COVID‐19 and coagulation dysfunction in adults: A systematic review and meta‐analysis

Lin, Jing; Han, Yan; Chen, Hanchuan; He, Chen; Lin, Chunjin; He, Hongtao; Zhang, Sicheng; Shu, Shi; Lin, Kaiyang

doi:10.1002/jmv.26346

Cited by 84 publications

(87 citation statements)

References 57 publications

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“…The results of our phenotype analysis using mouse orthologs of shared human genes shows that phenotypic enrichment is consistent with the pathway enrichment using the human genes and is also consistent with pathologies associated with severe COVID-19: blood coagulation, inflammation and cardiovascular pathologies [36][37][38][39][40][41] . Since mice provide an attractive genetic system for disease modeling, we investigated the phenotypes associated with each of these genes in further detail.…”

Section: Identification Of Potential Mouse Models To Study Comorbiditsupporting

confidence: 81%

Investigation of COVID-19 comorbidities reveals genes and pathways coincident with the SARS-CoV-2 viral disease

Dolan

Hill

Mukherjee

et al. 2020

Sci Rep

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The emergence of the SARS-CoV-2 virus and subsequent COVID-19 pandemic initiated intense research into the mechanisms of action for this virus. It was quickly noted that COVID-19 presents more seriously in conjunction with other human disease conditions such as hypertension, diabetes, and lung diseases. We conducted a bioinformatics analysis of COVID-19 comorbidity-associated gene sets, identifying genes and pathways shared among the comorbidities, and evaluated current knowledge about these genes and pathways as related to current information about SARS-CoV-2 infection. We performed our analysis using GeneWeaver (GW), Reactome, and several biomedical ontologies to represent and compare common COVID-19 comorbidities. Phenotypic analysis of shared genes revealed significant enrichment for immune system phenotypes and for cardiovascular-related phenotypes, which might point to alleles and phenotypes in mouse models that could be evaluated for clues to COVID-19 severity. Through pathway analysis, we identified enriched pathways shared by comorbidity datasets and datasets associated with SARS-CoV-2 infection.

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Section: Identification Of Potential Mouse Models To Study Comorbiditsupporting

confidence: 81%

Investigation of COVID-19 comorbidities reveals genes and pathways coincident with the SARS-CoV-2 viral disease

Dolan

Hill

Mukherjee

et al. 2020

Sci Rep

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“…Coagulation dysfunction is a consistent observation in human COVID-19 and has been associated with disease severity [18][19][20][21][22]. Here, we performed a limited analysis of blood clotting times (PT and aPTT) and circulating fibrinogen levels to begin to characterize the coagulopathy in SARS-CoV-2-infected AGMs.…”

Section: Discussionmentioning

confidence: 99%

“…Transient increases in aPTT and in circulating fibrinogen levels were observed during the acute phase of infection. Increases in PT and/ or aPTT have been linked to severe human COVID-19 cases in some but not all studies [18][19][20][21][22]. However, nearly all severe COVID-19 cases have been associated with high levels of fibrinogen [20][21][22].…”

Section: Discussionmentioning

confidence: 99%

Intranasal exposure of African green monkeys to SARS-CoV-2 results in acute phase pneumonia with shedding and lung injury still present in the early convalescence phase

Cross

Agans

Prasad

et al. 2020

Virol J

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We recently reported the development of the first African green monkey (AGM) model for COVID-19 based on a combined liquid intranasal (i.n.) and intratracheal (i.t.) exposure to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Here, we followed up on this work by assessing an i.n. particle only route of exposure using the LMA mucosal atomization device (MAD). Six AGMs were infected with SARS-CoV-2; three animals were euthanized near the peak stage of virus replication (day 5) and three animals were euthanized during the early convalescence period (day 34). All six AGMs supported robust SARS-CoV-2 replication and developed respiratory disease. Evidence of coagulation dysfunction as noted by a transient increases in aPTT and circulating levels of fibrinogen was observed in all AGMs. The level of SARS-CoV-2 replication and lung pathology was not quite as pronounced as previously reported with AGMs exposed by the combined i.n. and i.t. routes; however, SARS-CoV-2 RNA was detected in nasal swabs of some animals as late as day 15 and rectal swabs as late as day 28 after virus challenge. Of particular importance to this study, all three AGMs that were followed until the early convalescence stage of COVID-19 showed substantial lung pathology at necropsy as evidenced by multifocal chronic interstitial pneumonia and increased collagen deposition in alveolar walls despite the absence of detectable SARS-CoV-2 in any of the lungs of these animals. These findings are consistent with human COVID-19 further demonstrating that the AGM faithfully reproduces the human condition.

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“…In addition, however, megakaryocytes have been observed to produce blood platelets within the alveolar capillaries of COVID-19 patients [ 33 ]. In addition to altered blood platelet numbers, COVID-19 patients also present with alterations in a number of other elements of hemostasis, including coagulation times (thrombin times and prothrombin times), d-dimer concentrations and fibrinogen levels [ 4 , 25 , 34 , 35 ].…”

Section: Blood Platelet Count and Platelet Activation In Covid-19mentioning

confidence: 99%

Modulation of Hemostasis in COVID-19; Blood Platelets May Be Important Pieces in the COVID-19 Puzzle

Ulanowska

Olas

2021

Pathogens

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Although the precise pathogenesis of coronavirus disease 2019 (COVID-19) currently remains unknown, its complex nature is gradually being revealed. COVID-19 is a disease caused by the SARS-CoV-2 virus and leads to respiratory dysfunction. Studies on hemostatic parameters have showed that COVID-19 significantly affects the disruption of the coagulation system and may contribute to coagulation and thrombotic events. A relevant cause of hemostasis disorders is inflammation and cytokine storms, which cause, for example, endothelial dysfunction in blood vessels. In order to prevent and treat states of hypercoagulability and thrombosis, the administration of anticoagulants, e.g., heparin, is recommended. The present mini-review describes the relationship between hemostasis and COVID-19, and discusses whether this relationship may cast light on the nature of COVID-19. The present short manuscript also examines the relationship between blood platelets and COVID-19. In addition, the paper explores the potential use of antiplatelet drugs in COVID-19 cases. The studies were identified by searching electronic databases, including PubMed and SCOPUS.

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COVID‐19 and coagulation dysfunction in adults: A systematic review and meta‐analysis

Cited by 84 publications

References 57 publications

Investigation of COVID-19 comorbidities reveals genes and pathways coincident with the SARS-CoV-2 viral disease

Investigation of COVID-19 comorbidities reveals genes and pathways coincident with the SARS-CoV-2 viral disease

Intranasal exposure of African green monkeys to SARS-CoV-2 results in acute phase pneumonia with shedding and lung injury still present in the early convalescence phase

Modulation of Hemostasis in COVID-19; Blood Platelets May Be Important Pieces in the COVID-19 Puzzle

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