Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coronavirus disease 2019 (COVID-19) emerged from the West District of Southern China Seafood Wholesale Market in late December 2019 and has been declared a global pandemic by the World Health Organization (WHO). Infection with severe acute respiratory syndrome coronavirus (SARS-CoV-2) presents with upper respiratory symptoms like cough, fever, and lethargy. At the same time, in later stages, critical COVID-19 patients develop acute respiratory distress syndrome (ARDS), venous thromboembolism (VTE), and multiple organ failure from cytokine storm and coagulation hyperactivity. Primary manifestations of thrombotic events include deep vein thrombosis (DVT), disseminated intravascular coagulation (DIC) and pulmonary embolism (PE). Initial coagulopathy in COVID-19 patients presents with elevated fibrin degradation products, especially D-dimers. In contrast, late presentations show evidence of prolonged prothrombin time (PT) and activated partial thromboplastin (aPTT), increased platelets, and fibrinogen levels. Diagnosis and monitoring of disease progression are done by regular screening of laboratory parameters, including D-dimer and fibrinogen. Management of coagulopathy in COVID-19 patients is like that of critically ill patients, including thromboprophylaxis. Coagulopathy is a poor prognostic factor, and optimum strategies should be developed for early diagnosis, prevention, and prompt treatment of VTE in COVID-19 patients. Thrombosis prophylaxis with low molecular weight heparin (LMWH) has shown beneficial results in preventing coagulopathy a reducing risk of mortality due to thrombotic events. We will discuss VTE in COVID-19 patients highlighting the role of D-dimer, fibrinogen, and interleukin-6 (IL-6).
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PMID:D-Dimer, Fibrinogen, and IL-6 in COVID-19 Patients with Suspected Venous Thromboembolism: A Narrative Review. 3322 33

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for an unprecedented global pandemic of COVID-19. Animal models are urgently needed to study the pathogenesis of COVID-19 and to screen vaccines and treatments. We show that African green monkeys (AGMs) support robust SARS-CoV-2 replication and develop pronounced respiratory disease, which may more accurately reflect human COVID-19 cases than other nonhuman primate species. SARS-CoV-2 was detected in mucosal samples, including rectal swabs, as late as 15 days after exposure. Marked inflammation and coagulopathy in blood and tissues were prominent features. Transcriptome analysis demonstrated stimulation of interferon and interleukin-6 pathways in bronchoalveolar lavage samples and repression of natural killer cell- and T cell-associated transcripts in peripheral blood. Despite a slight waning in antibody titers after primary challenge, enhanced antibody and cellular responses contributed to rapid clearance after re-challenge with an identical strain. These data support the utility of AGM for studying COVID-19 pathogenesis and testing medical countermeasures.
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PMID:Establishment of an African green monkey model for COVID-19 and protection against re-infection. 3251 77


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