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These conclusions position EBNA-3a similar to a critical modulator of B cellular proliferation and survival during EBV latency, and being a relevant CD8⁺ T mobile goal in The 2 simple immunological experiments and translational examine.
Amid these latency proteins, EBNA-3a plays a supportive but non-important part in B mobile transformation: EBV mutants lacking EBNA-3a can however change B cells, but with considerably decreased performance.
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EBNA-3a appears to manage a subset of cellular genes, lots of which overlap with People today controlled by EBNA2. The 2 proteins can act antagonistically or cooperatively to control gene expression.
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