AI Article Synopsis
- Kaposi's sarcoma (KS) is the most prevalent cancer among HIV patients, driven by the Kaposi's sarcoma-associated herpesvirus (KSHV) and characterized by hyperinflammation.
- The study reveals that KSHV promotes hyperinflammation by increasing IL-1α and decreasing IL-1Ra through mechanisms involving KSHV miRNAs and vFLIP that activate the NF-κB pathway.
- Dexamethasone, an anti-inflammatory drug, can mitigate KSHV-induced hyperinflammation and tumor growth by enhancing glucocorticoid receptor signaling, suggesting IL-1-related inflammation as a promising treatment target.
Article Abstract
Kaposi's sarcoma (KS) is the most common cancer in HIV-infected patients caused by Kaposi's sarcoma-associated herpesvirus (KSHV) infection. Hyperinflammation is the hallmark of KS. In this study, we have shown that KSHV mediates hyperinflammation by inducing IL-1α and suppressing IL-1Ra. Mechanistically, KSHV miRNAs and vFLIP induce hyperinflammation by activating the NF-κB pathway. A common anti-inflammatory agent dexamethasone blocks KSHV-induced hyperinflammation and tumorigenesis by activating glucocorticoid receptor signaling to suppress IL-1α and induce IL-1Ra. This work has identified IL-1-mediated inflammation as a potential therapeutic target and dexamethasone as a potential therapeutic agent for KSHV-induced malignancies.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10790708 | PMC |
| http://dx.doi.org/10.1128/mbio.03011-23 | DOI Listing |
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