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<p>Zika virus (ZIKV) infection can cause severe neurological complications, yet the role of CD8<sup>+</sup> T cells in controlling viral pathogenesis in the brain remains unclear. Using <i>Ifnar1</i><sup>−</sup>/<sup>−</sup> mice, which lack type I interferon signaling, we demonstrate that ZIKV infection triggers significant infiltration of CD8<sup>+</sup> T cells into the brain, accompanied by neurological defects. ZIKV-experienced CD8<sup>+</sup> T cells exhibit enhanced cytotoxic potential, and adoptive transfer of these cells improves survival. In contrast, blocking their infiltration exacerbates brain inflammatory and injury-associated signatures, highlighting their protective contribution. Furthermore, PD-1 blockade worsens ZIKV pathology, suggesting that PD-1 expression reflects an activated rather than exhausted state. These findings underscore an important role of infiltrating CD8<sup>+</sup> T cells in reducing ZIKV-induced CNS inflammation and suggest that modulating their response could serve as a potential therapeutic strategy for ZIKV-associated neurological disease.</p>

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Brain-infiltrating CD8 T cells retain functional activity to protect against acute Zika virus infection

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年1月5日

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  • Jaehui Kim,
  • Wooseong Lee,
  • Do Yeon Kim,
  • Keun Bon Ku,
  • Young-Chan Kwon,
  • Kyun-Do Kim,
  • Chonsaeng Kim,
  • Dae-Gyun Ahn,
  • Seong-Jun Kim,
  • Sungjun Park

摘要

Zika virus (ZIKV) infection can cause severe neurological complications, yet the role of CD8+ T cells in controlling viral pathogenesis in the brain remains unclear. Using Ifnar1−/− mice, which lack type I interferon signaling, we demonstrate that ZIKV infection triggers significant infiltration of CD8+ T cells into the brain, accompanied by neurological defects. ZIKV-experienced CD8+ T cells exhibit enhanced cytotoxic potential, and adoptive transfer of these cells improves survival. In contrast, blocking their infiltration exacerbates brain inflammatory and injury-associated signatures, highlighting their protective contribution. Furthermore, PD-1 blockade worsens ZIKV pathology, suggesting that PD-1 expression reflects an activated rather than exhausted state. These findings underscore an important role of infiltrating CD8+ T cells in reducing ZIKV-induced CNS inflammation and suggest that modulating their response could serve as a potential therapeutic strategy for ZIKV-associated neurological disease.