Open AccessTh17 cell master transcription factor RORC2 regulates HIV-1 gene expression and viral outgrowth
Author(s) -
Tomas Raul Wiche Salinas,
Yuwei Zhang,
Daniele Sarnello,
Alexander Zhyvoloup,
Laurence Raymond Marchand,
Augustine Fert,
Delphine Planas,
Manivel Lodha,
Debashree Chatterjee,
Katarzyna Karwacz,
Sally Oxenford,
JeanPierre Routy,
David M. Irlbeck,
Heather Amrine-Madsen,
Petronela Ancuța,
Ariberto Fassati
Publication year - 2021
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.2105927118
Subject(s) - biology , viremia , retinoic acid , viral replication , enhancer , transcription factor , gene expression , virology , microbiology and biotechnology , gene , virus , genetics
Significance HIV-1 infects CD4 T cells, and, among these, T helper 17 (Th17) cells are known to be particularly permissive for virus replication. The infection of Th17 cells is critical for AIDS pathogenesis and viral persistence. It is, however, not clear why these cells are highly permissive to HIV-1. We found that Th17 cell permissiveness depends on the expression of the hormone receptor RORC2, which is the master transcriptional regulator of Th17 cell differentiation. We identify RORC2 as a cell-specific host-dependency factor that can be targeted by small molecules. Our results suggest that RORC2 may be a cell-specific target to mitigate the loss of Th17 cells as a consequence of their preferential HIV-1 infection.