AGT and Hypertension: Allosteric modulators bind sites topologically distinct from viral recognition and catalytic domains [33], enabling critical advantages: (1) Selective viral entry disruption through transmitted conformational changes interfering with spike engagement without occupying binding epitopes [34,35]; (2) Preserved angiotensin II processing via spatial separation from catalytic machinery, ensuring protective angiotensin-(1–7) production [28,29,36]; (3) Maintained cardiovascular homeostasis preventing hypertension, inflammation, and thrombosis associated with angiotensin II excess [28,29].