A hypothesis: Bitter taste receptors as a therapeutic target for the clinical symptoms of SARS-CoV-2.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has paralysed the livelihood of the global population by inflicting higher mortality among the affected patients. Nearly the entire human physiological system can get disrupted by the virulence of SARS-CoV-2, which exemplifies the significance of discovering a potential drug target. Similar to angiotensin-converting enzyme 2 (ACE2), bitter taste receptors (T2Rs) unequivocally expressed on all vital human organs, particularly on nasal/oral respiratory tract, gastrointestinal organs, innate immune cells, heart, brain and urogenital cells are susceptible to SARS-CoV-2 virulence. Activation of T2Rs by bitter agonists restores vital functions to these organs via activation of large conductance, Ca2+-dependent potassium (K+) channels (BKca), and inducible nitric oxide synthase. T2R activation in the gustatory system can act as the first defence mechanism, primarily preventing or mitigating SARS-CoV-2 entry to the respiratory tract. Moreover, T2R activation is crucial for the improved vasodilation accompanied by the attenuation of systemic inflammation; hyper-innate immune responses; gastrointestinal disorders; defective neurological functions; acute kidney injury; and impotency witnessed in severe SARS-CoV-2 cases. This review discusses the potential for bitter taste receptors to act as drug targets for SARS-CoV-2 symptoms and the use of existing bitter agonists to restore T2R function.