Sodium regulatory disorders are frequently related to defective sodium ion channel function. Specific viral fusion proteins appear to be related to cell membrane fusion proteins . In general, viral proteins activate the Na + channel, allowing Na + to infiltrate the cell . The cell's Na + /Ca +2 exchange pump subsequently discharges some Na + and absorbs Ca +2 . S1 and S2 of the SARS-COV-2 S protein contain LCN type CS-α/β domain. LCN type CS-α/β denotes the cysteine-stabilized -helix/-sheet. The LCN type CS-α/β interacts to the extracellular -scorpion and anemone toxin receptors of the Na + channel . It activates the Na + channel, then a large number of sodium ions into the cell. Na + /K + ATPase pumps 3 Na + out of the cell and 2 K + into the cell (active transport) . Na + /K + -ATPase is required for the proper functioning of numerous cell activities. When the K + concentration inside the cell is greater than the K + concentration of outer, K + can release from the cell via the potassium ion channel (diffusion transport) . The majority of short-chain toxins LCN type CS-α/β are capable of inhibiting voltage-dependent or Ca +2 -activated K + channels . So LCN type CS-α/β can activate Na + /K + pumps and Na + channels while simultaneously inactivating K + channels. It may result in many Na + entering the cell and a large amount of K + accumulating within the cell. Simultaneously, the Na + /Ca +2 exchange pump outputs Na + and inputs Ca + in "the reverse" mode . Na + can also enter the cell via the Na + channels. The results in an electrolytic environment outside the cell with hyponatremia, hypocalcemia and hypokalemia. A neurotoxic of the LCN type CS-α/β domain is found in scorpion venom, sea anemone venom, and snake venom.