ArticleProceedings of the National Academy of Sciences of the United States of America2026
Cellular antibody affinity-based CRISPR screening identifies JUNB as a broadly acting antiviral factor.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
CRISPR screening is a powerful approach to identify genetic perturbations that impact viral infection. However, most virus-focused CRISPR screens utilize selection strategies that limit the ability to identify genes important for infection. Here, we developed a CRISPR screening pipeline to identify cellular determinants of human cytomegalovirus (HCMV) infection based on virally induced remodeling of cellular antibody affinity (VIRCAA), which is scalable for large libraries and can identify cellular genes that impact HCMV infection at different life cycle stages. We utilized this pipeline to interrogate proteomic and transcriptomic datasets associated with the HCMV UL26 protein, which blocks antiviral signaling during infection. We find that JUNB drives antiviral gene expression, induces protein ISGylation, and suppresses diverse viral infections. Further, UL26 interacts with JUNB and suppresses JUNB-mediated condensation of viral DNA replication compartments. These results highlight the VIRCAA pipeline's utility for identifying important determinants of viral infection.
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