Barrier-to-autointegration factor 1 promotes gammaherpesvirus reactivation from latency

Grant Broussard, Guoxin Ni, Zhigang Zhang, Qian Li, Patricio Cano, Dirk P. Dittmer and Blossom Damania ()
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Grant Broussard: University of North Carolina at Chapel Hill
Guoxin Ni: University of North Carolina at Chapel Hill
Zhigang Zhang: University of North Carolina at Chapel Hill
Qian Li: University of North Carolina at Chapel Hill
Patricio Cano: University of North Carolina at Chapel Hill
Dirk P. Dittmer: University of North Carolina at Chapel Hill
Blossom Damania: University of North Carolina at Chapel Hill

Nature Communications, 2023, vol. 14, issue 1, 1-14

Abstract: Abstract Gammaherpesviruses, including Kaposi sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV), are DNA viruses that are globally associated with human cancers and establish lifelong latency in the human population. Detection of gammaherpesviral infection by the cGAS-STING innate immune DNA-sensing pathway is critical for suppressing viral reactivation from latency, a process that promotes viral pathogenesis and transmission. We report that barrier-to-autointegration factor 1 (BAF)-mediated suppression of the cGAS-STING signaling pathway is necessary for reactivation of KSHV and EBV. We demonstrate a role for BAF in destabilizing cGAS expression and show that inhibiting BAF expression in latently infected, reactivating, or uninfected cells leads to increased type I interferon-mediated antiviral responses and decreased viral replication. Furthermore, BAF overexpression resulted in decreased cGAS expression at the protein level. These results establish BAF as a key regulator of the lifecycle of gammaherpesviruses and a potential target for treating viral infections and malignancies.

Date: 2023
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DOI: 10.1038/s41467-023-35898-2

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