RANTES was the only chemokine that showed a clear-cut suppressive
effect on HIV replication in both culture systems, although inhibitory
effects were frequently also observed with MIP-1, MCP-3, and,
occasionally, with MCP-1. In contrast, MCP-1 frequently enhanced HIV
production in most patients’ cultures or cocultures that were
characterized by secreting relatively low levels (<20 ng/mL) of MCP-1.
When CD8-depleted PBMC of HIV+ individuals were
cocultivated with ATCB of uninfected healthy donors, a positive
correlation was observed between MCP-1 concentrations and the
enhancement of HIV-1 replication occurring after depletion of
CD8+ cells from donors’ cells. Depletion of
CD14+ cells (monocytes) from ATCB resulted in the
down-regulation of virus replication during co-cultivation with
CD8-depleted PBMC of infected individuals. Of interest, MCP-1
up-regulated HIV production in these CD14-depleted ATCB cocultures.
Altogether these observations suggest that MCP-1 may represent an
important factor enhancing HIV spreading, particularly in anatomical
sites, such as the brain, where infection of macrophages and microglial
cells plays a dominant role.
Key Words: patients • CD8 • CD14
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