T cell signaling mechanisms that regulate HIV-1 infection

• Published in: Immunologic research 2001-01, Vol.23 (2-3), p.167-177
• Main Author: Unutmaz, D
• Format: Article
• Language: English
• Subjects: Antigen-Presenting Cells - immunology; CD4-Positive T-Lymphocytes - immunology; CD4-Positive T-Lymphocytes - virology; Cell Adhesion Molecules; Cytokines - physiology; Dendritic Cells - immunology; Gene Products, nef - physiology; HIV; HIV Infections - immunology; HIV Infections - virology; HIV-1 - physiology; Human immunodeficiency virus; Human immunodeficiency virus 1; Humans; Immunologic Memory; Immunology; Infections; Lectins - physiology; Lectins, C-Type; Lymphocyte Activation; Lymphoid Tissue - immunology; nef Gene Products, Human Immunodeficiency Virus; Proteins; Receptors, Cell Surface - physiology; Signal Transduction - physiology; T cell receptors; T-Lymphocyte Subsets - physiology; T-Lymphocyte Subsets - virology; Virus Replication - physiology
• ISSN: 0257-277X; 0257-277X; 1559-0755
• DOI: 10.1385/IR:23:2-3:167

The ability of human immunodeficiency virus type-1 (HIV-1) to establish a persistent infection is critically dependent on the cellular signals that regulate HIV-1 replication within target cells. The balance between numerous host factors that either enhance or suppress viral infection determines the clinical outcome. Perturbation of the steady-state level of viral replication can significantly influence the course and the speed at which the infection develops into clinical disease. Activation signals delivered to T cells by cytokines and antigen-presenting cells (APC), are key modulators of viral replication. Our laboratory seeks to decipher how HIV-1 exploits T cell signaling mechanisms and host factors that regulate viral replication. Elucidation of the molecular mechanisms by which cellular signals regulate the HIV-1 life cycle within target cells will significantly advance our understanding of host-virus interactions.