A concurrent human papilloma virus (HPV) infection potentiates the efficacy of ionizing radiation for treatment of head and neck cancer by promoting apoptosis. Studies in cell culture indicated an opposite effect for photodynamic therapy (PDT) when this leads to mitochondrial and ER photodamage. The explanation for this difference in PDT efficacy remains to be established. While apoptosis was impaired in HPV(-) cells, such cells can be killed via photodamage directed at the ER: this leads to a nonapoptotic death pathway termed paraptosis. No differences in photosensitizer uptake or reactive oxygen species (ROS) production were observed in HPV(+) vs. HPV(-) tumors. We now provide evidence that death pathways initiated by ER/mitochondrial photodamage leading to either paraptosis or apoptosis are impaired in an HPV(+) head and neck cell line. These results illustrate the complex determinants of PDT efficacy, a topic that has yet to be fully explored.

中文翻译：

---

PDT 反应受损的特征

并发的人乳头瘤病毒（HPV）感染可通过促进细胞凋亡来增强电离辐射治疗头颈癌的疗效。细胞培养研究表明，当光动力疗法 (PDT) 导致线粒体和内质网光损伤时，会产生相反的效果。PDT 疗效差异的解释仍有待确定。虽然 HPV(-) 细胞的凋亡受到损害，但此类细胞可以通过针对 ER 的光损伤而被杀死：这会导致称为细胞凋亡的非凋亡死亡途径。在 HPV(+) 与 HPV(-) 肿瘤中未观察到光敏剂摄取或活性氧 (ROS) 产生存在差异。我们现在提供的证据表明，由 ER/线粒体光损伤引发的死亡途径导致 HPV(+) 头颈细胞系中的细胞凋亡或细胞凋亡受到损害。这些结果说明了 PDT 疗效的复杂决定因素，这是一个尚未得到充分探讨的话题。