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LitCovid-PubTator

LitCovid-PMC-OGER-BB

LitCovid-PD-FMA-UBERON

LitCovid_AGAC

{"project":"LitCovid_AGAC","denotations":[{"id":"p17634s1","span":{"begin":1309,"end":1318},"obj":"PosReg"},{"id":"p17634s2","span":{"begin":1319,"end":1328},"obj":"CPA"}],"text":"Recent Advances in the Treatment of 2019-Novel Coronavirus\n\nRemdesivir and chloroquine[33]\nUsing clinical isolates of 2019-nCoV, Wang et al., 2020 evaluated the efficacy of seven agents (ribavirin, penciclovir, nitazoxanide, nafamostat, chloroquine, remdesivir [GS5734], and favipiravir [T-705]) in in vitro conditions. Cytotoxicity was evaluated in vero E6 cells, which was followed by infection of the cells with 2019-nCoV clinical isolates, and the test drug was evaluated at different doses. Reverse transcription polymerase chain reaction-based quantification was done to get the viral yield, which was later confirmed by immunofluorescence microscopy (nucleocapsid protein visualization). Both chloroquine and remdesivir inhibited virus infection at micromolar level (0.77–1.13 μM) and with high selectivity.[33]\nBeing an adenosine analog, remdesivir gets incorporated into viral RNA and causes premature chain termination.[34] The importance of chloroquine as an antiviral agent is coming up. Chloroquine even showed efficacy as a potent antiviral against SARS-CoV infection and spread.[35] Pretreatment with chloroquine renders vero E6 cells refractory to SARS CoV infection. Moreover, in the postinfection period, treatment with chloroquine prevents the spread of SARS-CoV infection.[35] Chloroquine increases endosomal pH and thus makes the environment unfavorable for the virus/cell fusion. Chloroquine also affects the glycosylation process of angiotensin-converting enzyme 2 (ACE-2, receptor for binding of viral spike protein, which is essential for interaction with the host).[35] Being nonexpensive and easily available agent, chloroquine may prove as a promising candidate.\n\nBaricitinib\nThe SARSCoV and the 2019nCoV both enters host cells through ACE2 receptormediated entry, especially through AT2 cells present in lungs.[36] Downstream signaling of this receptor mediates the endocytosis process, and AP2-associated protein kinase 1 (AAK1) plays a major role in this process. Thus, AAK1 represents an important target. Richardson et al., 2020 evaluated 378 ligands, of which 47 were already approved for use in other conditions. Among these ligands, six inhibited AAK1 with high affinity. Considering the side effect profile, they found janus kinase inhibitor baricitinib to be the most important agent. In addition to AAK1, baricitinib also binds to another endocytosis regulator protein (cyclin G-associated kinase). Thus, the authors suggest that baricitinib can be evaluated in the in vitro conditions as well as in the clinical trial settings for 2019-nCoV.[37]\n\nLimitations of current research\nLack of high-quality evidence (especially randomized controlled trails [RCTs]) is the most important limitation of the current CoV research. As most of the CoV strains are genetically different and the outbreaks occur extremely randomly, conducting an RCT is extremely difficult, and we have to rely on observational studies (most of which do not have proper control group), which hamper the estimation of proper treatment effect."}

LitCovid-PD-MONDO

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T46","span":{"begin":387,"end":396},"obj":"Disease"},{"id":"T47","span":{"begin":737,"end":752},"obj":"Disease"},{"id":"T48","span":{"begin":743,"end":752},"obj":"Disease"},{"id":"T49","span":{"begin":1063,"end":1081},"obj":"Disease"},{"id":"T50","span":{"begin":1072,"end":1081},"obj":"Disease"},{"id":"T51","span":{"begin":1164,"end":1168},"obj":"Disease"},{"id":"T52","span":{"begin":1173,"end":1182},"obj":"Disease"},{"id":"T53","span":{"begin":1273,"end":1291},"obj":"Disease"},{"id":"T54","span":{"begin":1282,"end":1291},"obj":"Disease"}],"attributes":[{"id":"A46","pred":"mondo_id","subj":"T46","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A47","pred":"mondo_id","subj":"T47","obj":"http://purl.obolibrary.org/obo/MONDO_0005108"},{"id":"A48","pred":"mondo_id","subj":"T48","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A49","pred":"mondo_id","subj":"T49","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A50","pred":"mondo_id","subj":"T50","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A51","pred":"mondo_id","subj":"T51","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A52","pred":"mondo_id","subj":"T52","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A53","pred":"mondo_id","subj":"T53","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A54","pred":"mondo_id","subj":"T54","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"}],"text":"Recent Advances in the Treatment of 2019-Novel Coronavirus\n\nRemdesivir and chloroquine[33]\nUsing clinical isolates of 2019-nCoV, Wang et al., 2020 evaluated the efficacy of seven agents (ribavirin, penciclovir, nitazoxanide, nafamostat, chloroquine, remdesivir [GS5734], and favipiravir [T-705]) in in vitro conditions. Cytotoxicity was evaluated in vero E6 cells, which was followed by infection of the cells with 2019-nCoV clinical isolates, and the test drug was evaluated at different doses. Reverse transcription polymerase chain reaction-based quantification was done to get the viral yield, which was later confirmed by immunofluorescence microscopy (nucleocapsid protein visualization). Both chloroquine and remdesivir inhibited virus infection at micromolar level (0.77–1.13 μM) and with high selectivity.[33]\nBeing an adenosine analog, remdesivir gets incorporated into viral RNA and causes premature chain termination.[34] The importance of chloroquine as an antiviral agent is coming up. Chloroquine even showed efficacy as a potent antiviral against SARS-CoV infection and spread.[35] Pretreatment with chloroquine renders vero E6 cells refractory to SARS CoV infection. Moreover, in the postinfection period, treatment with chloroquine prevents the spread of SARS-CoV infection.[35] Chloroquine increases endosomal pH and thus makes the environment unfavorable for the virus/cell fusion. Chloroquine also affects the glycosylation process of angiotensin-converting enzyme 2 (ACE-2, receptor for binding of viral spike protein, which is essential for interaction with the host).[35] Being nonexpensive and easily available agent, chloroquine may prove as a promising candidate.\n\nBaricitinib\nThe SARSCoV and the 2019nCoV both enters host cells through ACE2 receptormediated entry, especially through AT2 cells present in lungs.[36] Downstream signaling of this receptor mediates the endocytosis process, and AP2-associated protein kinase 1 (AAK1) plays a major role in this process. Thus, AAK1 represents an important target. Richardson et al., 2020 evaluated 378 ligands, of which 47 were already approved for use in other conditions. Among these ligands, six inhibited AAK1 with high affinity. Considering the side effect profile, they found janus kinase inhibitor baricitinib to be the most important agent. In addition to AAK1, baricitinib also binds to another endocytosis regulator protein (cyclin G-associated kinase). Thus, the authors suggest that baricitinib can be evaluated in the in vitro conditions as well as in the clinical trial settings for 2019-nCoV.[37]\n\nLimitations of current research\nLack of high-quality evidence (especially randomized controlled trails [RCTs]) is the most important limitation of the current CoV research. As most of the CoV strains are genetically different and the outbreaks occur extremely randomly, conducting an RCT is extremely difficult, and we have to rely on observational studies (most of which do not have proper control group), which hamper the estimation of proper treatment effect."}

LitCovid-PD-CLO

LitCovid-PD-CHEBI

LitCovid-PD-GO-BP

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T8","span":{"begin":496,"end":517},"obj":"http://purl.obolibrary.org/obo/GO_0001171"},{"id":"T9","span":{"begin":504,"end":517},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T10","span":{"begin":1389,"end":1400},"obj":"http://purl.obolibrary.org/obo/GO_0140253"},{"id":"T11","span":{"begin":1389,"end":1400},"obj":"http://purl.obolibrary.org/obo/GO_0045026"},{"id":"T12","span":{"begin":1389,"end":1400},"obj":"http://purl.obolibrary.org/obo/GO_0000768"},{"id":"T13","span":{"begin":1389,"end":1400},"obj":"http://purl.obolibrary.org/obo/GO_0000747"},{"id":"T14","span":{"begin":1431,"end":1444},"obj":"http://purl.obolibrary.org/obo/GO_0070085"},{"id":"T15","span":{"begin":1564,"end":1589},"obj":"http://purl.obolibrary.org/obo/GO_0051701"},{"id":"T16","span":{"begin":1855,"end":1864},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T17","span":{"begin":1873,"end":1906},"obj":"http://purl.obolibrary.org/obo/GO_0006898"},{"id":"T18","span":{"begin":1895,"end":1906},"obj":"http://purl.obolibrary.org/obo/GO_0006897"},{"id":"T19","span":{"begin":2262,"end":2278},"obj":"http://purl.obolibrary.org/obo/GO_0033673"},{"id":"T20","span":{"begin":2378,"end":2389},"obj":"http://purl.obolibrary.org/obo/GO_0006897"},{"id":"T21","span":{"begin":2409,"end":2415},"obj":"http://purl.obolibrary.org/obo/GO_0016538"}],"text":"Recent Advances in the Treatment of 2019-Novel Coronavirus\n\nRemdesivir and chloroquine[33]\nUsing clinical isolates of 2019-nCoV, Wang et al., 2020 evaluated the efficacy of seven agents (ribavirin, penciclovir, nitazoxanide, nafamostat, chloroquine, remdesivir [GS5734], and favipiravir [T-705]) in in vitro conditions. Cytotoxicity was evaluated in vero E6 cells, which was followed by infection of the cells with 2019-nCoV clinical isolates, and the test drug was evaluated at different doses. Reverse transcription polymerase chain reaction-based quantification was done to get the viral yield, which was later confirmed by immunofluorescence microscopy (nucleocapsid protein visualization). Both chloroquine and remdesivir inhibited virus infection at micromolar level (0.77–1.13 μM) and with high selectivity.[33]\nBeing an adenosine analog, remdesivir gets incorporated into viral RNA and causes premature chain termination.[34] The importance of chloroquine as an antiviral agent is coming up. Chloroquine even showed efficacy as a potent antiviral against SARS-CoV infection and spread.[35] Pretreatment with chloroquine renders vero E6 cells refractory to SARS CoV infection. Moreover, in the postinfection period, treatment with chloroquine prevents the spread of SARS-CoV infection.[35] Chloroquine increases endosomal pH and thus makes the environment unfavorable for the virus/cell fusion. Chloroquine also affects the glycosylation process of angiotensin-converting enzyme 2 (ACE-2, receptor for binding of viral spike protein, which is essential for interaction with the host).[35] Being nonexpensive and easily available agent, chloroquine may prove as a promising candidate.\n\nBaricitinib\nThe SARSCoV and the 2019nCoV both enters host cells through ACE2 receptormediated entry, especially through AT2 cells present in lungs.[36] Downstream signaling of this receptor mediates the endocytosis process, and AP2-associated protein kinase 1 (AAK1) plays a major role in this process. Thus, AAK1 represents an important target. Richardson et al., 2020 evaluated 378 ligands, of which 47 were already approved for use in other conditions. Among these ligands, six inhibited AAK1 with high affinity. Considering the side effect profile, they found janus kinase inhibitor baricitinib to be the most important agent. In addition to AAK1, baricitinib also binds to another endocytosis regulator protein (cyclin G-associated kinase). Thus, the authors suggest that baricitinib can be evaluated in the in vitro conditions as well as in the clinical trial settings for 2019-nCoV.[37]\n\nLimitations of current research\nLack of high-quality evidence (especially randomized controlled trails [RCTs]) is the most important limitation of the current CoV research. As most of the CoV strains are genetically different and the outbreaks occur extremely randomly, conducting an RCT is extremely difficult, and we have to rely on observational studies (most of which do not have proper control group), which hamper the estimation of proper treatment effect."}

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T80","span":{"begin":0,"end":58},"obj":"Sentence"},{"id":"T81","span":{"begin":60,"end":90},"obj":"Sentence"},{"id":"T82","span":{"begin":91,"end":319},"obj":"Sentence"},{"id":"T83","span":{"begin":320,"end":495},"obj":"Sentence"},{"id":"T84","span":{"begin":496,"end":694},"obj":"Sentence"},{"id":"T85","span":{"begin":695,"end":818},"obj":"Sentence"},{"id":"T86","span":{"begin":819,"end":999},"obj":"Sentence"},{"id":"T87","span":{"begin":1000,"end":1183},"obj":"Sentence"},{"id":"T88","span":{"begin":1184,"end":1401},"obj":"Sentence"},{"id":"T89","span":{"begin":1402,"end":1690},"obj":"Sentence"},{"id":"T90","span":{"begin":1692,"end":1703},"obj":"Sentence"},{"id":"T91","span":{"begin":1704,"end":1994},"obj":"Sentence"},{"id":"T92","span":{"begin":1995,"end":2037},"obj":"Sentence"},{"id":"T93","span":{"begin":2038,"end":2147},"obj":"Sentence"},{"id":"T94","span":{"begin":2148,"end":2207},"obj":"Sentence"},{"id":"T95","span":{"begin":2208,"end":2322},"obj":"Sentence"},{"id":"T96","span":{"begin":2323,"end":2437},"obj":"Sentence"},{"id":"T97","span":{"begin":2438,"end":2585},"obj":"Sentence"},{"id":"T98","span":{"begin":2587,"end":2618},"obj":"Sentence"},{"id":"T99","span":{"begin":2619,"end":2759},"obj":"Sentence"},{"id":"T100","span":{"begin":2760,"end":3049},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Recent Advances in the Treatment of 2019-Novel Coronavirus\n\nRemdesivir and chloroquine[33]\nUsing clinical isolates of 2019-nCoV, Wang et al., 2020 evaluated the efficacy of seven agents (ribavirin, penciclovir, nitazoxanide, nafamostat, chloroquine, remdesivir [GS5734], and favipiravir [T-705]) in in vitro conditions. Cytotoxicity was evaluated in vero E6 cells, which was followed by infection of the cells with 2019-nCoV clinical isolates, and the test drug was evaluated at different doses. Reverse transcription polymerase chain reaction-based quantification was done to get the viral yield, which was later confirmed by immunofluorescence microscopy (nucleocapsid protein visualization). Both chloroquine and remdesivir inhibited virus infection at micromolar level (0.77–1.13 μM) and with high selectivity.[33]\nBeing an adenosine analog, remdesivir gets incorporated into viral RNA and causes premature chain termination.[34] The importance of chloroquine as an antiviral agent is coming up. Chloroquine even showed efficacy as a potent antiviral against SARS-CoV infection and spread.[35] Pretreatment with chloroquine renders vero E6 cells refractory to SARS CoV infection. Moreover, in the postinfection period, treatment with chloroquine prevents the spread of SARS-CoV infection.[35] Chloroquine increases endosomal pH and thus makes the environment unfavorable for the virus/cell fusion. Chloroquine also affects the glycosylation process of angiotensin-converting enzyme 2 (ACE-2, receptor for binding of viral spike protein, which is essential for interaction with the host).[35] Being nonexpensive and easily available agent, chloroquine may prove as a promising candidate.\n\nBaricitinib\nThe SARSCoV and the 2019nCoV both enters host cells through ACE2 receptormediated entry, especially through AT2 cells present in lungs.[36] Downstream signaling of this receptor mediates the endocytosis process, and AP2-associated protein kinase 1 (AAK1) plays a major role in this process. Thus, AAK1 represents an important target. Richardson et al., 2020 evaluated 378 ligands, of which 47 were already approved for use in other conditions. Among these ligands, six inhibited AAK1 with high affinity. Considering the side effect profile, they found janus kinase inhibitor baricitinib to be the most important agent. In addition to AAK1, baricitinib also binds to another endocytosis regulator protein (cyclin G-associated kinase). Thus, the authors suggest that baricitinib can be evaluated in the in vitro conditions as well as in the clinical trial settings for 2019-nCoV.[37]\n\nLimitations of current research\nLack of high-quality evidence (especially randomized controlled trails [RCTs]) is the most important limitation of the current CoV research. As most of the CoV strains are genetically different and the outbreaks occur extremely randomly, conducting an RCT is extremely difficult, and we have to rely on observational studies (most of which do not have proper control group), which hamper the estimation of proper treatment effect."}

2_test

{"project":"2_test","denotations":[{"id":"32201439-32020029-47219433","span":{"begin":87,"end":89},"obj":"32020029"},{"id":"32201439-32020029-47219434","span":{"begin":815,"end":817},"obj":"32020029"},{"id":"32201439-26934220-47219435","span":{"begin":930,"end":932},"obj":"26934220"},{"id":"32201439-16115318-47219436","span":{"begin":1094,"end":1096},"obj":"16115318"},{"id":"32201439-16115318-47219437","span":{"begin":1293,"end":1295},"obj":"16115318"},{"id":"32201439-16115318-47219438","span":{"begin":1592,"end":1594},"obj":"16115318"},{"id":"32201439-32032529-47219439","span":{"begin":2582,"end":2584},"obj":"32032529"},{"id":"T41189","span":{"begin":87,"end":89},"obj":"32020029"},{"id":"T4625","span":{"begin":815,"end":817},"obj":"32020029"},{"id":"T49263","span":{"begin":930,"end":932},"obj":"26934220"},{"id":"T96382","span":{"begin":1094,"end":1096},"obj":"16115318"},{"id":"T21534","span":{"begin":1293,"end":1295},"obj":"16115318"},{"id":"T99419","span":{"begin":1592,"end":1594},"obj":"16115318"},{"id":"T4041","span":{"begin":2582,"end":2584},"obj":"32032529"}],"text":"Recent Advances in the Treatment of 2019-Novel Coronavirus\n\nRemdesivir and chloroquine[33]\nUsing clinical isolates of 2019-nCoV, Wang et al., 2020 evaluated the efficacy of seven agents (ribavirin, penciclovir, nitazoxanide, nafamostat, chloroquine, remdesivir [GS5734], and favipiravir [T-705]) in in vitro conditions. Cytotoxicity was evaluated in vero E6 cells, which was followed by infection of the cells with 2019-nCoV clinical isolates, and the test drug was evaluated at different doses. Reverse transcription polymerase chain reaction-based quantification was done to get the viral yield, which was later confirmed by immunofluorescence microscopy (nucleocapsid protein visualization). Both chloroquine and remdesivir inhibited virus infection at micromolar level (0.77–1.13 μM) and with high selectivity.[33]\nBeing an adenosine analog, remdesivir gets incorporated into viral RNA and causes premature chain termination.[34] The importance of chloroquine as an antiviral agent is coming up. Chloroquine even showed efficacy as a potent antiviral against SARS-CoV infection and spread.[35] Pretreatment with chloroquine renders vero E6 cells refractory to SARS CoV infection. Moreover, in the postinfection period, treatment with chloroquine prevents the spread of SARS-CoV infection.[35] Chloroquine increases endosomal pH and thus makes the environment unfavorable for the virus/cell fusion. Chloroquine also affects the glycosylation process of angiotensin-converting enzyme 2 (ACE-2, receptor for binding of viral spike protein, which is essential for interaction with the host).[35] Being nonexpensive and easily available agent, chloroquine may prove as a promising candidate.\n\nBaricitinib\nThe SARSCoV and the 2019nCoV both enters host cells through ACE2 receptormediated entry, especially through AT2 cells present in lungs.[36] Downstream signaling of this receptor mediates the endocytosis process, and AP2-associated protein kinase 1 (AAK1) plays a major role in this process. Thus, AAK1 represents an important target. Richardson et al., 2020 evaluated 378 ligands, of which 47 were already approved for use in other conditions. Among these ligands, six inhibited AAK1 with high affinity. Considering the side effect profile, they found janus kinase inhibitor baricitinib to be the most important agent. In addition to AAK1, baricitinib also binds to another endocytosis regulator protein (cyclin G-associated kinase). Thus, the authors suggest that baricitinib can be evaluated in the in vitro conditions as well as in the clinical trial settings for 2019-nCoV.[37]\n\nLimitations of current research\nLack of high-quality evidence (especially randomized controlled trails [RCTs]) is the most important limitation of the current CoV research. As most of the CoV strains are genetically different and the outbreaks occur extremely randomly, conducting an RCT is extremely difficult, and we have to rely on observational studies (most of which do not have proper control group), which hamper the estimation of proper treatment effect."}

PMC:7074432 / 11879-14928 JSONTXT

Annnotations TAB JSON ListView MergeView

PMC:7074432 / 11879-14928 JSON TXT