cxuvatr4

Property	Value
?:abstract	The global Coronavirus Disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has led to unprecedented social and economic consequences The risk of morbidity and mortality due to COVID-19 increases dramatically in the presence of co-existing medical conditions while the underlying mechanisms remain unclear Furthermore, there are no proven effective therapies for COVID-19 This study aims to identify SARS-CoV-2 pathogenesis, diseases manifestations, and COVID-19 therapies using network medicine methodologies along with clinical and multi-omics observations We incorporate SARS-CoV-2 virus-host protein-protein interactions, transcriptomics, and proteomics into the human interactome Network proximity measure revealed underlying pathogenesis for broad COVID-19-associated manifestations Multi-modal analyses of single-cell RNA-sequencing data showed that co-expression of ACE2 and TMPRSS2 was elevated in absorptive enterocytes from the inflamed ileal tissues of Crohn\'s disease patients compared to uninflamed tissues, revealing shared pathobiology by COVID-19 and inflammatory bowel disease Integrative analyses of metabolomics and transcriptomics (bulk and single-cell) data from asthma patients indicated that COVID-19 shared intermediate inflammatory endophenotypes with asthma (including IRAK3 and ADRB2) To prioritize potential treatment, we combined network-based prediction and propensity score (PS) matching observational study of 18,118 patients from a COVID-19 registry We identified that melatonin (odds ratio (OR) = 0 36, 95% confidence interval (CI) 0 22-0 59) was associated with 64% reduced likelihood of a positive laboratory test result for SARS-CoV-2 Using PS-matching user active comparator design, melatonin was associated with 54% reduced likelihood of SARS-CoV-2 positive test result compared to angiotensin Ireceptor blockers or angiotensin-converting enzyme inhibitors (OR = 0 46, 95% C0 24-0 86) The global Coronavirus Disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has led to unprecedented social and economic consequences. The risk of morbidity and mortality due to COVID-19 increases dramatically in the presence of co-existing medical conditions while the underlying mechanisms remain unclear. Furthermore, there are no proven effective therapies for COVID-19. This study aims to identify SARS-CoV-2 pathogenesis, diseases manifestations, and COVID-19 therapies using network medicine methodologies along with clinical and multi-omics observations. We incorporate SARS-CoV-2 virus-host protein-protein interactions, transcriptomics, and proteomics into the human interactome. Network proximity measure revealed underlying pathogenesis for broad COVID-19-associated manifestations. Multi-modal analyses of single-cell RNA-sequencing data showed that co-expression of ACE2 and TMPRSS2 was elevated in absorptive enterocytes from the inflamed ileal tissues of Crohn\'s disease patients compared to uninflamed tissues, revealing shared pathobiology by COVID-19 and inflammatory bowel disease. Integrative analyses of metabolomics and transcriptomics (bulk and single-cell) data from asthma patients indicated that COVID-19 shared intermediate inflammatory endophenotypes with asthma (including IRAK3 and ADRB2). To prioritize potential treatment, we combined network-based prediction and propensity score (PS) matching observational study of 18,118 patients from a COVID-19 registry. We identified that melatonin (odds ratio (OR) = 0.36, 95% confidence interval (CI) 0.22-0.59) was associated with 64% reduced likelihood of a positive laboratory test result for SARS-CoV-2. Using PS-matching user active comparator design, melatonin was associated with 54% reduced likelihood of SARS-CoV-2 positive test result compared to angiotensin II receptor blockers or angiotensin-converting enzyme inhibitors (OR = 0.46, 95% CI 0.24-0.86).
is ?:annotates of	<https://research.tib.eu/covid-19/entity/cxuvatr4_hasAnnotation_C0003015> <https://research.tib.eu/covid-19/entity/cxuvatr4_hasAnnotation_C0013227> <https://research.tib.eu/covid-19/entity/cxuvatr4_hasAnnotation_C0162327> <https://research.tib.eu/covid-19/entity/cxuvatr4_hasAnnotation_C0682447> <https://research.tib.eu/covid-19/entity/cxuvatr4_hasAnnotation_C1334136> <https://research.tib.eu/covid-19/entity/cxuvatr4_hasAnnotation_C1336641> <https://research.tib.eu/covid-19/entity/cxuvatr4_hasAnnotation_C1422064> <https://research.tib.eu/covid-19/entity/cxuvatr4_hasAnnotation_C5203676>
?:creator	<https://research.tib.eu/covid-19/entity/Zhou%2C_Yadi%3B_Hou%2C_Yuan%3B_Shen%2C_Jiayu%3B_Kallianpur%2C_Asha%3B_Zein%2C_Joe%3B_Culver%2C_Daniel_A%3B_Farha%2C_Samar%3B_Comhair%2C_Suzy%3B_Fiocchi%2C_Claudio%3B_Gack%2C_Michaela_U%3B_Mehra%2C_Reena%3B_Stappenbeck%2C_Thaddeus%3B_Chan%2C_Timothy%3B_Eng%2C_Charis%3B_Jung%2C_Jae_U%3B_Jehi%2C_Lara%3B_Erzurum%2C_Serpil%3B_Cheng%2C_Feixiong> <https://research.tib.eu/covid-19/entity/Zhou%2C_Yadi_Hou_Yuan_Shen_Jiayu_Kallianpur_Asha_Zein_Joe_Culver_Daniel_A.%3B_Farha%2C_Samar_Comhair_Suzy_Fiocchi_Claudio_Gack_Michaela_U.%3B_Mehra%2C_Reena_Stappenbeck_Thaddeus_Chan_Timothy_Eng_Charis_Jung_Jae_U.%3B_Jehi%2C_Lara_Erzurum_Serpil_Cheng_Feixiong>
?:license	unk
?:publication_isRelatedTo_Disease	<https://research.tib.eu/covid-19/entity/COVID-19>
is ?:relation_isRelatedTo_publication of	<https://research.tib.eu/covid-19/entity/cxuvatr4_HAS_C1336641_STIMULATES_C0682610> <https://research.tib.eu/covid-19/entity/cxuvatr4_HAS_C1422064_STIMULATES_C0682610> <https://research.tib.eu/covid-19/entity/cxuvatr4_HAS_C5203676_CAUSES_C5203670>
?:source	WHO
?:title	A Network Medicine Approach to Investigation and Population-based Validation of Disease Manifestations and Drug Repurposing for COVID-19
?:type	<https://research.tib.eu/covid-19/vocab/Publication>
?:who_covidence_id	#1027422 #472
?:year	2020

Property

Value

?:abstract

The global Coronavirus Disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has led to unprecedented social and economic consequences The risk of morbidity and mortality due to COVID-19 increases dramatically in the presence of co-existing medical conditions while the underlying mechanisms remain unclear Furthermore, there are no proven effective therapies for COVID-19 This study aims to identify SARS-CoV-2 pathogenesis, diseases manifestations, and COVID-19 therapies using network medicine methodologies along with clinical and multi-omics observations We incorporate SARS-CoV-2 virus-host protein-protein interactions, transcriptomics, and proteomics into the human interactome Network proximity measure revealed underlying pathogenesis for broad COVID-19-associated manifestations Multi-modal analyses of single-cell RNA-sequencing data showed that co-expression of ACE2 and TMPRSS2 was elevated in absorptive enterocytes from the inflamed ileal tissues of Crohn\'s disease patients compared to uninflamed tissues, revealing shared pathobiology by COVID-19 and inflammatory bowel disease Integrative analyses of metabolomics and transcriptomics (bulk and single-cell) data from asthma patients indicated that COVID-19 shared intermediate inflammatory endophenotypes with asthma (including IRAK3 and ADRB2) To prioritize potential treatment, we combined network-based prediction and propensity score (PS) matching observational study of 18,118 patients from a COVID-19 registry We identified that melatonin (odds ratio (OR) = 0 36, 95% confidence interval (CI) 0 22-0 59) was associated with 64% reduced likelihood of a positive laboratory test result for SARS-CoV-2 Using PS-matching user active comparator design, melatonin was associated with 54% reduced likelihood of SARS-CoV-2 positive test result compared to angiotensin Ireceptor blockers or angiotensin-converting enzyme inhibitors (OR = 0 46, 95% C0 24-0 86)
The global Coronavirus Disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has led to unprecedented social and economic consequences. The risk of morbidity and mortality due to COVID-19 increases dramatically in the presence of co-existing medical conditions while the underlying mechanisms remain unclear. Furthermore, there are no proven effective therapies for COVID-19. This study aims to identify SARS-CoV-2 pathogenesis, diseases manifestations, and COVID-19 therapies using network medicine methodologies along with clinical and multi-omics observations. We incorporate SARS-CoV-2 virus-host protein-protein interactions, transcriptomics, and proteomics into the human interactome. Network proximity measure revealed underlying pathogenesis for broad COVID-19-associated manifestations. Multi-modal analyses of single-cell RNA-sequencing data showed that co-expression of ACE2 and TMPRSS2 was elevated in absorptive enterocytes from the inflamed ileal tissues of Crohn\'s disease patients compared to uninflamed tissues, revealing shared pathobiology by COVID-19 and inflammatory bowel disease. Integrative analyses of metabolomics and transcriptomics (bulk and single-cell) data from asthma patients indicated that COVID-19 shared intermediate inflammatory endophenotypes with asthma (including IRAK3 and ADRB2). To prioritize potential treatment, we combined network-based prediction and propensity score (PS) matching observational study of 18,118 patients from a COVID-19 registry. We identified that melatonin (odds ratio (OR) = 0.36, 95% confidence interval (CI) 0.22-0.59) was associated with 64% reduced likelihood of a positive laboratory test result for SARS-CoV-2. Using PS-matching user active comparator design, melatonin was associated with 54% reduced likelihood of SARS-CoV-2 positive test result compared to angiotensin II receptor blockers or angiotensin-converting enzyme inhibitors (OR = 0.46, 95% CI 0.24-0.86).

is ?:annotates of