ArticlePrion2021
Hypothesis: AA amyloidosis is a factor causing systemic complications after coronavirus disease.
Article in Prion, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 37 citations in OpenAlex.
- Key charged residues influence the amyloidogenic propensity of the helix-1 region of serum amyloid A.Biochimica et biophysica acta. General subjects · 2024Article
- Promising Strategies to Reduce the SARS-CoV-2 Amyloid Deposition in the Brain and Prevent COVID-19-Exacerbated Dementia and Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Coronavirus Disease 2019 Outcomes in Amyloid A Protein Amyloidosis Secondary to Rheumatic Conditions and Signs of Post- Coronavirus Disease 2019 Proteinuria Progression.European journal of rheumatology · 2024Article
- Article
- Exploring the Potential Long-term Impact of SARS-CoV-2 on Protein Misfolding and Amyloid-related Conditions.Protein and peptide letters · 2024Review
- Viruses and amyloids - a vicious liaison.Prion · 2023Review
- Article
- Gastrointestinal AA Amyloidosis following Recurrent SARS-CoV-2 Infection: A Case Report.Yonsei medical journal · 2023Article
- COVID-19 Infection and Vaccination and Its Relation to Amyloidosis: What Do We Know Currently?Vaccines · 2023Review
- Controversial Properties of Amyloidogenic Proteins and Peptides: New Data in the COVID Era.Biomedicines · 2023Review
- Elevated Serum Amyloid A Levels Contribute to Increased Platelet Adhesion in COVID-19 Patients.International journal of molecular sciences · 2022Article
- SARS-CoV-2-Induced Amyloidgenesis: Not One, but Three Hypotheses for Cerebral COVID-19 Outcomes.Metabolites · 2022Article
- A comprehensive mini-review on amyloidogenesis of different SARS-CoV-2 proteins and its effect on amyloid formation in various host proteins.3 Biotech · 2022Review
- The deciphering of the immune cells and marker signature in COVID-19 pathogenesis: An update.Journal of medical virology · 2022Review
- COVID-GWAB: A Web-Based Prediction of COVID-19 Host Genes via Network Boosting of Genome-Wide Association Data.Biomolecules · 2022Article
- Neurotoxic amyloidogenic peptides in the proteome of SARS-COV2: potential implications for neurological symptoms in COVID-19.Nature communications · 2022Article
- Deciphering the link between Diabetes mellitus and SARS-CoV-2 infection through differential targeting of microRNAs in the human pancreas.Journal of endocrinological investigation · 2022Article
- Presence of a SARS-CoV-2 Protein Enhances Amyloid Formation of Serum Amyloid A.The journal of physical chemistry. B · 2021Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The severe course of COVID-19 causes systemic chronic inflammation and thrombosis in a wide variety of organs and tissues. The nature of these inflammations remains a mystery, although they are known to occur against the background of a high level of cytokine production. The high level of cytokines provokes overproduction of the Serum amyloid A (SAA) protein. Moreover, the number of studies has shown that the severe COVID-19 causes SAA overproduction. The authors of these works regard a high level of SAA exclusively as a biomarker of COVID-19. However, it should be borne in mind that overproduction of SAA can cause systemic AA amyloidosis. SAA forms cytotoxic amyloid deposits in various organs and induces inflammation and thrombosis. The consequences of COVID-19 infection are surprisingly similar to the clinical picture that is observed in AA amyloidosis. Here I present the hypothesis that AA amyloidosis is a factor causing systemic complications after coronavirus disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.