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Therefore, this therapy could be useful for those viruses that do not generate latency, such as SARS-CoV-2, but could be detrimental for viruses that do, since it promotes the increase of latent cells by increasing oxidative stress

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The most studied mechanisms include: upregulation of growth hormone receptors in fibroblasts (increasing sensitivity to healing signals), activation of the FAK-paxillin pathway (promoting cell adhesion and migration), modulation of the nitric oxide system through Src-Caveolin-1-eNOS phosphorylation (enhancing vascular function), and dual activation of the Egr-1/NAB2 gene loop (promoting organized, non-chaotic blood vessel growth)

Part I: complications and pathology and a review of designs