Macrophages and lymphocytes differentially modulate the ability of RANTES to inhibit HIV-1 infection (original) (raw)
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Immunology and Inflammation Center, North Shore-LIJ Research Institute
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New York
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Immunology and Inflammation Center, North Shore-LIJ Research Institute
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New York
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Immunology and Inflammation Center, North Shore-LIJ Research Institute
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New York
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Department of Medicine, Albert Einstein College of Medicine
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New York
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Immunology and Inflammation Center, North Shore-LIJ Research Institute
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New York
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Immunology and Inflammation Center, North Shore-LIJ Research Institute
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New York
Correspondence: North Shore-LIJ Research Institute, 350 Community Drive, Manhasset, NY 11030. E-mail: HSchmidt@nshs.edu
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Revision received:
16 June 2003
Published:
01 November 2003
Cite
Eleanore Gross, Carol A Amella, Lorena Pompucci, Giovanni Franchin, Barbara Sherry, Helena Schmidtmayerova, Macrophages and lymphocytes differentially modulate the ability of RANTES to inhibit HIV-1 infection, Journal of Leukocyte Biology, Volume 74, Issue 5, November 2003, Pages 781–790, https://doi.org/10.1189/jlb.0403187
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Abstract
The β-chemokines MIP-1α, MIP-1β, and RANTES inhibit HIV-1 infection of CD4+ T cells by inhibiting interactions between the virus and CCR5 receptors. However, while β-chemokine-mediated inhibition of HIV-1 infection of primary lymphocytes is well documented, conflicting results have been obtained using primary macrophages as the virus target. Here, we show that the β-chemokine RANTES inhibits virus entry into both cellular targets of the virus, lymphocytes and macrophages. However, while virus entry is inhibited at the moment of infection in both cell types, the amount of virus progeny is lowered only in lymphocytes. In macrophages, early-entry restriction is lost during long-term cultivation, and the amount of virus produced by RANTES-treated macrophages is similar to the untreated cultures, suggesting an enhanced virus replication. We further show that at least two distinct cellular responses to RANTES treatment in primary lymphocytes and macrophages contribute to this phenomenon. In lymphocytes, exposure to RANTES significantly increases the pool of inhibitory β-chemokines through intracellular signals that result in increased production of MIP-1α and MIP-1β, thereby amplifying the antiviral effects of RANTES. In macrophages this amplification step does not occur. In fact, RANTES added to the macrophages is efficiently cleared from the culture, without inducing synthesis of β-chemokines. Our results demonstrate dichotomous effects of RANTES on HIV-1 entry at the moment of infection, and on production and spread of virus progeny in primary macrophages. Since macrophages serve as a reservoir of HIV-1, this may contribute to the failure of endogenous chemokines to successfully eradicate the virus.
© 2003 Society for Leukocyte Biology
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