Trace element homeostasis in the neurological system after SARS-CoV-2 infection: Insight into potential biochemical mechanisms

Background: Several studies have suggested that COVID-19 is a systemic disease that can affect several organs, including the brain. In the brain, specifically, viral infection can cause dyshomeostasis of some trace elements that promote complex biochemical reactions in specialized neurological functions.Objective: Understand the neurovirulence of SARS-CoV-2 and the relationship between trace elements and neurological disorders after infection, and provide new insights on the drug development for the treatment of SARS-CoV-2 infections.Methods: The main databases were used to search studies published up September 2021, focusing on the role of trace elements during viral infection and on the correct functioning of the brain. Results: The imbalance of important trace elements can accelerate SARS-CoV-2 neurovirulence and increase the neurotoxicity since many neurological processes can be associated with the homeostasis of metal and metalloproteins. Some studies involving animals and humans have suggested the synapse as a vulnerable region of the brain to neurological disorders after viral infection. Considering the combined evidence, some mechanisms have been suggested to understand the relationship between neurological disorders and imbalance of trace elements in the brain after viral infection. Conclusion: Trace elements play important roles in viral infections, such as helping to activate immune cells, produce antibodies, and inhibit virus replication. However, the relationship between trace elements and virus infections is complex since the specific functions of several elements remain largely undefined. Therefore, there is still a lot to be explored to understand the biochemical mechanisms involved between trace elements and viral infections, especially in the brain.

Automated summary

Viral infection can lead to an imbalance of trace elements in the brain, increasing neurovirulence and neurotoxicity. Synapse vulnerability has been suggested as a potential mechanism for neurological disorders following viral infection. Trace elements play crucial roles in viral infections, although their specific functions remain largely undefined.