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<p>HIV-transcribing cells can perpetuate chronic inflammation in ART-suppressed people with HIV (PWH) and likely contribute to viral rebound after ART interruption. However, these cells are difficult to study using single-cell RNA-seq (scRNA-seq) due to their low frequency and low levels of HIV transcripts, which are usually not polyadenylated. By spiking in capture sequences targeting conserved regions of HIV during scRNA-seq – a new method we call “HIV-seq” - we detect double the mean number of HIV reads per cell from PWH. HIV RNA+ cells are enriched among T effector memory cells during both viremia and ART suppression but exhibit a cytotoxic signature during viremia only. In contrast, HIV-transcribing cells from ART-suppressed timepoints exhibit a distinct anti-inflammatory signature involving elevated TGF-β and diminished IFN signaling. These findings demonstrate that HIV-seq is a useful tool to better understand the mechanisms by which HIV-transcribing cells can persist during ART.</p>

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HIV-seq reveals gene expression differences between HIV-transcribing cells from viremic and suppressed people with HIV

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月3日

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  • Julie Frouard,
  • Sushama Telwatte,
  • Xiaoyu Luo,
  • Natalie Gill,
  • Reuben Thomas,
  • Douglas Arneson,
  • Pavitra Roychoudhury,
  • Atul J. Butte,
  • Joseph K. Wong,
  • Rebecca Hoh,
  • Steven G. Deeks,
  • Sulggi A. Lee,
  • Nadia R. Roan,
  • Steven A. Yukl

摘要

HIV-transcribing cells can perpetuate chronic inflammation in ART-suppressed people with HIV (PWH) and likely contribute to viral rebound after ART interruption. However, these cells are difficult to study using single-cell RNA-seq (scRNA-seq) due to their low frequency and low levels of HIV transcripts, which are usually not polyadenylated. By spiking in capture sequences targeting conserved regions of HIV during scRNA-seq – a new method we call “HIV-seq” - we detect double the mean number of HIV reads per cell from PWH. HIV RNA+ cells are enriched among T effector memory cells during both viremia and ART suppression but exhibit a cytotoxic signature during viremia only. In contrast, HIV-transcribing cells from ART-suppressed timepoints exhibit a distinct anti-inflammatory signature involving elevated TGF-β and diminished IFN signaling. These findings demonstrate that HIV-seq is a useful tool to better understand the mechanisms by which HIV-transcribing cells can persist during ART.