Facial paralysis induced by ear inoculation of herpes simplex virus in rat

The etiology of Bell’s palsy: a review

“…The reactivation of HSV-1 centered around the geniculate ganglion, and thus potentially linked to BP, was first outlined by McCormick [25]. An association with HSV-1 is supported by the presence of HSV-1 DNA in clinical specimens (i.e., intra-temporal facial nerve endo-neural fluid) [26] in BP patients, as well as its capability to cause facial paralysis in animal models after initial infection [27] and reactivation incited by immune modulation [28,29]. A possible cause of HSV-1-mediated neural dysfunction is the activation of apoptotic pathways and intra-axonal degradation, which are driven by the axon's local indirect and direct responses to the viruses themselves in susceptible phenotypes.…”

“…Bell's palsy seems to usually coincide with the narrower fallopian tube of the patient [13,14] The mean width was significantly smaller at the labyrinthine section of the facial canal in the influenced temporal bone than the equivalent in the uninfluenced (p = 0.00) [14] Significant relationship was found between the HB grade and the facial canal diameter at the level of second genu (p = 0.02) [9] In patients with higher primary HB-scores, their 6-month later HB-scores were also higher. In patients with higher 6-month HB score; their IAC inlet and mid-canal values were lower Table 2 Summary of key evidence for the etiological theory about virus infection Key references Summary of evidence [21][22][23][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 endoneural fluid in Bell's palsy patients [27][28][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.…”

Cox4i2 Triggers an Increase in Reactive Oxygen Species, Leading to Ferroptosis and Apoptosis in HHV7 Infected Schwann Cells

“…LuxolFastBlue (LFB) staining was used to observe the demyelination of the nerve tracts, and it was performed according to standard techniques (Fujiwara et al, 2017). Briefly, paraffin sections were immersed in a 0.1% LFB reagent for 8-16 h at 60 • C. After this, 0.05% lithium carbonate aqueous solution and 70% alcohol, 0.25% tar violet solution, and glacial acetic acid dyeing solution were used to redye all specimens for 10 min.…”

Análise facial digital de pacientes com paralisia facial, após laserterapia e aplicação de toxina botulínica: estudo triplo-cego, randomizado, placebo controlado

“…Lazarini e colaboradores (2006), Lázaro (2009) e Zimmermann et al ( 2019), apresentando a hipótese em que a PB pode ocorrer por reativação do HVS-1 e do ZVZ latente no gânglio geniculado (Sugita, 1993;Fujiwara et al, 2017).…”

“…As PFP de causa viral têm sido demonstradas atualmente na literatura como causadoras de muitas das paralisias; o VZV é responsável por 18% dos casos (Hato et al, 2000;Gilchrist, 2009), conforme de achados de DNA viral em saliva, lágrima e gânglio geniculado (Lazarini et al, 2006;Teixeira, 2008;Garro;Nigrovic, 2018). A reação de polimerase em cadeia (Polymerase Chain Reaction -PCR) e a sorologia para anticorpos do HVS-1 têm sido consideradas para diagnóstico, demonstrando positividade entre 20 e 79% dos casos (Takasu et al, 1992;Burgess et al, 1994;Murakami et al, 1996;Furuta et al, 1998;Lazarini et al, 2006;Khine et al, 2008;Teixeira, 2008) Há evidências literárias de que a Paralisia de Bell ocorre por reativação do HVS-1 e do VZV (Stjernquist-Desatnik et al, 2006) latentes no gânglio geniculado (Adour et al, 1996;Murakami et al, 1996;Furuta et al, 1997;Hato et al, 2000;Teixeira, 2008;Lackner et al, 2010;Turgeon et al, 2015;Fujiwara et al, 2017). Estudos recentes também demonstram o possível envolvimento do Herpes vírus do tipo 6 (HHV-6) como fator predisponente da PB.…”