GBS is generally regarded as a post-infection immune-mediated disease. JEV infection is an important etiology of GBS in endemic regions [
5]. Most patients with JEV-associated GBS did not receive the JE vaccination previously [
6].Our patient is similar to the case reported by Chung, et al [
3] of a patient who had also received JE vaccination in childhood. The high ratio of IgG to IgM is a distinction between rapid seroconversion of IgM and IgG due to acute infections and IgG antibodies derived from previous vaccine viruses. All available vaccines belong to the JEV genotype 3 strain. A partial cross-protection between JEV genotype 1 and genotype 3 strain [
1,
7] and the inferior protective efficacy due to inadequate neutralizing antibody levels probably explain why JE vaccination could not provide complete protection.
Liaoning province is located in northeast of China, where neither Zika nor Dengue virus [
8,
9] are endemic. Although Liaoning province had a low prevalence of JE [
10], there was an outbreak of 69 cases with a 30.4% fatality rate in the summer of 2018, which was very similar to the prevalence of JEV infection in the north of Ningxia in 2018 [
11]. JEV genotype 1 was the pathogen in that outbreak, and no cases were reported in children, indicating that the JEV vaccine was still effective. The chance of JEV detection by PCR in the blood and CSF is extremely low [
4,
8].Our patient was confirmed with JEV infection by positive anti-JEV IgM antibody in serum, a sensitive, specific, and early indicator of JEV infection. His characteristic clinical manifestation included weakness of the four extremities and respiratory myoparalysis accompanied by the involvement of several cranial nerves. Electrophysiology examination suggested decreased evoked potential amplitude and slowed conduction speed of motor nerves. Acute disseminated encephalomyelitis and acute transverse myelitis were excluded based on normal brain and spinal MRI images [
4,
12]. Glucocorticoid-induced myopathy was also ruled out as his muscle paralysis preceded glucocorticoid application [
13]. We must also differentiate between anterior horn cell myelitis [
3,
14] and GBS [
5,
15,
16]. Viral myelitis tends to present with a fever and a moderate pleocytosis in the CSF, while GBS typically presents a prodromal infection 1–2 weeks prior and an albumin cytologic dissociation in the CSF. However, anterior horn cell myelitis was not supported by the normal MRI of the spinal cord and slowed motor nerves conduction speed. Therefore, GBS was finally considered. The mortality of GBS is 2–10% [
17]. GBS was involved in the pathogenesis of humoral and cellular immunity [
16]. The underlying mechanism for the clusters of GBS cases in 2018 was unclear [
11]. Molecular mimicry, antiglycolipid autoantibody, and immune complexes were implicated in the pathogenesis of GBS, which caused a kind of demyelinating neuropathy or axonal neuropathy [
18,
19]. Although this patient received two doses of JEV vaccine in childhood, another booster vaccine should be provided by reason of the reduced protective antibody levels over time or primary “low-responders” [
20]. Moreover, the presence of high levels of anti-JEV IgG in early serum provided the possibility that antibody-dependent enhancement (ADE) between pre-existing antibody targeting genotype 3-derived JE vaccine and subsequent genotype 1 virus infection may play a role in the development of GBS [
21].
In summary, JE combined with GBS shows an increasing trend in recent years. Rapid diagnosis and early application of intravenous Ig or plasma exchange will be beneficial for GBS while glucocorticoids are not recommended [
17,
21,
22]. JEV genotype 1 is currently circulating in China [
23]. The longevity and titers of protective antibody responses induced by the JE vaccine depend on the type of vaccine, number of doses, and the immune status of hosts. Up to now, there is no standardized protocol for a neutralization test. A commercial kit for neutralizing antibody detection is unavailable. Therefore, another booster dose should be recommended approximately a decade after the first booster immunization. The protective role of genotype 3-derived JE vaccine in preventing genotype 1 virus infection needs additional attention.