ZFIN Image: Wu et al., 2021, Fig. 8

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Fig. 8

Proposed model illustrating how histone H2A is utilized by SVCV to evade host immune response. Histone H2A is nuclear-localized in the absence of pathogen infection. SVCV infection promotes histone H2A nuclear/cytoplasmic trafficking. In the cytoplasm, histone H2A degrades TBK1 and IRF3, which lead to the impaired formation of TBK1-IRF3 functional complex and the decreased expression of nuclear IRF3 protein. In the cell nucleus, the impaired expressions of IRF3 and/or histone H2A inhibit transcriptional regulation of immune genes, and impede the production of type I IFNs and ISGs in response to SVCV infection.

Acknowledgments

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