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EBNA-3a–deficient LCLs proliferate more slowly but surely and exhibit improved apoptosis when compared to wild-form virus–derived LCLs.
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These conclusions placement EBNA-3a similar to a vital modulator of B mobile proliferation and survival all through EBV latency, and for a relevant CD8⁺ T mobile objective in the two basic immunological experiments and translational examine.
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