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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
The invisible agitators: exploring the viral interplay in psoriatic immune dysregulation
Snehasis Nayak1, Budhera Nithika Reddy2, Sri Vaibhav Kintali2
1University of Visayas Gullas College of Medicine, Cebu City, Banilad, 6000, Philippines. snehasisnayak37@gmail.com.
Abstract:
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.
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