KSHV miRNAs target STING to evade innate immunity and facilitate KSHV lytic reactivation from latency
Kaposi sarcoma-associated herpesvirus (KSHV) employs various strategies to evade host immune surveillance and maintain lifelong latency. The cyclic GMP-AMP synthase (cGAS)/stimulator of interferon genes (STING) DNA sensing pathway is a key innate immunity pathway that detects viral DNA and restricts KSHV lytic replication upon reactivation from latency. Here, we identify three KSHV microRNAs (miRNAs), miR-K12-6-3p, miR-K12-7-3p, and miR-K12-11-3p, that directly bind to STING1 mRNA to repress its translation and inhibit downstream immune signaling. Exogenous delivery of these KSHV miRNAs led to decreased STING expression and attenuated cGAS/STING signaling in response to STING agonist stimulation. Conversely, genetic deletion of these KSHV miRNAs rescued STING and interferon-stimulated gene expression in latent KSHV cell lines, delaying KSHV lytic reactivation and reducing KSHV lytic gene expression. These findings shed light on the immune evasion strategy of KSHV miRNA-mediated STING repression, representing the discovery of viral miRNAs that target STING.
Authors
- Kimberly Paulsen
- Lauren A. Gay (ORCID: https://orcid.org/0000-0001-5715-6717)
- Zhe Ma (ORCID: https://orcid.org/0000-0002-7222-2556)
- Rosenna Chan
Institutions
- University of Florida Health (US)
- University of Florida (US)
- Florida College (US)
Publication Details
- Journal
- Cell Reports
- Published
- 2025-05-24
- DOI
- https://doi.org/10.1016/j.celrep.2025.115741
- Citations
- 3
- Primary Topic
- Viral Infections and Vectors
- Type
- article
- Field-Weighted Citation Impact
- 4.19
Funders
- American Cancer Society
- University of Florida
- University of Florida Health
- National Cancer Institute
- National Institute of Allergy and Infectious Diseases