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As SARS-CoV-2 virus has 80 % homology to SARS coronavirus, it probably uses similar mechanisms (Reference Koyama, Platt and Parida36)
Concurrent inhibition or deletion of GCN2 may permit sustained mitochondrial and anabolic activity, which can increase ROS generation, while preventing activation of stress-response pathways that otherwise restrain T cell proliferation and effector differentiation
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