Journal of Clinical and Cellular Immunology
Open Access

Abstract

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

Rajeev Mehla, Debjani Guha and Velpandi Ayyavoo

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.