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LitCovid-PubTator

LitCovid-PD-FMA-UBERON

LitCovid-PD-UBERON

LitCovid-PD-MONDO

LitCovid-PD-CLO

LitCovid-PD-CHEBI

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T27","span":{"begin":63,"end":68},"obj":"Chemical"},{"id":"T28","span":{"begin":201,"end":206},"obj":"Chemical"},{"id":"T29","span":{"begin":2618,"end":2621},"obj":"Chemical"},{"id":"T30","span":{"begin":2652,"end":2659},"obj":"Chemical"},{"id":"T31","span":{"begin":2870,"end":2872},"obj":"Chemical"}],"attributes":[{"id":"A27","pred":"chebi_id","subj":"T27","obj":"http://purl.obolibrary.org/obo/CHEBI_24433"},{"id":"A28","pred":"chebi_id","subj":"T28","obj":"http://purl.obolibrary.org/obo/CHEBI_24433"},{"id":"A29","pred":"chebi_id","subj":"T29","obj":"http://purl.obolibrary.org/obo/CHEBI_138181"},{"id":"A30","pred":"chebi_id","subj":"T30","obj":"http://purl.obolibrary.org/obo/CHEBI_36080"},{"id":"A31","pred":"chebi_id","subj":"T31","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A32","pred":"chebi_id","subj":"T31","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"}],"text":"Discussion\nThe SARS-Coronavirus-2 belongs to the β-coronavirus group which includes several human pathogenic viruses including middle east respiratory syndrome (MERS) coronavirus and SARS-CoV-1. These group of coronaviruses are associated with respiratory symptoms. Additional neurological symptoms including delirium, dizziness, and headaches have also been reported with other coronavirus infections prior to the SARS-CoV-2 outbreak [4]. The case series of patients from Wuhan, China, with COVID-19 disease, included both central and peripheral neurological manifestations (i.e., headache, dizziness, impaired consciousness, cerebrovascular disease, and neuralgia) [2]. Seizures were not reported as a direct manifestation of SARS-CoV-2 infection. The patients described in our series developed focal seizures and, in the second case, even progressed to non-convulsive status epilepticus. Seizures may be a CNS manifestation of COVID-19 disease. Further investigations are needed to elucidate the mechanism of neurological symptoms in SARS-CoV-2 infection.\nHuman coronaviruses (HCoV) have been established to infect human astrocytes and microglia in neural cell cultures as well as detection of viral RNA in a study of human brain autopsy samples supporting their neurotropic and neuroinvasive properties [5]. A case report of SARS-CoV-1 infection with CNS symptoms during the SARS epidemic also isolated the virus within a brain tissue specimen [6]. Although direct evidence of a neurotropic effect of SARS-Cov-2 has not been reported as yet through either cerebrospinal fluid (CSF) or autopsy studies, the presence of neurological symptoms in patients with COVID-19 disease during this current pandemic, and the similarity between the two strains of human coronaviruses (CoV-1 and CoV-2), makes this mechanism highly suggestive. Acute symptomatic seizures may be the result of a possible neurotropic effect of the virus or can be a marker of severity of systemic disease itself since CNS symptoms were found mainly in patients with severe COVID-19 disease. After penetration of the blood–brain barrier, the virus can slow the cerebral microcirculation, possibly through the creation of a hypercoagulable state. This allows increased interaction of SARS-CoV-2 with the endothelial receptors and receptors on glial tissue [7]. The interaction at the glia may predispose patients to seizures as seen in other neurological diseases [8, 9].\nPrevious studies of SARS-coronaviruses have described the proliferation of pro-inflammatory cytokines that are active in promoting blood–barrier breakdown, namely interleukin-8 (IL8) and monocyte chemoattractant protein-1 (MCP1) [10, 11]. A description of coronavirus infections in a Japanese encephalitis mouse model demonstrated CNS viral infection induced astrocyte and microglia proliferation, leading to increased release of IL-8 in the CSF [10]. MCP1 is another pro-inflammatory mediator that is expressed in CNS cells including astrocytes, neurons, and microglia. MCP1 may be up-regulated in conditions which target and degrade the blood–brain barrier and can recruit additional inflammatory cells as the monocytes migrate across the blood–brain barrier [11]. We hypothesize that as a result of the accumulation of inflammatory markers, there may be local cortical irritation that precipitates seizures related to COVID-19 infection. Although cerebrospinal fluid may contain markers of inflammation, the treatment of this infection is largely supportive, and with the additional risk of coagulopathy precipitated by SARS-CoV-2, a lumbar puncture may not be justifiable unless there is an alternative diagnosis to be sought. A limitation of our case series is that cerebrospinal fluid was unable to be obtained due to patient factors that made a lumbar puncture relatively contraindicated and that a CSF-PCR test for SARS-CoV-2 was not yet commercially available. As this disease continues to spread, we will continue to learn about its direct and/or indirect epileptogenesis."}

LitCovid-PD-GO-BP

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T5","span":{"begin":2585,"end":2594},"obj":"http://purl.obolibrary.org/obo/GO_0009056"},{"id":"T6","span":{"begin":2775,"end":2790},"obj":"http://purl.obolibrary.org/obo/GO_0016032"},{"id":"T7","span":{"begin":3433,"end":3445},"obj":"http://purl.obolibrary.org/obo/GO_0006954"}],"text":"Discussion\nThe SARS-Coronavirus-2 belongs to the β-coronavirus group which includes several human pathogenic viruses including middle east respiratory syndrome (MERS) coronavirus and SARS-CoV-1. These group of coronaviruses are associated with respiratory symptoms. Additional neurological symptoms including delirium, dizziness, and headaches have also been reported with other coronavirus infections prior to the SARS-CoV-2 outbreak [4]. The case series of patients from Wuhan, China, with COVID-19 disease, included both central and peripheral neurological manifestations (i.e., headache, dizziness, impaired consciousness, cerebrovascular disease, and neuralgia) [2]. Seizures were not reported as a direct manifestation of SARS-CoV-2 infection. The patients described in our series developed focal seizures and, in the second case, even progressed to non-convulsive status epilepticus. Seizures may be a CNS manifestation of COVID-19 disease. Further investigations are needed to elucidate the mechanism of neurological symptoms in SARS-CoV-2 infection.\nHuman coronaviruses (HCoV) have been established to infect human astrocytes and microglia in neural cell cultures as well as detection of viral RNA in a study of human brain autopsy samples supporting their neurotropic and neuroinvasive properties [5]. A case report of SARS-CoV-1 infection with CNS symptoms during the SARS epidemic also isolated the virus within a brain tissue specimen [6]. Although direct evidence of a neurotropic effect of SARS-Cov-2 has not been reported as yet through either cerebrospinal fluid (CSF) or autopsy studies, the presence of neurological symptoms in patients with COVID-19 disease during this current pandemic, and the similarity between the two strains of human coronaviruses (CoV-1 and CoV-2), makes this mechanism highly suggestive. Acute symptomatic seizures may be the result of a possible neurotropic effect of the virus or can be a marker of severity of systemic disease itself since CNS symptoms were found mainly in patients with severe COVID-19 disease. After penetration of the blood–brain barrier, the virus can slow the cerebral microcirculation, possibly through the creation of a hypercoagulable state. This allows increased interaction of SARS-CoV-2 with the endothelial receptors and receptors on glial tissue [7]. The interaction at the glia may predispose patients to seizures as seen in other neurological diseases [8, 9].\nPrevious studies of SARS-coronaviruses have described the proliferation of pro-inflammatory cytokines that are active in promoting blood–barrier breakdown, namely interleukin-8 (IL8) and monocyte chemoattractant protein-1 (MCP1) [10, 11]. A description of coronavirus infections in a Japanese encephalitis mouse model demonstrated CNS viral infection induced astrocyte and microglia proliferation, leading to increased release of IL-8 in the CSF [10]. MCP1 is another pro-inflammatory mediator that is expressed in CNS cells including astrocytes, neurons, and microglia. MCP1 may be up-regulated in conditions which target and degrade the blood–brain barrier and can recruit additional inflammatory cells as the monocytes migrate across the blood–brain barrier [11]. We hypothesize that as a result of the accumulation of inflammatory markers, there may be local cortical irritation that precipitates seizures related to COVID-19 infection. Although cerebrospinal fluid may contain markers of inflammation, the treatment of this infection is largely supportive, and with the additional risk of coagulopathy precipitated by SARS-CoV-2, a lumbar puncture may not be justifiable unless there is an alternative diagnosis to be sought. A limitation of our case series is that cerebrospinal fluid was unable to be obtained due to patient factors that made a lumbar puncture relatively contraindicated and that a CSF-PCR test for SARS-CoV-2 was not yet commercially available. As this disease continues to spread, we will continue to learn about its direct and/or indirect epileptogenesis."}

LitCovid-PD-HP

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T82","span":{"begin":0,"end":10},"obj":"Sentence"},{"id":"T83","span":{"begin":11,"end":194},"obj":"Sentence"},{"id":"T84","span":{"begin":195,"end":265},"obj":"Sentence"},{"id":"T85","span":{"begin":266,"end":439},"obj":"Sentence"},{"id":"T86","span":{"begin":440,"end":671},"obj":"Sentence"},{"id":"T87","span":{"begin":672,"end":749},"obj":"Sentence"},{"id":"T88","span":{"begin":750,"end":890},"obj":"Sentence"},{"id":"T89","span":{"begin":891,"end":947},"obj":"Sentence"},{"id":"T90","span":{"begin":948,"end":1058},"obj":"Sentence"},{"id":"T91","span":{"begin":1059,"end":1311},"obj":"Sentence"},{"id":"T92","span":{"begin":1312,"end":1452},"obj":"Sentence"},{"id":"T93","span":{"begin":1453,"end":1832},"obj":"Sentence"},{"id":"T94","span":{"begin":1833,"end":2060},"obj":"Sentence"},{"id":"T95","span":{"begin":2061,"end":2214},"obj":"Sentence"},{"id":"T96","span":{"begin":2215,"end":2328},"obj":"Sentence"},{"id":"T97","span":{"begin":2329,"end":2439},"obj":"Sentence"},{"id":"T98","span":{"begin":2440,"end":2678},"obj":"Sentence"},{"id":"T99","span":{"begin":2679,"end":2891},"obj":"Sentence"},{"id":"T100","span":{"begin":2892,"end":3010},"obj":"Sentence"},{"id":"T101","span":{"begin":3011,"end":3206},"obj":"Sentence"},{"id":"T102","span":{"begin":3207,"end":3380},"obj":"Sentence"},{"id":"T103","span":{"begin":3381,"end":3670},"obj":"Sentence"},{"id":"T104","span":{"begin":3671,"end":3909},"obj":"Sentence"},{"id":"T105","span":{"begin":3910,"end":4022},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Discussion\nThe SARS-Coronavirus-2 belongs to the β-coronavirus group which includes several human pathogenic viruses including middle east respiratory syndrome (MERS) coronavirus and SARS-CoV-1. These group of coronaviruses are associated with respiratory symptoms. Additional neurological symptoms including delirium, dizziness, and headaches have also been reported with other coronavirus infections prior to the SARS-CoV-2 outbreak [4]. The case series of patients from Wuhan, China, with COVID-19 disease, included both central and peripheral neurological manifestations (i.e., headache, dizziness, impaired consciousness, cerebrovascular disease, and neuralgia) [2]. Seizures were not reported as a direct manifestation of SARS-CoV-2 infection. The patients described in our series developed focal seizures and, in the second case, even progressed to non-convulsive status epilepticus. Seizures may be a CNS manifestation of COVID-19 disease. Further investigations are needed to elucidate the mechanism of neurological symptoms in SARS-CoV-2 infection.\nHuman coronaviruses (HCoV) have been established to infect human astrocytes and microglia in neural cell cultures as well as detection of viral RNA in a study of human brain autopsy samples supporting their neurotropic and neuroinvasive properties [5]. A case report of SARS-CoV-1 infection with CNS symptoms during the SARS epidemic also isolated the virus within a brain tissue specimen [6]. Although direct evidence of a neurotropic effect of SARS-Cov-2 has not been reported as yet through either cerebrospinal fluid (CSF) or autopsy studies, the presence of neurological symptoms in patients with COVID-19 disease during this current pandemic, and the similarity between the two strains of human coronaviruses (CoV-1 and CoV-2), makes this mechanism highly suggestive. Acute symptomatic seizures may be the result of a possible neurotropic effect of the virus or can be a marker of severity of systemic disease itself since CNS symptoms were found mainly in patients with severe COVID-19 disease. After penetration of the blood–brain barrier, the virus can slow the cerebral microcirculation, possibly through the creation of a hypercoagulable state. This allows increased interaction of SARS-CoV-2 with the endothelial receptors and receptors on glial tissue [7]. The interaction at the glia may predispose patients to seizures as seen in other neurological diseases [8, 9].\nPrevious studies of SARS-coronaviruses have described the proliferation of pro-inflammatory cytokines that are active in promoting blood–barrier breakdown, namely interleukin-8 (IL8) and monocyte chemoattractant protein-1 (MCP1) [10, 11]. A description of coronavirus infections in a Japanese encephalitis mouse model demonstrated CNS viral infection induced astrocyte and microglia proliferation, leading to increased release of IL-8 in the CSF [10]. MCP1 is another pro-inflammatory mediator that is expressed in CNS cells including astrocytes, neurons, and microglia. MCP1 may be up-regulated in conditions which target and degrade the blood–brain barrier and can recruit additional inflammatory cells as the monocytes migrate across the blood–brain barrier [11]. We hypothesize that as a result of the accumulation of inflammatory markers, there may be local cortical irritation that precipitates seizures related to COVID-19 infection. Although cerebrospinal fluid may contain markers of inflammation, the treatment of this infection is largely supportive, and with the additional risk of coagulopathy precipitated by SARS-CoV-2, a lumbar puncture may not be justifiable unless there is an alternative diagnosis to be sought. A limitation of our case series is that cerebrospinal fluid was unable to be obtained due to patient factors that made a lumbar puncture relatively contraindicated and that a CSF-PCR test for SARS-CoV-2 was not yet commercially available. As this disease continues to spread, we will continue to learn about its direct and/or indirect epileptogenesis."}

2_test

{"project":"2_test","denotations":[{"id":"32462412-10982334-75539779","span":{"begin":1308,"end":1309},"obj":"10982334"},{"id":"32462412-16163626-75539780","span":{"begin":1449,"end":1450},"obj":"16163626"},{"id":"32462412-32167747-75539781","span":{"begin":2325,"end":2326},"obj":"32167747"},{"id":"32462412-18336559-75539782","span":{"begin":2436,"end":2437},"obj":"18336559"},{"id":"32462412-28103598-75539783","span":{"begin":2670,"end":2672},"obj":"28103598"},{"id":"32462412-24051980-75539784","span":{"begin":2674,"end":2676},"obj":"24051980"},{"id":"32462412-28103598-75539785","span":{"begin":2887,"end":2889},"obj":"28103598"},{"id":"32462412-24051980-75539786","span":{"begin":3202,"end":3204},"obj":"24051980"}],"text":"Discussion\nThe SARS-Coronavirus-2 belongs to the β-coronavirus group which includes several human pathogenic viruses including middle east respiratory syndrome (MERS) coronavirus and SARS-CoV-1. These group of coronaviruses are associated with respiratory symptoms. Additional neurological symptoms including delirium, dizziness, and headaches have also been reported with other coronavirus infections prior to the SARS-CoV-2 outbreak [4]. The case series of patients from Wuhan, China, with COVID-19 disease, included both central and peripheral neurological manifestations (i.e., headache, dizziness, impaired consciousness, cerebrovascular disease, and neuralgia) [2]. Seizures were not reported as a direct manifestation of SARS-CoV-2 infection. The patients described in our series developed focal seizures and, in the second case, even progressed to non-convulsive status epilepticus. Seizures may be a CNS manifestation of COVID-19 disease. Further investigations are needed to elucidate the mechanism of neurological symptoms in SARS-CoV-2 infection.\nHuman coronaviruses (HCoV) have been established to infect human astrocytes and microglia in neural cell cultures as well as detection of viral RNA in a study of human brain autopsy samples supporting their neurotropic and neuroinvasive properties [5]. A case report of SARS-CoV-1 infection with CNS symptoms during the SARS epidemic also isolated the virus within a brain tissue specimen [6]. Although direct evidence of a neurotropic effect of SARS-Cov-2 has not been reported as yet through either cerebrospinal fluid (CSF) or autopsy studies, the presence of neurological symptoms in patients with COVID-19 disease during this current pandemic, and the similarity between the two strains of human coronaviruses (CoV-1 and CoV-2), makes this mechanism highly suggestive. Acute symptomatic seizures may be the result of a possible neurotropic effect of the virus or can be a marker of severity of systemic disease itself since CNS symptoms were found mainly in patients with severe COVID-19 disease. After penetration of the blood–brain barrier, the virus can slow the cerebral microcirculation, possibly through the creation of a hypercoagulable state. This allows increased interaction of SARS-CoV-2 with the endothelial receptors and receptors on glial tissue [7]. The interaction at the glia may predispose patients to seizures as seen in other neurological diseases [8, 9].\nPrevious studies of SARS-coronaviruses have described the proliferation of pro-inflammatory cytokines that are active in promoting blood–barrier breakdown, namely interleukin-8 (IL8) and monocyte chemoattractant protein-1 (MCP1) [10, 11]. A description of coronavirus infections in a Japanese encephalitis mouse model demonstrated CNS viral infection induced astrocyte and microglia proliferation, leading to increased release of IL-8 in the CSF [10]. MCP1 is another pro-inflammatory mediator that is expressed in CNS cells including astrocytes, neurons, and microglia. MCP1 may be up-regulated in conditions which target and degrade the blood–brain barrier and can recruit additional inflammatory cells as the monocytes migrate across the blood–brain barrier [11]. We hypothesize that as a result of the accumulation of inflammatory markers, there may be local cortical irritation that precipitates seizures related to COVID-19 infection. Although cerebrospinal fluid may contain markers of inflammation, the treatment of this infection is largely supportive, and with the additional risk of coagulopathy precipitated by SARS-CoV-2, a lumbar puncture may not be justifiable unless there is an alternative diagnosis to be sought. A limitation of our case series is that cerebrospinal fluid was unable to be obtained due to patient factors that made a lumbar puncture relatively contraindicated and that a CSF-PCR test for SARS-CoV-2 was not yet commercially available. As this disease continues to spread, we will continue to learn about its direct and/or indirect epileptogenesis."}

PMC:7253233 / 10598-14620 JSONTXT

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PMC:7253233 / 10598-14620 JSON TXT