Table 2.

Summary of key evidence for the etiological theory about virus infection

Key references	Summary of evidence
[21–24]	The α-HV which target peripheral neurons (e.g., HSV-1, HSV-2, and VZV) can establish lifelong infections and infectivity potential in the host including in the autonomic and sensory ganglia of the head, neck and cranial
[25]	Reactivation of HSV-1 centered around the geniculate ganglion was first outlined by McCormick in 1972
[26]	The presence of HSV-1 deoxyribonucleic acid (DNA) was detected in clinical specimens, i.e., intra-temporal facial nerve endo-neural fluid in Bell’s palsy patients
[27–29]	Animal models have the capability to cause facial paralysis through initial infection and virus reactivation incited by immune modulation
[36, 37]	Earlier work examining cellular electrophysiology in the setting of herpes infection demonstrated a pathway for the quick and dynamic control of excitability in sensory neurons by internalization of sodium channels. The processes of intra-axonal degeneration would drive the abrupt onset of Bell’s palsy
[38]	The aquaporin 1 water channel protein (AQP1) in Schwann cells of intratemporal facial nerve is involved in the evolution of facial palsy caused by HSV-1 and may play an important role in the pathogenesis of this disease
[39]	Decreasing LAT levels in neurons reduced the ability of the virus to reactivate. This suggests the potential of reverse validation of bell’s palsy as a virus reactivation