研究团队提出用 Crispr 作为「泛流感」抗病毒策略，核心是利用 Cas13 专攻 RNA：流感病毒基因组全是 RNA，Cas13 在导引 RNA 的指引下切断病毒 RNA，让复制链条中断。构想的给药型态是鼻喷或注射，用脂质奈米粒子把两段讯息送进呼吸道感染细胞：一段 mRNA 让细胞制造 Cas13，另一段导引 RNA 精准锁定病毒序列；亦被设想成流行季的短期预防工具。

需求端的数字很直观：仅流感 A 型在美国每年约造成 12,000 到 52,000 人死亡，随季节严重度上下波动，显示现有药物与防护仍不稳定。传统抗病毒药如 Tamiflu 多针对特定株，容易快速出现抗药性；相较之下，Cas13 可被设计去瞄准「保守区段」——几乎所有流感株都共有、且对存活关键的 RNA 片段，以降低株别差异带来的失效风险。

风险与验证也被量化到「可观察」层级：外源细菌蛋白可能引发免疫反应，且存在 off-target 风险（误切人体 RNA）。哈佛 Wyss 以人类肺与血管细胞建立 lung-on-a-chip，报告显示 Cas13 系统可抑制多株流感（包含 2009 年 H1N1 与本季较严重的 H3N2），且未观察到明显 off-target，同时降低发炎介质；但真正把载体送达肺深部肺泡细胞仍是工程难题。另一路线是用 Cas9 调整宿主因子：敲除筛选指出流感依赖 SLC35A1（影响细胞表面糖受体），未来可能探索在特定组织、短暂下调而非永久移除的策略。

Researchers propose a “pan-influenza” antiviral approach using CRISPR, centered on Cas13, which targets RNA. Because influenza’s genome is entirely RNA, Cas13 can be guided to cut viral RNA and halt replication. The delivery concept is a nasal spray or injection using lipid nanoparticles carrying two instructions: an mRNA that makes cells produce Cas13 and a guide RNA that directs it to conserved viral sequences. The same setup is framed as both treatment and short-term prophylaxis during severe seasons.

The numerical public-health case is stark: influenza A alone is cited as killing about 12,000 to 52,000 Americans annually, with wide season-to-season swings. Existing antivirals such as Tamiflu tend to be strain-limited and can quickly select for resistance, motivating strategies that target conserved regions shared across most strains. Other “pan-flu” ideas mentioned include monoclonal antibodies aimed at conserved targets and drugs that boost interferon signaling.

Key risks are immune reactions to a foreign bacterial protein and off-target cleavage of human RNAs. A Harvard Wyss “lung-on-a-chip” safety assessment reports Cas13-equipped cells suppressed replication of multiple strains, including 2009 H1N1 and H3N2, with no observed off-target effects and reduced inflammatory mediators, but delivery to deep alveolar cells remains difficult. A second CRISPR route uses Cas9 to find host factors; gene knockout screens highlight SLC35A1, suggesting transient, localized downregulation could potentially blunt influenza entry while limiting toxicity.