By Giulio Zampogna

Concluding my research in plant and comparative immunology, I theorized that immunity is fundamentally the genetic program’s ability to resist change and maintain homeostasis. All immunological phenomena are governed not by molecular discontinuities mediated by receptor-ligand interactions—known as Continuity Theory—but more specifically by discontinuities that ultimately disrupt the program’s stability. Immunity is the program’s ability to stabilize—to resist natural selection—as replication perpetuates existence. Perceived this way, immunity may be considered the program’s intrinsic predisposition toward adaptation, with evolution originating as the interplay between immunity and natural selection.

Requisite for biological life is the genetic program’s abilities of replication and stability under environmental forces. Polymerization/replication coexists with the reverse reaction of depolymerization/de-replication. Genetic code strand variants formed through imperfect replication might interfere with the parent molecule’s stability; therefore, parent molecules may—as a form of resistance—catalyze the depolymerization of interfering progeny. Progeny resistant to this degradation could persist and outcompete inferior, less stable replicants. To test this hypothesis and support the aforementioned theory, we must conduct experiments involving competition among identical self-replicating ribozymes occupying finite space and resources, and analyze the resultant spectrum, respective concentration, 3D structure, and catalytic capabilities of ribozyme variants formed over time.


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Giulio Zampogna



Published: 26 Jan, 2019

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