PMC:7445716 / 2372-4185 JSON TXT

Annnotations TAB JSON ListView MergeView

LitCovid-PD-FMA-UBERON

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T7","span":{"begin":272,"end":278},"obj":"Body_part"},{"id":"T8","span":{"begin":389,"end":408},"obj":"Body_part"},{"id":"T9","span":{"begin":410,"end":413},"obj":"Body_part"},{"id":"T10","span":{"begin":762,"end":771},"obj":"Body_part"},{"id":"T11","span":{"begin":979,"end":995},"obj":"Body_part"},{"id":"T12","span":{"begin":1147,"end":1158},"obj":"Body_part"}],"attributes":[{"id":"A7","pred":"fma_id","subj":"T7","obj":"http://purl.org/sig/ont/fma/fma9721"},{"id":"A8","pred":"fma_id","subj":"T8","obj":"http://purl.org/sig/ont/fma/fma20935"},{"id":"A9","pred":"fma_id","subj":"T9","obj":"http://purl.org/sig/ont/fma/fma20935"},{"id":"A10","pred":"fma_id","subj":"T10","obj":"http://purl.org/sig/ont/fma/fma79876"},{"id":"A11","pred":"fma_id","subj":"T11","obj":"http://purl.org/sig/ont/fma/fma65239"},{"id":"A12","pred":"fma_id","subj":"T12","obj":"http://purl.org/sig/ont/fma/fma82816"}],"text":"GBS represents the most common cause of acute flaccid paralysis [57]. The classic form is an immune-mediated acute-onset demyelinating polyradiculoneuropathy (acute inflammatory demyelinating polyneuropathy—AIDP) typically presenting with ascending weakness, loss of deep tendon reflexes, and sensory deficits. Diagnosis of GBS relies on the results of clinical, electrophysiological, and cerebrospinal fluid (CSF) examinations (classically albuminocytological dissociation) [57–59]. The clinical spectrum of GBS encompasses a classic sensorimotor form, Miller Fisher syndrome (MFS), bilateral facial palsy with paraesthesia, pure motor, pure sensory, paraparetic, pharyngeal–cervical–brachial variants, polyneuritis cranialis (GBS–MFS overlap), and Bickerstaff brainstem encephalitis [57–60]. As regard electrophysiological features, three main subtypes are recognized: AIDP, acute motor axonal neuropathy (AMAN), and acute motor sensory axonal neuropathy (AMSAN) [57, 58, 61]. Peripheral nerve damage is thought to be provoked by an aberrant immune response to infections, in some cases driven by the production of autoreactive antibodies (anti-ganglioside antibodies) [57–59]. Potential triggering pathogens include both viruses [e.g., cytomegalovirus (CMV), Epstein–Barr virus (EBV), influenza virus, hepatitis E virus, and Zika virus] and bacteria (e.g., Campylobacter Jejuni, Mycoplasma Pneumoniae) [57, 58, 62]. However, a relationship with other events has been also described (e.g., vaccinations, surgery, administration of checkpoint inhibitors, and malignancy) [57, 58]. Given that a potential causal association with beta-coronaviruses [Middle East Respiratory Syndrome (MERS-CoV)] has already been speculated, the relationship between COVID-19 and GBS deserves undoubtedly further attention [63, 64]."}

LitCovid-PD-UBERON

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T3","span":{"begin":272,"end":278},"obj":"Body_part"},{"id":"T4","span":{"begin":389,"end":408},"obj":"Body_part"},{"id":"T5","span":{"begin":762,"end":771},"obj":"Body_part"},{"id":"T6","span":{"begin":990,"end":995},"obj":"Body_part"}],"attributes":[{"id":"A3","pred":"uberon_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/UBERON_0000043"},{"id":"A4","pred":"uberon_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/UBERON_0001359"},{"id":"A5","pred":"uberon_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/UBERON_0002298"},{"id":"A6","pred":"uberon_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/UBERON_0001021"}],"text":"GBS represents the most common cause of acute flaccid paralysis [57]. The classic form is an immune-mediated acute-onset demyelinating polyradiculoneuropathy (acute inflammatory demyelinating polyneuropathy—AIDP) typically presenting with ascending weakness, loss of deep tendon reflexes, and sensory deficits. Diagnosis of GBS relies on the results of clinical, electrophysiological, and cerebrospinal fluid (CSF) examinations (classically albuminocytological dissociation) [57–59]. The clinical spectrum of GBS encompasses a classic sensorimotor form, Miller Fisher syndrome (MFS), bilateral facial palsy with paraesthesia, pure motor, pure sensory, paraparetic, pharyngeal–cervical–brachial variants, polyneuritis cranialis (GBS–MFS overlap), and Bickerstaff brainstem encephalitis [57–60]. As regard electrophysiological features, three main subtypes are recognized: AIDP, acute motor axonal neuropathy (AMAN), and acute motor sensory axonal neuropathy (AMSAN) [57, 58, 61]. Peripheral nerve damage is thought to be provoked by an aberrant immune response to infections, in some cases driven by the production of autoreactive antibodies (anti-ganglioside antibodies) [57–59]. Potential triggering pathogens include both viruses [e.g., cytomegalovirus (CMV), Epstein–Barr virus (EBV), influenza virus, hepatitis E virus, and Zika virus] and bacteria (e.g., Campylobacter Jejuni, Mycoplasma Pneumoniae) [57, 58, 62]. However, a relationship with other events has been also described (e.g., vaccinations, surgery, administration of checkpoint inhibitors, and malignancy) [57, 58]. Given that a potential causal association with beta-coronaviruses [Middle East Respiratory Syndrome (MERS-CoV)] has already been speculated, the relationship between COVID-19 and GBS deserves undoubtedly further attention [63, 64]."}

LitCovid-PD-MONDO

LitCovid-PD-CLO

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T18","span":{"begin":272,"end":278},"obj":"http://www.ebi.ac.uk/cellline#tendon"},{"id":"T19","span":{"begin":272,"end":278},"obj":"http://www.ebi.ac.uk/efo/EFO_0000952"},{"id":"T20","span":{"begin":525,"end":526},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T21","span":{"begin":990,"end":995},"obj":"http://purl.obolibrary.org/obo/UBERON_0001021"},{"id":"T22","span":{"begin":1224,"end":1231},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"},{"id":"T23","span":{"begin":1275,"end":1280},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"},{"id":"T24","span":{"begin":1298,"end":1303},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"},{"id":"T25","span":{"begin":1317,"end":1322},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"},{"id":"T26","span":{"begin":1333,"end":1338},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"},{"id":"T27","span":{"begin":1344,"end":1352},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_2"},{"id":"T28","span":{"begin":1428,"end":1429},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T29","span":{"begin":1461,"end":1464},"obj":"http://purl.obolibrary.org/obo/CLO_0051582"},{"id":"T30","span":{"begin":1593,"end":1594},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T31","span":{"begin":1694,"end":1697},"obj":"http://purl.obolibrary.org/obo/CLO_0051582"}],"text":"GBS represents the most common cause of acute flaccid paralysis [57]. The classic form is an immune-mediated acute-onset demyelinating polyradiculoneuropathy (acute inflammatory demyelinating polyneuropathy—AIDP) typically presenting with ascending weakness, loss of deep tendon reflexes, and sensory deficits. Diagnosis of GBS relies on the results of clinical, electrophysiological, and cerebrospinal fluid (CSF) examinations (classically albuminocytological dissociation) [57–59]. The clinical spectrum of GBS encompasses a classic sensorimotor form, Miller Fisher syndrome (MFS), bilateral facial palsy with paraesthesia, pure motor, pure sensory, paraparetic, pharyngeal–cervical–brachial variants, polyneuritis cranialis (GBS–MFS overlap), and Bickerstaff brainstem encephalitis [57–60]. As regard electrophysiological features, three main subtypes are recognized: AIDP, acute motor axonal neuropathy (AMAN), and acute motor sensory axonal neuropathy (AMSAN) [57, 58, 61]. Peripheral nerve damage is thought to be provoked by an aberrant immune response to infections, in some cases driven by the production of autoreactive antibodies (anti-ganglioside antibodies) [57–59]. Potential triggering pathogens include both viruses [e.g., cytomegalovirus (CMV), Epstein–Barr virus (EBV), influenza virus, hepatitis E virus, and Zika virus] and bacteria (e.g., Campylobacter Jejuni, Mycoplasma Pneumoniae) [57, 58, 62]. However, a relationship with other events has been also described (e.g., vaccinations, surgery, administration of checkpoint inhibitors, and malignancy) [57, 58]. Given that a potential causal association with beta-coronaviruses [Middle East Respiratory Syndrome (MERS-CoV)] has already been speculated, the relationship between COVID-19 and GBS deserves undoubtedly further attention [63, 64]."}

LitCovid-PD-CHEBI

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T2","span":{"begin":1147,"end":1158},"obj":"Chemical"},{"id":"T3","span":{"begin":1544,"end":1554},"obj":"Chemical"},{"id":"T4","span":{"begin":1629,"end":1633},"obj":"Chemical"}],"attributes":[{"id":"A2","pred":"chebi_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/CHEBI_28892"},{"id":"A3","pred":"chebi_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/CHEBI_35222"},{"id":"A4","pred":"chebi_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/CHEBI_10545"}],"text":"GBS represents the most common cause of acute flaccid paralysis [57]. The classic form is an immune-mediated acute-onset demyelinating polyradiculoneuropathy (acute inflammatory demyelinating polyneuropathy—AIDP) typically presenting with ascending weakness, loss of deep tendon reflexes, and sensory deficits. Diagnosis of GBS relies on the results of clinical, electrophysiological, and cerebrospinal fluid (CSF) examinations (classically albuminocytological dissociation) [57–59]. The clinical spectrum of GBS encompasses a classic sensorimotor form, Miller Fisher syndrome (MFS), bilateral facial palsy with paraesthesia, pure motor, pure sensory, paraparetic, pharyngeal–cervical–brachial variants, polyneuritis cranialis (GBS–MFS overlap), and Bickerstaff brainstem encephalitis [57–60]. As regard electrophysiological features, three main subtypes are recognized: AIDP, acute motor axonal neuropathy (AMAN), and acute motor sensory axonal neuropathy (AMSAN) [57, 58, 61]. Peripheral nerve damage is thought to be provoked by an aberrant immune response to infections, in some cases driven by the production of autoreactive antibodies (anti-ganglioside antibodies) [57–59]. Potential triggering pathogens include both viruses [e.g., cytomegalovirus (CMV), Epstein–Barr virus (EBV), influenza virus, hepatitis E virus, and Zika virus] and bacteria (e.g., Campylobacter Jejuni, Mycoplasma Pneumoniae) [57, 58, 62]. However, a relationship with other events has been also described (e.g., vaccinations, surgery, administration of checkpoint inhibitors, and malignancy) [57, 58]. Given that a potential causal association with beta-coronaviruses [Middle East Respiratory Syndrome (MERS-CoV)] has already been speculated, the relationship between COVID-19 and GBS deserves undoubtedly further attention [63, 64]."}

LitCovid-PD-GO-BP

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T1","span":{"begin":1044,"end":1059},"obj":"http://purl.obolibrary.org/obo/GO_0006955"}],"text":"GBS represents the most common cause of acute flaccid paralysis [57]. The classic form is an immune-mediated acute-onset demyelinating polyradiculoneuropathy (acute inflammatory demyelinating polyneuropathy—AIDP) typically presenting with ascending weakness, loss of deep tendon reflexes, and sensory deficits. Diagnosis of GBS relies on the results of clinical, electrophysiological, and cerebrospinal fluid (CSF) examinations (classically albuminocytological dissociation) [57–59]. The clinical spectrum of GBS encompasses a classic sensorimotor form, Miller Fisher syndrome (MFS), bilateral facial palsy with paraesthesia, pure motor, pure sensory, paraparetic, pharyngeal–cervical–brachial variants, polyneuritis cranialis (GBS–MFS overlap), and Bickerstaff brainstem encephalitis [57–60]. As regard electrophysiological features, three main subtypes are recognized: AIDP, acute motor axonal neuropathy (AMAN), and acute motor sensory axonal neuropathy (AMSAN) [57, 58, 61]. Peripheral nerve damage is thought to be provoked by an aberrant immune response to infections, in some cases driven by the production of autoreactive antibodies (anti-ganglioside antibodies) [57–59]. Potential triggering pathogens include both viruses [e.g., cytomegalovirus (CMV), Epstein–Barr virus (EBV), influenza virus, hepatitis E virus, and Zika virus] and bacteria (e.g., Campylobacter Jejuni, Mycoplasma Pneumoniae) [57, 58, 62]. However, a relationship with other events has been also described (e.g., vaccinations, surgery, administration of checkpoint inhibitors, and malignancy) [57, 58]. Given that a potential causal association with beta-coronaviruses [Middle East Respiratory Syndrome (MERS-CoV)] has already been speculated, the relationship between COVID-19 and GBS deserves undoubtedly further attention [63, 64]."}

LitCovid-PubTator

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T20","span":{"begin":0,"end":69},"obj":"Sentence"},{"id":"T21","span":{"begin":70,"end":310},"obj":"Sentence"},{"id":"T22","span":{"begin":311,"end":483},"obj":"Sentence"},{"id":"T23","span":{"begin":484,"end":793},"obj":"Sentence"},{"id":"T24","span":{"begin":794,"end":978},"obj":"Sentence"},{"id":"T25","span":{"begin":979,"end":1179},"obj":"Sentence"},{"id":"T26","span":{"begin":1180,"end":1418},"obj":"Sentence"},{"id":"T27","span":{"begin":1419,"end":1581},"obj":"Sentence"},{"id":"T28","span":{"begin":1582,"end":1813},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"GBS represents the most common cause of acute flaccid paralysis [57]. The classic form is an immune-mediated acute-onset demyelinating polyradiculoneuropathy (acute inflammatory demyelinating polyneuropathy—AIDP) typically presenting with ascending weakness, loss of deep tendon reflexes, and sensory deficits. Diagnosis of GBS relies on the results of clinical, electrophysiological, and cerebrospinal fluid (CSF) examinations (classically albuminocytological dissociation) [57–59]. The clinical spectrum of GBS encompasses a classic sensorimotor form, Miller Fisher syndrome (MFS), bilateral facial palsy with paraesthesia, pure motor, pure sensory, paraparetic, pharyngeal–cervical–brachial variants, polyneuritis cranialis (GBS–MFS overlap), and Bickerstaff brainstem encephalitis [57–60]. As regard electrophysiological features, three main subtypes are recognized: AIDP, acute motor axonal neuropathy (AMAN), and acute motor sensory axonal neuropathy (AMSAN) [57, 58, 61]. Peripheral nerve damage is thought to be provoked by an aberrant immune response to infections, in some cases driven by the production of autoreactive antibodies (anti-ganglioside antibodies) [57–59]. Potential triggering pathogens include both viruses [e.g., cytomegalovirus (CMV), Epstein–Barr virus (EBV), influenza virus, hepatitis E virus, and Zika virus] and bacteria (e.g., Campylobacter Jejuni, Mycoplasma Pneumoniae) [57, 58, 62]. However, a relationship with other events has been also described (e.g., vaccinations, surgery, administration of checkpoint inhibitors, and malignancy) [57, 58]. Given that a potential causal association with beta-coronaviruses [Middle East Respiratory Syndrome (MERS-CoV)] has already been speculated, the relationship between COVID-19 and GBS deserves undoubtedly further attention [63, 64]."}

LitCovid-PD-HP

{"project":"LitCovid-PD-HP","denotations":[{"id":"T3","span":{"begin":54,"end":63},"obj":"Phenotype"},{"id":"T4","span":{"begin":121,"end":134},"obj":"Phenotype"},{"id":"T5","span":{"begin":178,"end":191},"obj":"Phenotype"},{"id":"T6","span":{"begin":192,"end":206},"obj":"Phenotype"},{"id":"T7","span":{"begin":259,"end":287},"obj":"Phenotype"},{"id":"T8","span":{"begin":584,"end":606},"obj":"Phenotype"},{"id":"T9","span":{"begin":704,"end":716},"obj":"Phenotype"},{"id":"T10","span":{"begin":772,"end":784},"obj":"Phenotype"},{"id":"T11","span":{"begin":883,"end":906},"obj":"Phenotype"},{"id":"T12","span":{"begin":931,"end":956},"obj":"Phenotype"},{"id":"T13","span":{"begin":979,"end":1002},"obj":"Phenotype"},{"id":"T14","span":{"begin":1305,"end":1314},"obj":"Phenotype"},{"id":"T15","span":{"begin":1393,"end":1403},"obj":"Phenotype"}],"attributes":[{"id":"A3","pred":"hp_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/HP_0003470"},{"id":"A4","pred":"hp_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/HP_0011096"},{"id":"A5","pred":"hp_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/HP_0011096"},{"id":"A6","pred":"hp_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/HP_0001271"},{"id":"A7","pred":"hp_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/HP_0001284"},{"id":"A8","pred":"hp_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/HP_0430025"},{"id":"A9","pred":"hp_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/HP_0031003"},{"id":"A10","pred":"hp_id","subj":"T10","obj":"http://purl.obolibrary.org/obo/HP_0002383"},{"id":"A11","pred":"hp_id","subj":"T11","obj":"http://purl.obolibrary.org/obo/HP_0007002"},{"id":"A12","pred":"hp_id","subj":"T12","obj":"http://purl.obolibrary.org/obo/HP_0003390"},{"id":"A13","pred":"hp_id","subj":"T13","obj":"http://purl.obolibrary.org/obo/HP_0009830"},{"id":"A14","pred":"hp_id","subj":"T14","obj":"http://purl.obolibrary.org/obo/HP_0012115"},{"id":"A15","pred":"hp_id","subj":"T15","obj":"http://purl.obolibrary.org/obo/HP_0002090"}],"text":"GBS represents the most common cause of acute flaccid paralysis [57]. The classic form is an immune-mediated acute-onset demyelinating polyradiculoneuropathy (acute inflammatory demyelinating polyneuropathy—AIDP) typically presenting with ascending weakness, loss of deep tendon reflexes, and sensory deficits. Diagnosis of GBS relies on the results of clinical, electrophysiological, and cerebrospinal fluid (CSF) examinations (classically albuminocytological dissociation) [57–59]. The clinical spectrum of GBS encompasses a classic sensorimotor form, Miller Fisher syndrome (MFS), bilateral facial palsy with paraesthesia, pure motor, pure sensory, paraparetic, pharyngeal–cervical–brachial variants, polyneuritis cranialis (GBS–MFS overlap), and Bickerstaff brainstem encephalitis [57–60]. As regard electrophysiological features, three main subtypes are recognized: AIDP, acute motor axonal neuropathy (AMAN), and acute motor sensory axonal neuropathy (AMSAN) [57, 58, 61]. Peripheral nerve damage is thought to be provoked by an aberrant immune response to infections, in some cases driven by the production of autoreactive antibodies (anti-ganglioside antibodies) [57–59]. Potential triggering pathogens include both viruses [e.g., cytomegalovirus (CMV), Epstein–Barr virus (EBV), influenza virus, hepatitis E virus, and Zika virus] and bacteria (e.g., Campylobacter Jejuni, Mycoplasma Pneumoniae) [57, 58, 62]. However, a relationship with other events has been also described (e.g., vaccinations, surgery, administration of checkpoint inhibitors, and malignancy) [57, 58]. Given that a potential causal association with beta-coronaviruses [Middle East Respiratory Syndrome (MERS-CoV)] has already been speculated, the relationship between COVID-19 and GBS deserves undoubtedly further attention [63, 64]."}

LitCovid-PMC-OGER-BB

2_test

{"project":"2_test","denotations":[{"id":"32840686-31541214-63205623","span":{"begin":65,"end":67},"obj":"31541214"},{"id":"32840686-31541214-63205624","span":{"begin":476,"end":478},"obj":"31541214"},{"id":"32840686-26948435-63205624","span":{"begin":476,"end":478},"obj":"26948435"},{"id":"32840686-30310069-63205624","span":{"begin":476,"end":478},"obj":"30310069"},{"id":"32840686-31541214-63205625","span":{"begin":786,"end":788},"obj":"31541214"},{"id":"32840686-26948435-63205625","span":{"begin":786,"end":788},"obj":"26948435"},{"id":"32840686-30310069-63205625","span":{"begin":786,"end":788},"obj":"30310069"},{"id":"32840686-26369515-63205625","span":{"begin":786,"end":788},"obj":"26369515"},{"id":"32840686-31541214-63205626","span":{"begin":966,"end":968},"obj":"31541214"},{"id":"32840686-26948435-63205627","span":{"begin":970,"end":972},"obj":"26948435"},{"id":"32840686-30419502-63205628","span":{"begin":974,"end":976},"obj":"30419502"},{"id":"32840686-31541214-63205629","span":{"begin":1172,"end":1174},"obj":"31541214"},{"id":"32840686-26948435-63205629","span":{"begin":1172,"end":1174},"obj":"26948435"},{"id":"32840686-30310069-63205629","span":{"begin":1172,"end":1174},"obj":"30310069"},{"id":"32840686-31541214-63205630","span":{"begin":1406,"end":1408},"obj":"31541214"},{"id":"32840686-26948435-63205631","span":{"begin":1410,"end":1412},"obj":"26948435"},{"id":"32840686-32518150-63205632","span":{"begin":1414,"end":1416},"obj":"32518150"},{"id":"32840686-31541214-63205633","span":{"begin":1573,"end":1575},"obj":"31541214"},{"id":"32840686-26948435-63205634","span":{"begin":1577,"end":1579},"obj":"26948435"},{"id":"32840686-32860084-63205635","span":{"begin":1809,"end":1811},"obj":"32860084"}],"text":"GBS represents the most common cause of acute flaccid paralysis [57]. The classic form is an immune-mediated acute-onset demyelinating polyradiculoneuropathy (acute inflammatory demyelinating polyneuropathy—AIDP) typically presenting with ascending weakness, loss of deep tendon reflexes, and sensory deficits. Diagnosis of GBS relies on the results of clinical, electrophysiological, and cerebrospinal fluid (CSF) examinations (classically albuminocytological dissociation) [57–59]. The clinical spectrum of GBS encompasses a classic sensorimotor form, Miller Fisher syndrome (MFS), bilateral facial palsy with paraesthesia, pure motor, pure sensory, paraparetic, pharyngeal–cervical–brachial variants, polyneuritis cranialis (GBS–MFS overlap), and Bickerstaff brainstem encephalitis [57–60]. As regard electrophysiological features, three main subtypes are recognized: AIDP, acute motor axonal neuropathy (AMAN), and acute motor sensory axonal neuropathy (AMSAN) [57, 58, 61]. Peripheral nerve damage is thought to be provoked by an aberrant immune response to infections, in some cases driven by the production of autoreactive antibodies (anti-ganglioside antibodies) [57–59]. Potential triggering pathogens include both viruses [e.g., cytomegalovirus (CMV), Epstein–Barr virus (EBV), influenza virus, hepatitis E virus, and Zika virus] and bacteria (e.g., Campylobacter Jejuni, Mycoplasma Pneumoniae) [57, 58, 62]. However, a relationship with other events has been also described (e.g., vaccinations, surgery, administration of checkpoint inhibitors, and malignancy) [57, 58]. Given that a potential causal association with beta-coronaviruses [Middle East Respiratory Syndrome (MERS-CoV)] has already been speculated, the relationship between COVID-19 and GBS deserves undoubtedly further attention [63, 64]."}

PMC:7445716 / 2372-4185 JSONTXT

Annnotations TAB JSON ListView MergeView

PMC:7445716 / 2372-4185 JSON TXT