Isolation of a TRAIL antagonist from the serum of HIV-infected patients

David J. Schnepple, Brett Shepard, Gary D. Bren, Nathan W. Cummins, Sekar Natesampillai, Sergey Trushin, Alicia Algeciras-Schimnich, Xue W. Meng, Amy M. Sainski, Stacey A. Rizza, Scott H. Kaufmann, Andrew D. Badley

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


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

Original languageEnglish (US)
Pages (from-to)35742-35754
Number of pages13
JournalJournal of Biological Chemistry
Issue number41
StatePublished - Oct 14 2011

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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