Nayak Snehasis, Reddy Budhera Nithika, Kintali Sri Vaibhav
University of Visayas Gullas College of Medicine, Cebu City, Banilad, 6000, Philippines.
Immunol Res. 2025 Oct 4;73(1):140. doi: 10.1007/s12026-025-09692-9.
This review explores the complex interplay between viral infections and psoriasis. It emphasizes how viruses like HIV, hepatitis, herpes, human papillomavirus, and SARS-CoV-2 can provoke and worsen psoriatic inflammation by disturbing immune balance. A key focus of the discussion is the IL-23/Th-17 pathway, which drives the production of proinflammatory cytokines that promote keratinocyte overgrowth and perpetuate chronic skin inflammation. Our article further investigates how disrupted intracellular pathways-such as those involving PI3K, Wnt signaling, and caveolin-affect the severity of the disease. This review supports the idea that viral infections can not only trigger psoriatic lesions but may also increase the risk of additional viral reactivation, thereby complicating the clinical picture of psoriasis. This thorough evaluation highlights the necessity for focused research to create innovative therapeutic strategies aimed at these viral triggers.
本综述探讨了病毒感染与银屑病之间复杂的相互作用。它强调了诸如艾滋病毒、肝炎病毒、疱疹病毒、人乳头瘤病毒和新型冠状病毒等病毒如何通过扰乱免疫平衡引发并加重银屑病炎症。讨论的一个关键焦点是白细胞介素-23/辅助性T细胞17（IL-23/Th-17）途径，该途径驱动促炎细胞因子的产生，促进角质形成细胞过度生长并使慢性皮肤炎症持续存在。我们的文章进一步研究了诸如涉及磷脂酰肌醇-3激酶（PI3K）、Wnt信号传导和小窝蛋白的细胞内途径紊乱如何影响疾病的严重程度。本综述支持这样一种观点，即病毒感染不仅可以引发银屑病皮损，还可能增加额外病毒再激活的风险，从而使银屑病的临床情况复杂化。这种全面评估凸显了开展针对性研究以制定针对这些病毒触发因素的创新治疗策略的必要性。
