The C-X-C chemokine IP-10 stimulates HIV-1 replication

• Published in: Virology (New York, N.Y.) Vol. 307; no. 1; pp. 122 - 134
• Main Authors: Lane, Brian R, King, Steven R, Bock, Paul J, Strieter, Robert M, Coffey, Michael J, Markovitz, David M
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.03.2003
• Subjects: Cell Adhesion; Cells, Cultured; DNA Primers; DNA, Viral - genetics; Gene Expression Regulation, Viral; Genes, Reporter; HIV Long Terminal Repeat; HIV-1 - genetics; HIV-1 - pathogenicity; HIV-1 - physiology; Humans; Leukocytes, Mononuclear - physiology; Leukocytes, Mononuclear - virology; Luciferases - genetics; Lymphocytes - physiology; Lymphocytes - virology; Polymerase Chain Reaction - methods; Receptors, Chemokine - physiology; Receptors, CXCR3; Recombinant Proteins - metabolism; RNA-Directed DNA Polymerase - analysis; Transfection; Virus Replication - physiology
• ISSN: 0042-6822; 1096-0341
• DOI: 10.1016/S0042-6822(02)00045-4

Chemokines play critical roles in HIV-1 infection, serving both to modulate viral replication and to recruit target cells to sites of infection. Interferon-γ-inducible protein 10 (IP-10/CXCL10) is a C-X-C chemokine that acts specifically upon activated T cells and macrophages and attracts T cells into the cerebrospinal fluid (CSF) in HIV-associated neurological disease. We now demonstrate that IP-10 stimulates HIV-1 replication in monocyte-derived macrophages and peripheral blood lymphocytes. We further demonstrate that neutralization of endogenous IP-10 or blocking the function of its receptor, CXCR3, reduces HIV-1 replication in these same cells. Therefore, blocking the interaction between IP-10 and CXCR3 represents a possible new target for anti-retroviral therapy.