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<p>Achieving durable viral remission without antiretroviral therapy (ART) remains a central challenge in HIV-1 cure research. Using a pathogenic SIV model in male cynomolgus macaques, we investigated mucosal and systemic immune features associated with post-treatment control (PTC). Chronic SIV infection disrupts intestinal macrophage homeostasis, skewing the compartment toward a CX3CR1<sup>low</sup> inflammatory phenotype marked by increased expression of costimulatory and homing markers. This polarization is associated with mucosal CD4<sup>+</sup> T cell depletion, elevated neutrophil activation, and systemic cytokine induction. Non-controllers exhibit a similar inflammatory profile. In contrast, PTCs maintain CX3CR1<sup>high</sup> macrophages, preserve regulatory CD4 + T cells, and exhibit attenuated mucosal and systemic immune activation, resembling uninfected animals. CX3CR1<sup>high</sup> macrophage abundance inversely correlates with viral burden, T cell activation, and pro-inflammatory cytokines, suggesting a potential role in post-treatment control. These findings identify CX3CR1-expressing intestinal macrophages as a potential biomarker of mucosal immune regulation and highlight their relevance as targets in HIV cure strategies.</p>

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Maintenance of intestinal CX3CR1+ macrophage homeostasis defines post-treatment control in SIV-infected macaques

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月24日

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  • Stéphane Hua,
  • Keltouma Benmeziane,
  • Delphine Desjardins,
  • Nastasia Dimant,
  • Marco Leonec,
  • Laetitia Bossevot,
  • Julien Lemaitre,
  • Adeline Mélard,
  • Francis Relouzat,
  • Véronique Avettand-Fenoël,
  • Nathalie Dereuddre-Bosquet,
  • Asier Sáez-Cirión,
  • Roger Le Grand,
  • Mariangela Cavarelli

摘要

Achieving durable viral remission without antiretroviral therapy (ART) remains a central challenge in HIV-1 cure research. Using a pathogenic SIV model in male cynomolgus macaques, we investigated mucosal and systemic immune features associated with post-treatment control (PTC). Chronic SIV infection disrupts intestinal macrophage homeostasis, skewing the compartment toward a CX3CR1low inflammatory phenotype marked by increased expression of costimulatory and homing markers. This polarization is associated with mucosal CD4+ T cell depletion, elevated neutrophil activation, and systemic cytokine induction. Non-controllers exhibit a similar inflammatory profile. In contrast, PTCs maintain CX3CR1high macrophages, preserve regulatory CD4 + T cells, and exhibit attenuated mucosal and systemic immune activation, resembling uninfected animals. CX3CR1high macrophage abundance inversely correlates with viral burden, T cell activation, and pro-inflammatory cytokines, suggesting a potential role in post-treatment control. These findings identify CX3CR1-expressing intestinal macrophages as a potential biomarker of mucosal immune regulation and highlight their relevance as targets in HIV cure strategies.