Endosymbiotic Actinidic Archaea and Viroids-Role in Genomic Regulation

Ravikumar Kurup A., Parameswara Achutha Kurup

Abstract


Aim: A hypothesis regarding the role of endosymbiotic actinidic archaea and viroids in genomic regulation is put forward. Endogenous digoxin has been related to the pathogenesis of huntington’s disease and trisomy 21. The possibility of endogenous digoxin synthesis by endosymbiotic bacteria with a mevalonate pathway and cholesterol catabolism was considered and explored in the study. The role of archaeal viroids was also studied. Methods: Cholesterol substrate was added to the plasma of the patients and the generation of cytochrome F420, free RNA, free DNA, polycyclic aromatic hydrocarbon, hydrogen peroxide, pyruvate, glutamate, cytochrome C, hexokinase, ATP synthase, HMG CoA redutase, digoxin and bile acids were studied. The changes with the addition of antibiotics and rutile to the patient’s plasma were also studied. Results: The study showed rutile dependent increase in archaea and RNA viroids in the sera of these patients. The generation of cholesterol catabolites- polycyclic aromatic hydrocarbon, hydrogen peroxide, pyruvate, glutamate, digoxin and bile acids was increased in the presence of rutile suggesting a rutile dependent alternate biochemistry. The mevalonate pathway, ATP synthase and glycolysis in this archaea were also rutile dependent. The addition of antibiotics to the patient’s serum decreased all these activities suggesting their archaeal origin. Conclusion: The study demonstrates the existence of a shadow biosphere of rutile dependent archaea and viroids in these disease states. The archaeal cholesterol catabolism and viroidal RNA interference is crucial to the pathogenesis of these diseases. Actinidic archaea and viroids can regulate genomic function.

Key words: Huntington’s disease; Trisomy 21; Actinides; Archaea; Viroids; Cholesterol Oxidase; HMG CoA reductase; Genomic function


Keywords


Huntington’s disease; Trisomy 21; Actinides; Archaea; Viroids; Cholesterol Oxidase; HMG CoA reductase; Genomic function



DOI: http://dx.doi.org/10.3968%2Fj.ans.1715787020120501.1135

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