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Neo-Darwinism conceptualizes evolution as the continuous succession of predominately random genetic variations disciplined by natural selection. In that frame, the primary interaction between cells and the virome is relegated to host-parasite dynamics governed by selective influences. Cognition-Based Evolution regards biological and evolutionary development as a reciprocating cognition-based informational interactome for the protection of self-referential cells. To sustain cellular homeorhesis, cognitive cells collaborate to assess the validity of ambiguous biological information. That collective interaction involves coordinate measurement, communication, and active deployment of resources as Natural Cellular Engineering. These coordinated activities drive multicellularity, biological development, and evolutionary change. The virome participates as the vital intercessory among the cellular domains to ensure their shared permanent perpetuation. The interactions between the virome and the cellular domains represent active virocellular cross-communications for the continual exchange of resources. Modular genetic transfers between viruses and cells carry bioactive potentials. Those exchanges are deployed as nonrandom flexible tools among the domains in their continuous confrontation with environmental stresses. This alternative framework fundamentally shifts our perspective on viral-cellular interactions, strengthening established principles of viral symbiogenesis. Pathogenesis can now be properly appraised as one expression of a range of outcomes between cells and viruses within a larger conceptual framework of Natural Viral Engineering as a co-engineering participant with cells. It is proposed that Natural Viral Engineering should be viewed as a co-existent facet of Natural Cellular Engineering within Cognition-Based Evolution.

Introduction: Brugada syndrome is an arrhythmogenic disorder that is a known cause of sudden cardiac death. It is characterized by a pattern of ST segment elevation in the precordial leads on an electrocardiogram (EKG) due to a sodium channelopathy. Case Report: This case report highlights the case of a five-year-old female who presented to the emergency department with a febrile viral illness and had an EKG consistent with Brugada syndrome. Discussion: Fever is known to accentuate or unmask EKG changes associated with Brugada due to temperature sensitivity of the sodium channels. Conclusion: Febrile patients with Brugada are at particular risk for fatal ventricular arrhythmias and fevers should be treated aggressively by the emergency medicine provider. Emergency medicine providers should also consider admitting febrile patients with Brugada syndrome who do not have an automatic implantable cardioverter-defibrillator for cardiac monitoring.