Expression Analysis of Cell Surface Markers: Cluster of Differentiation 4, Chemokine Receptor 5 and C-X-C Chemokine Receptor Type 4 in Different Cell Lines after Infection with HIV

S L Balakrishna,Bharti Gupta,Parikipandla Sridevi

doi:10.21767/2471-9676.100046

Abstract

The host cell infection by Human Immunodeficiency Virus (HIV) is initiated through the entry of the virus into the cell. The major target cells of HIV are cluster of differentiation 4 (CD4)+ T lymphocytes, which express co-receptors, chemokine receptor 5 (CCR5) or C-X-C chemokine receptor type 4 (CXCR4). HIV-1 envelope glycoprotein 120 (Gp120) binds to its primary receptor CD4, a member of the immunoglobulin superfamily enhances T-Cell Receptor (TCR)-mediated signaling, is absolutely required for the infection. Recent reports on cell surface marker expression levels by infecting CD4+ T cells with HIV-1 viruses gave an insight into host cell responses. In our study, we infected Jurkat, SupT1 cells and PBMCs with HIV-1 and analyzed the expression of cell surface markers gp120, CD4, CCR5 and CXCR4 levels by quantitative real time PCR (qRT-PCR) at different time intervals of post infection. Our study shows that there is ~ 5-fold increase in expression of gp120 1 h post infection and 1.5-fold increase in relative expression of CD4 and CCR5 at 2 h post infection, whereas CXCR4 showed differential up-regulation in different cell lines which needs further analysis.

Highlights

Human Immunodeficiency Virus (HIV) is a retrovirus that causes Acquired Immune deficiency Syndrome (AIDS)
HIV-1 entry is initiated by gp120 binding to cellular cluster of differentiation 4 (CD4) [3], which is a high-affinity interaction that facilitates the initial attachment of virus to the target cell
glycoprotein 120 (Gp120) up-regulated at 1 h after HIV infection and showed a steady decrease from 2 h to 4 h

Summary

Introduction

Human Immunodeficiency Virus (HIV) is a retrovirus that causes Acquired Immune deficiency Syndrome (AIDS). One of the principal cellular targets of HIV infection is the cluster differentiation 4 positive (CD4+) T lymphocytes [1]. HIV infects T cells via interaction between glycoprotein gp120 and the CD4 molecule [2]. Infection of T cells is assisted by the interaction of T cells with C-X-C Chemokine receptor type 4 (CXCR4) and C-C Chemokine receptor type 5 (CCR5) co-receptors. The envelope of HIV-1 mediates virus entry into cells, which comprises surface gp120 glycoproteins non-covalently linked to transmembrane gp glycoprotein that/which embed the complex into the viral membrane. HIV-1 entry is initiated by gp120 binding to cellular CD4 [3], which is a high-affinity interaction that facilitates the initial attachment of virus to the target cell. The binding of gp120 to receptor CD4 results in a conformational change in gp120 which exposes the binding site for chemokine receptors CCR5 or CXCR4 [4,5]

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