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ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
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Review Article

Chemokine Deregulation in HIV Infection: Role of Interferon Gamma Induced Th1-Chemokine Signaling

Rajeev Mehla*, Debjani Guha and Velpandi Ayyavoo*
Department of Infectious Disease and Microbiology, Graduate School of Public Health, University of Pittsburgh, PA, USA
Corresponding Authors : Rajeev Mehla, Ph.D
Department of Infectious, Diseases and Microbiology
University of Pittsburgh, 416, Parran Hall, 130
De Soto Street, Pittsburgh, PA 15261, USA
Tel: (412)-624-3062
E-mail: [email protected]
  Yong-Gook Jung
Department of Economics
Wayne State University
656 W. Kirby Street
Detroit, MI 48202, USA
Tel: +1 313 577 3231
Fax: +1 313 577 9564
E-mail: [email protected]
Received August 29, 2012; Accepted September 14, 2012; Published September 21, 2012
Citation: Mehla R, Guha D, Ayyavoo V (2012) Chemokine Deregulation in HIV Infection: Role of Interferon Gamma Induced Th1-Chemokine Signaling. J Clin Cell Immunol S7:004. doi:10.4172/2155-9899.S7-004
Copyright: © 2012 Mehla R, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

One of the hallmarks of AIDS is the progressive decline in CD4+ T cells in peripheral blood of HIV-infected individuals. This review focuses on how HIV-1 modulates inflammatory molecules, especially C-X-C chemokine ligand 10 (CXCL10), a Th1-chemoattractant chemokine to establish infection. HIV-infected T-cells, lead by Th1- agonist chemokines, gain access to the LNs where they die upon activation. The resultant T-cell death positively correlates with severe immunodeficiency and deteriorating HIV-1-infected patient’s health. CXCL10 is produced by wide range of cells (macrophages, neutrophils, endothelial cells, and astrocytes) in response to inflammation and attracts T-lymphocytes and NK cells to the site of infection. Increased level of CXCL10 is found in body fluids (Serum, and cerebrospinal fluid) of HIV-1 infected subjects and it correlates with disease severity. Furthermore, HIV-induced high levels of Th1 chemokines are accounted for failed taxing of effector T cells from lymphoid organs to the site of infection. Thus, the ability of effector T cells to combat viral infection comes to halt, failing ‘adaptive immunity’. CXCL10 is considered a positive indicator of the onset of HIV-associated neurocognitive disease in HIV-1 infected individuals. This review summarizes the current understanding of CXCL10 impact on development of central nervous system (CNS) abnormality. We hypothesize that drugs targeting chemotaxis of immune cells into brain might prove useful in the treatment of HIV-associated neurocognitive disorders (HAND). Further research in deciphering the role of chemotaxis will prove useful for better understanding of HIV pathogenesis both in periphery and brain.

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