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Divergent regulation of HIV-1 replication in PBMC of infected individuals by CC chemokines: suppression by RANTES, MIP-1alpha, and MCP-3, and enhancement by MCP-1.
J Leukoc Biol. 2000 Sep; 68(3):405-12.JL

Abstract

We investigated the role of different CC chemokines, including regulated upon activation normal T cell expressed and secreted (RANTES), macrophage inflammatory protein-lalpha (MIP-1alpha), 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-1alpha, 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.

Authors+Show Affiliations

AIDS Immunopathogenesis Unit, San Raffaele Scientific Institute, Milan, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10985258

Citation

Vicenzi, E, et al. "Divergent Regulation of HIV-1 Replication in PBMC of Infected Individuals By CC Chemokines: Suppression By RANTES, MIP-1alpha, and MCP-3, and Enhancement By MCP-1." Journal of Leukocyte Biology, vol. 68, no. 3, 2000, pp. 405-12.
Vicenzi E, Alfano M, Ghezzi S, et al. Divergent regulation of HIV-1 replication in PBMC of infected individuals by CC chemokines: suppression by RANTES, MIP-1alpha, and MCP-3, and enhancement by MCP-1. J Leukoc Biol. 2000;68(3):405-12.
Vicenzi, E., Alfano, M., Ghezzi, S., Gatti, A., Veglia, F., Lazzarin, A., Sozzani, S., Mantovani, A., & Poli, G. (2000). Divergent regulation of HIV-1 replication in PBMC of infected individuals by CC chemokines: suppression by RANTES, MIP-1alpha, and MCP-3, and enhancement by MCP-1. Journal of Leukocyte Biology, 68(3), 405-12.
Vicenzi E, et al. Divergent Regulation of HIV-1 Replication in PBMC of Infected Individuals By CC Chemokines: Suppression By RANTES, MIP-1alpha, and MCP-3, and Enhancement By MCP-1. J Leukoc Biol. 2000;68(3):405-12. PubMed PMID: 10985258.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Divergent regulation of HIV-1 replication in PBMC of infected individuals by CC chemokines: suppression by RANTES, MIP-1alpha, and MCP-3, and enhancement by MCP-1. AU - Vicenzi,E, AU - Alfano,M, AU - Ghezzi,S, AU - Gatti,A, AU - Veglia,F, AU - Lazzarin,A, AU - Sozzani,S, AU - Mantovani,A, AU - Poli,G, PY - 2000/9/14/pubmed PY - 2000/9/23/medline PY - 2000/9/14/entrez SP - 405 EP - 12 JF - Journal of leukocyte biology JO - J. Leukoc. Biol. VL - 68 IS - 3 N2 - We investigated the role of different CC chemokines, including regulated upon activation normal T cell expressed and secreted (RANTES), macrophage inflammatory protein-lalpha (MIP-1alpha), 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-1alpha, 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. SN - 0741-5400 UR - https://www.unboundmedicine.com/medline/citation/10985258/Divergent_regulation_of_HIV_1_replication_in_PBMC_of_infected_individuals_by_CC_chemokines:_suppression_by_RANTES_MIP_1alpha_and_MCP_3_and_enhancement_by_MCP_1_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&amp;sid=nlm:pubmed&amp;issn=0741-5400&amp;date=2000&amp;volume=68&amp;issue=3&amp;spage=405 DB - PRIME DP - Unbound Medicine ER -