Open AccessHIV elite control is associated with reduced TRAILshort expression
Author(s) -
Ana C. Paim,
Nathan W. Cummins,
Sekar Natesampillai,
Enrique Garcia-Rivera,
Leonardo Clemente,
Ujjwal Neogi,
Anders Sönnerborg,
Maike Sperk,
Gary D. Bren,
Steven G. Deeks,
Eric C. Polley,
Andrew D. Badley
Publication year - 2019
Publication title -
aids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.195
H-Index - 216
eISSN - 1473-5571
pISSN - 0269-9370
DOI - 10.1097/qad.0000000000002279
Subject(s) - context (archaeology) , peripheral blood mononuclear cell , biology , immunology , apoptosis , gene expression , programmed cell death , virology , gene , genetics , in vitro , paleontology
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) dependent apoptosis has been implicated in CD4 T-cell death and immunologic control of HIV-1 infection. We have described a splice variant called TRAILshort, which is a dominant negative ligand that antagonizes TRAIL-induced cell death in the context of HIV-1 infection. HIV-1 elite controllers naturally control viral replication for largely unknown reasons. Since enhanced death of infected cells might be responsible, as might occur in situations of low (or inhibited) TRAILshort, we tested whether there was an association between elite controller status and reduced levels of TRAILshort expression.