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

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 in...

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Published inVirology (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
LanguageEnglish
Published United States Elsevier Inc 01.03.2003
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Abstract 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.
AbstractList Chemokines play critical roles in HIV-1 infection, serving both to modulate viral replication and to recruit target cells to sites of infection. Interferon-gamma-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.
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.
Author Bock, Paul J
Strieter, Robert M
Coffey, Michael J
King, Steven R
Lane, Brian R
Markovitz, David M
Author_xml – sequence: 1
  givenname: Brian R
  surname: Lane
  fullname: Lane, Brian R
  organization: Division of Infectious Diseases, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI 48109-0640, USA
– sequence: 2
  givenname: Steven R
  surname: King
  fullname: King, Steven R
  organization: Division of Infectious Diseases, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI 48109-0640, USA
– sequence: 3
  givenname: Paul J
  surname: Bock
  fullname: Bock, Paul J
  organization: Division of Infectious Diseases, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI 48109-0640, USA
– sequence: 4
  givenname: Robert M
  surname: Strieter
  fullname: Strieter, Robert M
  organization: Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI 48109-0642, USA
– sequence: 5
  givenname: Michael J
  surname: Coffey
  fullname: Coffey, Michael J
  organization: Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI 48109-0642, USA
– sequence: 6
  givenname: David M
  surname: Markovitz
  fullname: Markovitz, David M
  email: dmarkov@umich.edu
  organization: Division of Infectious Diseases, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI 48109-0640, USA
BackLink https://www.ncbi.nlm.nih.gov/pubmed/12667820$$D View this record in MEDLINE/PubMed
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Snippet Chemokines play critical roles in HIV-1 infection, serving both to modulate viral replication and to recruit target cells to sites of infection....
Chemokines play critical roles in HIV-1 infection, serving both to modulate viral replication and to recruit target cells to sites of infection. Interferon-...
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SubjectTerms 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
Title The C-X-C chemokine IP-10 stimulates HIV-1 replication
URI https://dx.doi.org/10.1016/S0042-6822(02)00045-4
https://www.ncbi.nlm.nih.gov/pubmed/12667820
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https://search.proquest.com/docview/73161253
Volume 307
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