ReviewCellular and molecular life sciences : CMLS2021
Mechanisms and therapeutic potential of interactions between human amyloids and viruses.
Review in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Implications of virus-induced stress granules in tauopathies.Translational neurodegeneration · 2026Review
- Golgi Fragmentation as a Potential Link Between SARS-CoV-2 Infection and Alzheimer's Disease: Mechanisms and Implications for Neurodegeneration in Long COVID.Sub-cellular biochemistry · 2026Review
- From Pathology to Materials Science and Engineering: Harnessing the Amyloid State for Biotechnological Applications.ACS applied materials & interfaces · 2025Review
- Neurotropic Viruses as Acute and Insidious Drivers of Aging.Biomolecules · 2025Review
- α-Synuclein fibrils enhance HIV-1 infection of human T cells, macrophages and microglia.Nature communications · 2025Article
- Aggregating amyloid resources: A comprehensive review of databases on amyloid-like aggregation.Computational and structural biotechnology journal · 2024Review
- Influenza virus infection exacerbates gene expression related to neurocognitive dysfunction in brains of old mice.Immunity & ageing : I & A · 2024Article
- Neurotropic virus infection and neurodegenerative diseases: Potential roles of autophagy pathway.CNS neuroscience & therapeutics · 2024Review
- On-column refolding and off-column assembly of parvovirus B19 virus-like particles from bacteria-expressed protein.Applied microbiology and biotechnology · 2024Article
- Viruses and amyloids - a vicious liaison.Prion · 2023Review
- Spike Protein Fragments Promote Alzheimer's Amyloidogenesis.ACS applied materials & interfaces · 2023Article
- Peptide from NSP7 is able to form amyloid-like fibrils: Artifact or challenge to drug design?Biochimica et biophysica acta. Proteins and proteomics · 2023Article
- 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 potential role of ischaemia-reperfusion injury in chronic, relapsing diseases such as rheumatoid arthritis, Long COVID, and ME/CFS: evidence, mechanisms, and therapeutic implications.The Biochemical journal · 2022Review
- Viruses in neurodegenerative diseases: More than just suspects in crimes.PLoS pathogens · 2022Review
- Amyloidogenesis of SARS-CoV-2 Spike Protein.Journal of the American Chemical Society · 2022Article
- Article
- Metabolites of soil microorganisms modulate amyloid β production in Alzheimer's neurons.Scientific reports · 2022Article
- The role of Aβ in Alzheimer's Disease as an Evolutionary Outcome of Optimized Innate Immune Defense.The journal of prevention of Alzheimer's disease · 2022Article
- Nipah virus infection as a putative risk factor for Alzheimer's disease: A testable hypothesis.Journal of Alzheimer's disease reportsArticle
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
The aggregation of specific proteins and their amyloid deposition in affected tissue in disease has been studied for decades assuming a sole pathogenic role of amyloids. It is now clear that amyloids can also encode important cellular functions, one of which involves the interaction potential of amyloids with microbial pathogens, including viruses. Human expressed amyloids have been shown to act both as innate restriction molecules against viruses as well as promoting agents for viral infectivity. The underlying molecular driving forces of such amyloid-virus interactions are not completely understood. Starting from the well-described molecular mechanisms underlying amyloid formation, we here summarize three non-mutually exclusive hypotheses that have been proposed to drive amyloid-virus interactions. Viruses can indirectly drive amyloid depositions by affecting upstream molecular pathways or induce amyloid formation by a direct interaction with the viral surface or specific viral proteins. Finally, we highlight the potential of therapeutic interventions using the sequence specificity of amyloid interactions to drive viral interference.
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What OpenQuestion holds
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.