Isolation of a TRAIL Antagonist from the Serum of HIV-infected Patients

• DOI: 10.1074/jbc.m111.274639
• Publication Date: 2011-08-23T00:49:46Z
• Authors: David J. Schnepple; Brett Shepard; Gary D. Bren; Nathan W. Cummins; Sekar Natesampillai; Sergey Trushin; Alicia Algeciras-...; Xue W. Meng; Amy M. Sainski; Stacey A. Rizza; Scott H. Kaufmann; Andrew D. Badley
• Keywords: Male; 0301 basic medicine; 0303 health sciences; T-Lymphocytes; HIV; Apoptosis; HIV Infections; 3. Good health; TNF-Related Apoptosis-Inducing Ligand; Alternative Splicing; Jurkat Cells; Receptors, TNF-Related Apoptosis-Inducing Ligand; 03 medical and health sciences; HEK293 Cells; Humans; Female

Virus-host interactions are characterized by the selection of adaptive mechanisms which to evade pathogenic and defense mechanisms, respectively. In primary T cells infected with HIV, HIV infection up-regulates TNF-related apoptosis inducing ligand (TRAIL) death-inducing TRAIL receptors, but blockade TRAIL:TRAIL receptor interaction does not alter HIV-induced cell death. Instead, results in a novel splice variant that we call TRAIL-short (TRAIL-s), antagonizes TRAIL-R2. patients, plasma TRAIL-s concentration increases increasing viral load renders resistant TRAIL-induced Knockdown abrogates this resistance. We propose is mechanism resistance acquired HIV-infected avoid their elimination TRAIL-dependent effector mechanism.