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LitCovid-PD-FMA-UBERON

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T41","span":{"begin":2729,"end":2733},"obj":"Body_part"},{"id":"T42","span":{"begin":2767,"end":2779},"obj":"Body_part"},{"id":"T43","span":{"begin":2822,"end":2826},"obj":"Body_part"}],"attributes":[{"id":"A41","pred":"fma_id","subj":"T41","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A42","pred":"fma_id","subj":"T42","obj":"http://purl.org/sig/ont/fma/fma86578"},{"id":"A43","pred":"fma_id","subj":"T43","obj":"http://purl.org/sig/ont/fma/fma68646"}],"text":"Discussion\nWe confirmed that in a significantly proportion of COVID-19 patients, SARS-CoV-2 reactivation developed after discharging from hospital (9%). We reported clinical data from 5 patients with SARS-CoV-2 reactivation. The clinical characteristics of these patients with SARS-CoV-2 reactivation were similar to those of non-reactivated patients with COVID-19 infection. None of the 5 patients developed severe pneumonia or died, as of Feb. 24, 2020. Notably, based on our findings in these 5 patients, there is currently evidence to suggest that a proportion of recovered COVID-19 patients could reactivate.\nThe reactivated patients included 1 asymptomatic patient and 4 symptomatic patients, which suggests the reactivation potential of asymptomatic or minimally symptomatic patients. The time from SARS-CoV-2 negative to positive ranged from 4 to 17 days, suggesting that recovered patients still may be virus carriers and require additional round of viral detection and isolation.\nWe need better data to determine risk factors and mechanisms that cause SARS-CoV-2 reactivation. The timing of onset of SARS-CoV-2 reactivation can be variable depending upon the host factors, underlying disease and the type of immunosuppressive therapies. In our study, the recovered patients had positive RT-PCR test results 4–17 days later. The key risk factors for reactivation would include 3 categories: (1) host status, (2) virologic factors and (3) type and degree of immunosuppression. Host factors may include sex, older age, type of disease needing immunosuppression. Although we could not identify risk factors for these host factors in the current study, the potential requires further large cohort confirmation. The virologic factors associated with increased risk of reactivation include high baseline SARS-CoV-2 load and variable genotype. SARS-CoV-2 viral load would also linked to treatment response, disease severity and progression.8 The association of SARS-CoV-2 genotypes and viral load with SARS-CoV-2 reactivation will be an important question to address. In our study, all the patients received antiviral therapy (Oseltamivir or Arbidol). These cases suggest that SARS-CoV-2 reactivation may occur whatever the antiviral therapy used. These host and virologic factors are important considerations that may further increase the likelihood of SARS-CoV-2 reactivation. Therefore, the assessment of host as well as virologic risk factors should be important caveats to help decide whether to initiate prophylactic therapy and immunosuppression. Immunosuppressive therapies are the commonly used causative agents. These agents have a general mechanism that inhibits many immune functions. For example, steroid inhibits cell-mediated immunity by suppressing interleukins production which is important for T and B cell proliferation.9 It is thus not surprising that these general immunosuppressive effects result in broad immune dysfunctions and potential SARS-CoV-2 reactivation.\nSARS-CoV-2 reactivation will be a vexing and persistent problem. Considering numerous patients infected or previously exposed to the virus, such a problem poses a major public health burden in terms of global morbidity and possibly mortality. Currently, we did not find reliable markers in predicting the risk of SARS-CoV-2 reactivation, nor there are any validated tests to determine whether a particular drug or therapy is associated with SARS-CoV-2 reactivation. The latter point was often determined by our empirical experience. Although decades of the experiences helped us to identify important drugs and to manage these situations appropriately, we could not accurately evaluate the risk of the drugs prior to its clinical application.\nConsidering the significance of this ongoing global public health emergency, although our conclusions are limited by the small sample size, we believe that the findings are important to understand the clinical characteristics and SARS-CoV-2 reactivation potential in COVID-19 patients."}

LitCovid-PD-MONDO

LitCovid-PD-CLO

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T70","span":{"begin":32,"end":33},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T71","span":{"begin":552,"end":553},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T72","span":{"begin":912,"end":917},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"},{"id":"T73","span":{"begin":1304,"end":1308},"obj":"http://purl.obolibrary.org/obo/UBERON_0000473"},{"id":"T74","span":{"begin":2642,"end":2643},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T75","span":{"begin":2729,"end":2733},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T76","span":{"begin":2820,"end":2826},"obj":"http://purl.obolibrary.org/obo/CL_0000236"},{"id":"T77","span":{"begin":3021,"end":3022},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T78","span":{"begin":3122,"end":3127},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"},{"id":"T79","span":{"begin":3134,"end":3135},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T80","span":{"begin":3150,"end":3151},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T81","span":{"begin":3355,"end":3360},"obj":"http://purl.obolibrary.org/obo/UBERON_0000473"},{"id":"T82","span":{"begin":3382,"end":3383},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"}],"text":"Discussion\nWe confirmed that in a significantly proportion of COVID-19 patients, SARS-CoV-2 reactivation developed after discharging from hospital (9%). We reported clinical data from 5 patients with SARS-CoV-2 reactivation. The clinical characteristics of these patients with SARS-CoV-2 reactivation were similar to those of non-reactivated patients with COVID-19 infection. None of the 5 patients developed severe pneumonia or died, as of Feb. 24, 2020. Notably, based on our findings in these 5 patients, there is currently evidence to suggest that a proportion of recovered COVID-19 patients could reactivate.\nThe reactivated patients included 1 asymptomatic patient and 4 symptomatic patients, which suggests the reactivation potential of asymptomatic or minimally symptomatic patients. The time from SARS-CoV-2 negative to positive ranged from 4 to 17 days, suggesting that recovered patients still may be virus carriers and require additional round of viral detection and isolation.\nWe need better data to determine risk factors and mechanisms that cause SARS-CoV-2 reactivation. The timing of onset of SARS-CoV-2 reactivation can be variable depending upon the host factors, underlying disease and the type of immunosuppressive therapies. In our study, the recovered patients had positive RT-PCR test results 4–17 days later. The key risk factors for reactivation would include 3 categories: (1) host status, (2) virologic factors and (3) type and degree of immunosuppression. Host factors may include sex, older age, type of disease needing immunosuppression. Although we could not identify risk factors for these host factors in the current study, the potential requires further large cohort confirmation. The virologic factors associated with increased risk of reactivation include high baseline SARS-CoV-2 load and variable genotype. SARS-CoV-2 viral load would also linked to treatment response, disease severity and progression.8 The association of SARS-CoV-2 genotypes and viral load with SARS-CoV-2 reactivation will be an important question to address. In our study, all the patients received antiviral therapy (Oseltamivir or Arbidol). These cases suggest that SARS-CoV-2 reactivation may occur whatever the antiviral therapy used. These host and virologic factors are important considerations that may further increase the likelihood of SARS-CoV-2 reactivation. Therefore, the assessment of host as well as virologic risk factors should be important caveats to help decide whether to initiate prophylactic therapy and immunosuppression. Immunosuppressive therapies are the commonly used causative agents. These agents have a general mechanism that inhibits many immune functions. For example, steroid inhibits cell-mediated immunity by suppressing interleukins production which is important for T and B cell proliferation.9 It is thus not surprising that these general immunosuppressive effects result in broad immune dysfunctions and potential SARS-CoV-2 reactivation.\nSARS-CoV-2 reactivation will be a vexing and persistent problem. Considering numerous patients infected or previously exposed to the virus, such a problem poses a major public health burden in terms of global morbidity and possibly mortality. Currently, we did not find reliable markers in predicting the risk of SARS-CoV-2 reactivation, nor there are any validated tests to determine whether a particular drug or therapy is associated with SARS-CoV-2 reactivation. The latter point was often determined by our empirical experience. Although decades of the experiences helped us to identify important drugs and to manage these situations appropriately, we could not accurately evaluate the risk of the drugs prior to its clinical application.\nConsidering the significance of this ongoing global public health emergency, although our conclusions are limited by the small sample size, we believe that the findings are important to understand the clinical characteristics and SARS-CoV-2 reactivation potential in COVID-19 patients."}

LitCovid-PD-CHEBI

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T26","span":{"begin":918,"end":926},"obj":"Chemical"},{"id":"T27","span":{"begin":2110,"end":2119},"obj":"Chemical"},{"id":"T28","span":{"begin":2129,"end":2140},"obj":"Chemical"},{"id":"T29","span":{"begin":2226,"end":2235},"obj":"Chemical"},{"id":"T30","span":{"begin":2712,"end":2719},"obj":"Chemical"},{"id":"T31","span":{"begin":2767,"end":2779},"obj":"Chemical"},{"id":"T32","span":{"begin":3395,"end":3399},"obj":"Chemical"},{"id":"T33","span":{"begin":3590,"end":3595},"obj":"Chemical"},{"id":"T34","span":{"begin":3691,"end":3696},"obj":"Chemical"},{"id":"T35","span":{"begin":3719,"end":3730},"obj":"Chemical"}],"attributes":[{"id":"A26","pred":"chebi_id","subj":"T26","obj":"http://purl.obolibrary.org/obo/CHEBI_78059"},{"id":"A27","pred":"chebi_id","subj":"T27","obj":"http://purl.obolibrary.org/obo/CHEBI_22587"},{"id":"A28","pred":"chebi_id","subj":"T28","obj":"http://purl.obolibrary.org/obo/CHEBI_7798"},{"id":"A29","pred":"chebi_id","subj":"T29","obj":"http://purl.obolibrary.org/obo/CHEBI_22587"},{"id":"A30","pred":"chebi_id","subj":"T30","obj":"http://purl.obolibrary.org/obo/CHEBI_35341"},{"id":"A31","pred":"chebi_id","subj":"T31","obj":"http://purl.obolibrary.org/obo/CHEBI_52998"},{"id":"A32","pred":"chebi_id","subj":"T32","obj":"http://purl.obolibrary.org/obo/CHEBI_23888"},{"id":"A33","pred":"chebi_id","subj":"T33","obj":"http://purl.obolibrary.org/obo/CHEBI_23888"},{"id":"A34","pred":"chebi_id","subj":"T34","obj":"http://purl.obolibrary.org/obo/CHEBI_23888"},{"id":"A35","pred":"chebi_id","subj":"T35","obj":"http://purl.obolibrary.org/obo/CHEBI_33232"}],"text":"Discussion\nWe confirmed that in a significantly proportion of COVID-19 patients, SARS-CoV-2 reactivation developed after discharging from hospital (9%). We reported clinical data from 5 patients with SARS-CoV-2 reactivation. The clinical characteristics of these patients with SARS-CoV-2 reactivation were similar to those of non-reactivated patients with COVID-19 infection. None of the 5 patients developed severe pneumonia or died, as of Feb. 24, 2020. Notably, based on our findings in these 5 patients, there is currently evidence to suggest that a proportion of recovered COVID-19 patients could reactivate.\nThe reactivated patients included 1 asymptomatic patient and 4 symptomatic patients, which suggests the reactivation potential of asymptomatic or minimally symptomatic patients. The time from SARS-CoV-2 negative to positive ranged from 4 to 17 days, suggesting that recovered patients still may be virus carriers and require additional round of viral detection and isolation.\nWe need better data to determine risk factors and mechanisms that cause SARS-CoV-2 reactivation. The timing of onset of SARS-CoV-2 reactivation can be variable depending upon the host factors, underlying disease and the type of immunosuppressive therapies. In our study, the recovered patients had positive RT-PCR test results 4–17 days later. The key risk factors for reactivation would include 3 categories: (1) host status, (2) virologic factors and (3) type and degree of immunosuppression. Host factors may include sex, older age, type of disease needing immunosuppression. Although we could not identify risk factors for these host factors in the current study, the potential requires further large cohort confirmation. The virologic factors associated with increased risk of reactivation include high baseline SARS-CoV-2 load and variable genotype. SARS-CoV-2 viral load would also linked to treatment response, disease severity and progression.8 The association of SARS-CoV-2 genotypes and viral load with SARS-CoV-2 reactivation will be an important question to address. In our study, all the patients received antiviral therapy (Oseltamivir or Arbidol). These cases suggest that SARS-CoV-2 reactivation may occur whatever the antiviral therapy used. These host and virologic factors are important considerations that may further increase the likelihood of SARS-CoV-2 reactivation. Therefore, the assessment of host as well as virologic risk factors should be important caveats to help decide whether to initiate prophylactic therapy and immunosuppression. Immunosuppressive therapies are the commonly used causative agents. These agents have a general mechanism that inhibits many immune functions. For example, steroid inhibits cell-mediated immunity by suppressing interleukins production which is important for T and B cell proliferation.9 It is thus not surprising that these general immunosuppressive effects result in broad immune dysfunctions and potential SARS-CoV-2 reactivation.\nSARS-CoV-2 reactivation will be a vexing and persistent problem. Considering numerous patients infected or previously exposed to the virus, such a problem poses a major public health burden in terms of global morbidity and possibly mortality. Currently, we did not find reliable markers in predicting the risk of SARS-CoV-2 reactivation, nor there are any validated tests to determine whether a particular drug or therapy is associated with SARS-CoV-2 reactivation. The latter point was often determined by our empirical experience. Although decades of the experiences helped us to identify important drugs and to manage these situations appropriately, we could not accurately evaluate the risk of the drugs prior to its clinical application.\nConsidering the significance of this ongoing global public health emergency, although our conclusions are limited by the small sample size, we believe that the findings are important to understand the clinical characteristics and SARS-CoV-2 reactivation potential in COVID-19 patients."}

LitCovid-PD-GO-BP

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T2","span":{"begin":2729,"end":2751},"obj":"http://purl.obolibrary.org/obo/GO_0002456"},{"id":"T3","span":{"begin":2729,"end":2751},"obj":"http://purl.obolibrary.org/obo/GO_0002449"},{"id":"T4","span":{"begin":2767,"end":2790},"obj":"http://purl.obolibrary.org/obo/GO_0001816"},{"id":"T5","span":{"begin":2820,"end":2840},"obj":"http://purl.obolibrary.org/obo/GO_0042100"},{"id":"T6","span":{"begin":2822,"end":2840},"obj":"http://purl.obolibrary.org/obo/GO_0008283"}],"text":"Discussion\nWe confirmed that in a significantly proportion of COVID-19 patients, SARS-CoV-2 reactivation developed after discharging from hospital (9%). We reported clinical data from 5 patients with SARS-CoV-2 reactivation. The clinical characteristics of these patients with SARS-CoV-2 reactivation were similar to those of non-reactivated patients with COVID-19 infection. None of the 5 patients developed severe pneumonia or died, as of Feb. 24, 2020. Notably, based on our findings in these 5 patients, there is currently evidence to suggest that a proportion of recovered COVID-19 patients could reactivate.\nThe reactivated patients included 1 asymptomatic patient and 4 symptomatic patients, which suggests the reactivation potential of asymptomatic or minimally symptomatic patients. The time from SARS-CoV-2 negative to positive ranged from 4 to 17 days, suggesting that recovered patients still may be virus carriers and require additional round of viral detection and isolation.\nWe need better data to determine risk factors and mechanisms that cause SARS-CoV-2 reactivation. The timing of onset of SARS-CoV-2 reactivation can be variable depending upon the host factors, underlying disease and the type of immunosuppressive therapies. In our study, the recovered patients had positive RT-PCR test results 4–17 days later. The key risk factors for reactivation would include 3 categories: (1) host status, (2) virologic factors and (3) type and degree of immunosuppression. Host factors may include sex, older age, type of disease needing immunosuppression. Although we could not identify risk factors for these host factors in the current study, the potential requires further large cohort confirmation. The virologic factors associated with increased risk of reactivation include high baseline SARS-CoV-2 load and variable genotype. SARS-CoV-2 viral load would also linked to treatment response, disease severity and progression.8 The association of SARS-CoV-2 genotypes and viral load with SARS-CoV-2 reactivation will be an important question to address. In our study, all the patients received antiviral therapy (Oseltamivir or Arbidol). These cases suggest that SARS-CoV-2 reactivation may occur whatever the antiviral therapy used. These host and virologic factors are important considerations that may further increase the likelihood of SARS-CoV-2 reactivation. Therefore, the assessment of host as well as virologic risk factors should be important caveats to help decide whether to initiate prophylactic therapy and immunosuppression. Immunosuppressive therapies are the commonly used causative agents. These agents have a general mechanism that inhibits many immune functions. For example, steroid inhibits cell-mediated immunity by suppressing interleukins production which is important for T and B cell proliferation.9 It is thus not surprising that these general immunosuppressive effects result in broad immune dysfunctions and potential SARS-CoV-2 reactivation.\nSARS-CoV-2 reactivation will be a vexing and persistent problem. Considering numerous patients infected or previously exposed to the virus, such a problem poses a major public health burden in terms of global morbidity and possibly mortality. Currently, we did not find reliable markers in predicting the risk of SARS-CoV-2 reactivation, nor there are any validated tests to determine whether a particular drug or therapy is associated with SARS-CoV-2 reactivation. The latter point was often determined by our empirical experience. Although decades of the experiences helped us to identify important drugs and to manage these situations appropriately, we could not accurately evaluate the risk of the drugs prior to its clinical application.\nConsidering the significance of this ongoing global public health emergency, although our conclusions are limited by the small sample size, we believe that the findings are important to understand the clinical characteristics and SARS-CoV-2 reactivation potential in COVID-19 patients."}

LitCovid-PD-HP

{"project":"LitCovid-PD-HP","denotations":[{"id":"T41","span":{"begin":416,"end":425},"obj":"Phenotype"}],"attributes":[{"id":"A41","pred":"hp_id","subj":"T41","obj":"http://purl.obolibrary.org/obo/HP_0002090"}],"text":"Discussion\nWe confirmed that in a significantly proportion of COVID-19 patients, SARS-CoV-2 reactivation developed after discharging from hospital (9%). We reported clinical data from 5 patients with SARS-CoV-2 reactivation. The clinical characteristics of these patients with SARS-CoV-2 reactivation were similar to those of non-reactivated patients with COVID-19 infection. None of the 5 patients developed severe pneumonia or died, as of Feb. 24, 2020. Notably, based on our findings in these 5 patients, there is currently evidence to suggest that a proportion of recovered COVID-19 patients could reactivate.\nThe reactivated patients included 1 asymptomatic patient and 4 symptomatic patients, which suggests the reactivation potential of asymptomatic or minimally symptomatic patients. The time from SARS-CoV-2 negative to positive ranged from 4 to 17 days, suggesting that recovered patients still may be virus carriers and require additional round of viral detection and isolation.\nWe need better data to determine risk factors and mechanisms that cause SARS-CoV-2 reactivation. The timing of onset of SARS-CoV-2 reactivation can be variable depending upon the host factors, underlying disease and the type of immunosuppressive therapies. In our study, the recovered patients had positive RT-PCR test results 4–17 days later. The key risk factors for reactivation would include 3 categories: (1) host status, (2) virologic factors and (3) type and degree of immunosuppression. Host factors may include sex, older age, type of disease needing immunosuppression. Although we could not identify risk factors for these host factors in the current study, the potential requires further large cohort confirmation. The virologic factors associated with increased risk of reactivation include high baseline SARS-CoV-2 load and variable genotype. SARS-CoV-2 viral load would also linked to treatment response, disease severity and progression.8 The association of SARS-CoV-2 genotypes and viral load with SARS-CoV-2 reactivation will be an important question to address. In our study, all the patients received antiviral therapy (Oseltamivir or Arbidol). These cases suggest that SARS-CoV-2 reactivation may occur whatever the antiviral therapy used. These host and virologic factors are important considerations that may further increase the likelihood of SARS-CoV-2 reactivation. Therefore, the assessment of host as well as virologic risk factors should be important caveats to help decide whether to initiate prophylactic therapy and immunosuppression. Immunosuppressive therapies are the commonly used causative agents. These agents have a general mechanism that inhibits many immune functions. For example, steroid inhibits cell-mediated immunity by suppressing interleukins production which is important for T and B cell proliferation.9 It is thus not surprising that these general immunosuppressive effects result in broad immune dysfunctions and potential SARS-CoV-2 reactivation.\nSARS-CoV-2 reactivation will be a vexing and persistent problem. Considering numerous patients infected or previously exposed to the virus, such a problem poses a major public health burden in terms of global morbidity and possibly mortality. Currently, we did not find reliable markers in predicting the risk of SARS-CoV-2 reactivation, nor there are any validated tests to determine whether a particular drug or therapy is associated with SARS-CoV-2 reactivation. The latter point was often determined by our empirical experience. Although decades of the experiences helped us to identify important drugs and to manage these situations appropriately, we could not accurately evaluate the risk of the drugs prior to its clinical application.\nConsidering the significance of this ongoing global public health emergency, although our conclusions are limited by the small sample size, we believe that the findings are important to understand the clinical characteristics and SARS-CoV-2 reactivation potential in COVID-19 patients."}

LitCovid-sentences

LitCovid-PubTator

2_test

{"project":"2_test","denotations":[{"id":"32171867-17293163-61116998","span":{"begin":2841,"end":2842},"obj":"17293163"}],"text":"Discussion\nWe confirmed that in a significantly proportion of COVID-19 patients, SARS-CoV-2 reactivation developed after discharging from hospital (9%). We reported clinical data from 5 patients with SARS-CoV-2 reactivation. The clinical characteristics of these patients with SARS-CoV-2 reactivation were similar to those of non-reactivated patients with COVID-19 infection. None of the 5 patients developed severe pneumonia or died, as of Feb. 24, 2020. Notably, based on our findings in these 5 patients, there is currently evidence to suggest that a proportion of recovered COVID-19 patients could reactivate.\nThe reactivated patients included 1 asymptomatic patient and 4 symptomatic patients, which suggests the reactivation potential of asymptomatic or minimally symptomatic patients. The time from SARS-CoV-2 negative to positive ranged from 4 to 17 days, suggesting that recovered patients still may be virus carriers and require additional round of viral detection and isolation.\nWe need better data to determine risk factors and mechanisms that cause SARS-CoV-2 reactivation. The timing of onset of SARS-CoV-2 reactivation can be variable depending upon the host factors, underlying disease and the type of immunosuppressive therapies. In our study, the recovered patients had positive RT-PCR test results 4–17 days later. The key risk factors for reactivation would include 3 categories: (1) host status, (2) virologic factors and (3) type and degree of immunosuppression. Host factors may include sex, older age, type of disease needing immunosuppression. Although we could not identify risk factors for these host factors in the current study, the potential requires further large cohort confirmation. The virologic factors associated with increased risk of reactivation include high baseline SARS-CoV-2 load and variable genotype. SARS-CoV-2 viral load would also linked to treatment response, disease severity and progression.8 The association of SARS-CoV-2 genotypes and viral load with SARS-CoV-2 reactivation will be an important question to address. In our study, all the patients received antiviral therapy (Oseltamivir or Arbidol). These cases suggest that SARS-CoV-2 reactivation may occur whatever the antiviral therapy used. These host and virologic factors are important considerations that may further increase the likelihood of SARS-CoV-2 reactivation. Therefore, the assessment of host as well as virologic risk factors should be important caveats to help decide whether to initiate prophylactic therapy and immunosuppression. Immunosuppressive therapies are the commonly used causative agents. These agents have a general mechanism that inhibits many immune functions. For example, steroid inhibits cell-mediated immunity by suppressing interleukins production which is important for T and B cell proliferation.9 It is thus not surprising that these general immunosuppressive effects result in broad immune dysfunctions and potential SARS-CoV-2 reactivation.\nSARS-CoV-2 reactivation will be a vexing and persistent problem. Considering numerous patients infected or previously exposed to the virus, such a problem poses a major public health burden in terms of global morbidity and possibly mortality. Currently, we did not find reliable markers in predicting the risk of SARS-CoV-2 reactivation, nor there are any validated tests to determine whether a particular drug or therapy is associated with SARS-CoV-2 reactivation. The latter point was often determined by our empirical experience. Although decades of the experiences helped us to identify important drugs and to manage these situations appropriately, we could not accurately evaluate the risk of the drugs prior to its clinical application.\nConsidering the significance of this ongoing global public health emergency, although our conclusions are limited by the small sample size, we believe that the findings are important to understand the clinical characteristics and SARS-CoV-2 reactivation potential in COVID-19 patients."}

PMC:7102560 / 8332-12349 JSONTXT

Annnotations TAB JSON ListView MergeView

PMC:7102560 / 8332-12349 JSON TXT