Multiomic analysis of ART-interruption cohorts identifies cell-extrinsic and -intrinsic mechanisms driving lymphocyte-mediated control of HIV rebound
Tongcui Ma·Nadia R. Roan·Zichong Li·Sabrina M. Leddy·Mauricio Montaño·Douglas F. Nixon·Kyrlia C. Young·Christina Herrde·Maisha Adiba·Yusuke Matsui·Cédric Feschotte·Kailin Yin·Manickam Ashokkumar·Ulrike C. Lange·Min‐Gyoung Shin·Julia Prigann·Melanie Ott·Mohamed Abdel-Mohsen·Reuben Thomas·Julie Frouard·Edward P. Browne·Martin Tolstrup·Satish K. Pillai·Warner C. Greene·Ole S. Søgaard·Sulggi Lee·Jonathan Z. Li·Davey Smith·Nancie M. Archin·Robert Siliciano·Katherine S. Pollard·Steven Deeks·Ashley F. George
Immunological mechanisms regulating HIV rebound after antiretroviral therapy (ART) interruption remain unclear. We examined relationships between host factors, HIV reservoir, and HIV time-to-rebound after analytical treatment interruption (ATI) by characterizing pre-ATI peripheral blood mononuclear cells (PBMCs) from 75 ART-suppressed people with HIV (PWH) using high-parameter methods. Across interventional (CLEAR, TEACH, and REDUC) and non-interventional (A5345) cohorts, delayed rebound was not