King Irena V, Aid Malika, Kose Emek, Immonen Taina T, Goodman Charles A, Fennessey Christine M, Colarusso Alessandro, Walker-Sperling Victoria E K, Borducchi Erica N, Geleziunas Romas, Rinaldi William J, Ferguson Melissa J, Picker Louis J, Lifson Jeffrey D, Keele Brandon F, Barouch Dan H
Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Harvard-MIT Health Sciences and Technology Program, Cambridge, MA, USA.
bioRxiv. 2025 Aug 30:2025.08.30.673277. doi: 10.1101/2025.08.30.673277.
The vast majority of persons living with HIV-1 who discontinue antiretroviral therapy (ART) demonstrate viral rebound, but the tissue-level events that lead to rebound viremia are poorly understood. Here we report the origin, dynamics, and correlates of viral rebound in 16 rhesus macaques (RMs) infected with molecularly barcoded SIVmac239M, treated with ART for 70 weeks, and necropsied on day 12 after ART discontinuation. Barcode analysis of plasma following ART discontinuation identified 1 to 38 rebounding barcode-defined viral lineages per animal, with 1 to 4 rebounding lineages contributing to first measurable rebound viremia. Analysis of barcode viral RNA (vRNA) expression in necropsy tissues revealed presumptive anatomic origin sites for 56 of 175 total rebounding viral lineages, with significant enrichment in the gastrointestinal (GI) tract and GI-associated lymph nodes. Daily transcriptomic and proteomic profiling in peripheral blood following ART discontinuation showed upregulation of pathways related to T cell signaling, cytokine responses, and cellular metabolism prior to detectable rebound viremia. These data suggest that viral rebound following ART discontinuation is initiated by local tissue replication of a limited number of clonal lineages, followed by systemic expansion of the initial rebounding lineages and serial initiation of replication of multiple additional clonal lineages. These findings provide mechanistic insights into the processes that result in viral rebound following ART discontinuation and will contribute to next generation HIV-1 cure strategies.
绝大多数停止抗逆转录病毒疗法(ART)的HIV-1感染者会出现病毒反弹,但导致病毒血症反弹的组织水平事件却知之甚少。在此,我们报告了16只感染分子条形码SIVmac239M的恒河猴(RMs)的病毒反弹起源、动态变化及其相关因素。这些猴子接受了70周的ART治疗,并在停止ART治疗后的第12天进行了尸检。停止ART治疗后对血浆进行条形码分析,结果显示每只动物有1至38个由条形码定义的病毒谱系出现反弹,其中1至4个反弹谱系导致了首次可检测到的病毒血症反弹。对尸检组织中条形码病毒RNA(vRNA)表达的分析揭示了175个总反弹病毒谱系中56个的推定解剖起源部位,在胃肠道(GI)及与GI相关的淋巴结中显著富集。停止ART治疗后对外周血进行的每日转录组和蛋白质组分析显示,在可检测到的病毒血症反弹之前,与T细胞信号传导、细胞因子反应和细胞代谢相关的通路出现上调。这些数据表明,停止ART治疗后的病毒反弹是由有限数量的克隆谱系在局部组织中复制引发的,随后是初始反弹谱系的全身扩散以及多个其他克隆谱系复制的相继启动。这些发现为停止ART治疗后导致病毒反弹的过程提供了机制性见解,并将有助于下一代HIV-1治愈策略的制定。