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Patients with various degrees of TBI may suffer from a long period of secondary injury, which plays a key role in determining the final severity and recovery of nerve injury after TBI ( FIGURE 1 Inflammation Neuroinflammation is a key pathophysiological mechanism of secondary injury, as it can produce neurotoxic effects on neurons through oxidative stress, apoptosis, and excitotoxicity (Sulhan et al., 2020)

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Using the BioGRID database 26 as a reference, we find that interactions of 158 of these targets with human pathogenic viruses have been reported before, which represents a highly significant enrichment among reported interactions between enzymes and viruses (Fishers exact test p = 9.1 10 12 , odds ratio 1.93.4) and supports their central role in viral replication across diverse viruses

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