How SARS-CoV-2 (COVID-19) spreads within infected hosts — what we know so far

Sanyal, Sumana

doi:10.1042/etls20200165

Cited by 31 publications

(35 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The virus can enter human cells that express ACE-2, such as those in the lungs, heart, and renal and gastrointestinal tracts, with the help of its spike protein. A “cytokine storm” occurring after 7 to 14 days can lead to severe disease ( 25 , 26 ). The probability of severe disease depends, among other factors, on comorbidities.…”

Section: Discussion and Literature Reviewmentioning

confidence: 99%

Case Report: Myocarditis After COVID-19 Vaccination – Case Series and Literature Review

et al. 2022

View full text Add to dashboard Cite

BackgroundThe ongoing COVID-19 pandemic demands a series of measures and, above all, the vaccination of a substantial proportion of the population. Acute myocarditis is a rare complication of the widely used mRNA-based vaccines.Case PresentationWe present a case series of four patients (three men and one woman, 16 to 47 years old) with acute pericarditis/myocarditis 3 to 17 days after mRNA vaccination. They presented with chest pain, fever, and flu-like symptoms. Diagnosis was made based on the synopsis of clinical presentation, elevated levels of troponin T and NT-proBNP, impaired systolic function on echocardiography, and findings in non-invasive tissue characterization by cardiovascular magnetic resonance imaging. Two patients also underwent endomyocardial biopsies. As none of the patients showed signs of cardiogenic shock, they were discharged from ward care only a few days after their initial presentations.ConclusionsOur data are consistent with other case reports of myocarditis early after mRNA vaccination and demonstrate the need for multimodal diagnostics. In view of its rarity and mild course, the risk–benefit ratio of vaccination remains positive compared to potential SARS-CoV-2 infection.

show abstract

Section: Discussion and Literature Reviewmentioning

confidence: 99%

Case Report: Myocarditis After COVID-19 Vaccination – Case Series and Literature Review

et al. 2022

View full text Add to dashboard Cite

show abstract

“…This extends known KIPyV and MCPyV differences. Among interferon-response genes were CXCL10 and IGS15, involved in host antiviral response and found to induce cytokine storm in SARS-CoV-2 infected patients (Callahan et al, 2021;Sanyal, 2020). Interferon-induced proteins participate in inflammatory reactions and attract different cells of innate and adaptive immunity.…”

Section: Discussionmentioning

confidence: 99%

“…ISG15 (Interferon Stimulated Gene 15) encodes ubiquitin-like protein that is induced by type I interferons and involved in various processes related to host antiviral response, acting as extracellular and intracellular signalling protein (Perng & Lenschow, 2018). Its upregulation was detected in macrophages after infection by vaccinia and SARS-CoV-2 viruses (Sanyal, 2020;Yángüez et al, 2013). This protein is likely to be an important factor implicated in cytokine storms triggered by SARS-CoV-2.…”

Section: While Most Population and Gene Expression Changes Are Conserved Interferon-response Population Is Highly Enriched Upon Activatiomentioning

confidence: 99%

Activation of NLRP3 Inflammasome by Virus-like Particles of Human Polyomaviruses in Macrophages

Luciunait

Dalgėdienė

Žilionis

et al. 2021

Preprint

View full text Add to dashboard Cite

Viral antigens can activate phagocytes inducing inflammation but the mechanisms are barely explored. This study aimed to investigate the capability of viral oligomeric proteins of different structure to induce inflammatory response in macrophages. Human THP-1 cell line was used to prepare macrophages which were treated with filamentous nucleocapsid-like particles (NLPs) of paramyxoviruses and spherical virus-like particles (VLPs) of human polyomaviruses. The effects of viral proteins on cell viability, pro-inflammatory cytokines’ production and formation of NLRP3 inflammasome components, ASC specks, were investigated. Filamentous NLPs did not induce inflammation markers while spherical VLPs mediated inflammatory response followed by NLRP3 inflammasome activation. Inhibitors of cathepsins and K+ efflux decreased IL-1β levels and cell death indicating a complex inflammasome activation process. Similar activation pattern was observed in primary human macrophages treated with VLPs. Single cell RNAseq analysis of THP-1 cells revealed several cell activation states characterized by high expression of inflammation-related genes. This study provides new insights into interaction of viral proteins with innate immune cells and suggests that structural properties of oligomeric proteins may define cell activation pathways.

show abstract

“…The newly synthesized viral genomic RNA results in budding into the lumen of secretory vesicular compartments, which are then secreted from the infected cell by exocytosis. 7,12 The clinical presentations of COVID-19 are highly variable from one individual to another. COVID-19 ranges from asymptomatic to severe disease that could result in death.…”

Section: Pathogenesis Of Covid-19 Infectionmentioning

confidence: 99%

Thrombotic and Hypercoagulability Complications of COVID-19: An Update

Shibeeb¹,

Ahmad²

2021

JBM

View full text Add to dashboard Cite

The current COVID-19 pandemic emerged in December 2019, in China, affecting millions of people worldwide. COVID-19 is mainly a disease of the respiratory system, yet systematic complications have also been reported among SARS-CoV-2 infected patients. Thrombotic complications are one of the severe clinical outcomes of COVID-19, especially among critically ill patients, and are associated with poor prognosis. To date, many studies have concluded that COVID-19 increases the incidence of thrombotic events and coagulopathies; however, the exact mechanism behind such a disease outcome is not well known. Various pathophysiological mechanisms for thrombotic events in COVID-19 have been proposed, these include virus-induced endothelial cell damage, inflammation, and excess production of pro-inflammatory cytokines. As a result, most critically diseased COVID-19 patients are managed with prophylactic anticoagulant, yet some still develop thrombotic episodes. Therefore, better understanding of the mechanisms behind the thrombotic complications is needed to develop treatments that specifically target such pathways, which may aid in better disease management and improve the prognosis.

show abstract

How SARS-CoV-2 (COVID-19) spreads within infected hosts — what we know so far

Cited by 31 publications

References 56 publications

Case Report: Myocarditis After COVID-19 Vaccination – Case Series and Literature Review

Case Report: Myocarditis After COVID-19 Vaccination – Case Series and Literature Review

Activation of NLRP3 Inflammasome by Virus-like Particles of Human Polyomaviruses in Macrophages

Thrombotic and Hypercoagulability Complications of COVID-19: An Update

Contact Info

Product

Resources

About