Ebola: Destroys Na+/K+ Ion Exchange to Accelerate Electrolyte Imbalance by Scorpion Venom-like System

08 October 2021, Version 1
This content is a preprint and has not undergone peer review at the time of posting.


Ebola sickness is a hemorrhagic fever caused by the Ebola virus that has an extremely high fatality rate. Electrolyte imbalance is a typical sign in Ebola patients who have already contracted the virus. The use of bioinformatics calculation tools to research Ebola's electrolyte imbalance mechanism is critical for halting the development of the epidemic and saving lives. The computational method of conserved domain search was employed to investigate the protein function of EBOV in this work. This study demonstrates that L, N, S, VP24, and VP35 have LCN type CS-α/β domains. It is a peptide neurotoxin found in scorpions, sea anemone, and snake venom. It can activate Na+ channels and gradually deactivate them, and deactivate voltage- and Ca+2-activated K+ channels. S LCN type CS-α/β is a neurotoxin with a lengthy chain that can activate Na+ channels. VP24, VP35, and N LCN type CS-α/β are short-chain toxins that inhibit voltage-dependent or Ca+2-activated K+ channels and partially inactivate sodium channels. L contains both long- and short-chain LCN type CS-α/β toxins that can activate Na+ channels and inhibit K+ channels. These LCN type CS-α/β can activate Na+ channels and Na+/K+ pumps 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+ exchange pump outputs Na+ and inputs Ca+2 in “the reverse” mode. The results in an electrolytic environment outside the cell with hyponatremia, hypocalcemia and hypokalemia.


LCN type CS-α/β;Hyponatremia


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