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. 2023 Jul 12;9(28):eadg5175. doi: 10.1126/sciadv.adg5175

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Copyright © 2023 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC).

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Fig. 10. — Avian polymerase functions efficiently in avian cells due to high levels of vRNP assembly and strong chANP32A-vRNP interaction. However, in human cells, avian polymerase functions poorly due to limited vRNP assembly and weak huANP32A/B-vRNP interactions. Under infection conditions, the viral protein NS2 relies on its SIM to compensate for the defects in vRNP assembly and huANP32A/B-vRNP interactions, thereby greatly enhancing avian vPol activity and the replication capacity of AIVs. Impairment of SIM in NS2 caused it to lose its ability to promote vRNP assembly and huANP32A/B-vRNP interactions, thereby losing its avian polymerase-enhancing properties. Overall, we have identified a previously unknown mechanism by which AIVs use the SIM in NS2 to help their polymerase adapt to mammalian ANP32A/B.