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Finally, we illustrate the issues that need to be addressed to develop ICH as a therapeutic agent

In the lungs, after entering in type II alveolar cells, SARS-CoV-2 infected cells become defective for surfactant production (Ghati et al., 2021) and release cytokines, like IL-8 among others, which in turn activate alveolar macrophages to release IL-1, IL-6, and TNF-, that induce natural killer and dendritic cell differentiation and macrophage M1 polarization, enhancing the proinflammatory response with increased vasodilation causing neutrophil and activated T cell influx from the capillaries into the alveolus, all leading to the cytokine storm (Carcaterra and Caruso, 2021

Introducing EBNA1-targeting gRNAs into EBV-positive CNE2 cells resulted in substantially reduced GFP fluorescent signals (Fig

10.1016/j.xcrm.2024.101706 206 ZhuY.LiuC.NadimintyN.LouW.TummalaR.EvansC