Bell’s palsy is the most common cranial nerve paralysis, accounts for 60% - 70% of all causes of unilateral facial paralysis [1,2]. The etiology and pathological mechanism are still controversial. The main predispositions of Bell’s palsy include cold, fatigue, decreased resistance and immune deficiency. Most studies suggest that Bell’s palsy is related to an immune response after virus infection. Bell’s palsy usually occurs 1-2 weeks after virus infection, which might be an autoimmune demyelination disease following virus infection [2-4]. The herpes simplex virus 1 (HSV-1) genome found in endoneurial fluid from the facial nerve of patients with Bell’s palsy endorsed the hypothesis of an HSV-1 reactivation within the geniculate ganglion and subsequent inflammation and entrapment of the nerve at the meatal foramen or in the labyrinthine segment, which is believed to be the pathogenic mechanism of Bell’s palsy [3,4,10]. In addition, Bell’s palsy has some characteristics consistent with that of virus infection, such as seasonal prevalence [11,12].
COVID-19 is highly infectious and has caused an outbreak of pneumonia spreading from Wuhan, China to the whole world [5,6,9]. COVID-19 mainly causes respiratory symptoms in humans, and some patients can also have gastrointestinal, neurological, cardiovascular and other symptoms. Nervous system symptoms mainly include headache, dizziness and so on [5-6]. In addition, Chen et al  reported an asymptomatic case of COVID-19 pneumonia complicated with acute cerebral infarction of right corona radiate on March 2. Subsequently, on March 4, researchers from Beijing Ditan Hospital reported the first COVID-19 pneumonia complicated with encephalitis in the world, and confirmed the presence of SARS-CoV-2 RNA in cerebrospinal fluid of the patient by gene sequencing . These cases suggested COVID-19 could also develop neurological symptoms and even had neurological symptoms as the first manifestation, especially in patients with asymptomatic or mild infection.
In this case, the patient was diagnosed as Bell’s palsy without herpes zoster. Although Bell’s palsy was believed to be related to virus infection, the detection of viral antigens did not find the evidence of other viral infections, including herpes zoster virus. Surprisingly, we found that the patient was infected by SARS-CoV-2. Therefore, it is supposed that SARS-CoV-2 infection may be associated with Bell’s palsy in the patient reported here. It is found that angiotensin-converting enzyme 2 (ACE2) may be binded to the coronavirus and trigger functional changes in ACE2/Angiotensin Ⅱ Type 2 Receptor (AT2R), thereby resulting in an imbalance in the steady-state cytokine regulatory axis and a cytokine storm . ACE2 exists in nervous system and skeletal muscle. The expression and distribution of ACE2 suggest that SARS-CoV-2 may cause some neurological symptoms through direct or indirect mechanisms. The facial nerve damage might be attributed to an immune response caused by SARS-CoV-2, but needs to be further confirmed by future research.