ArticleProceedings of the National Academy of Sciences of the United States of America2024
Viral afterlife: SARS-CoV-2 as a reservoir of immunomimetic peptides that reassemble into proinflammatory supramolecular complexes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed.
- SARS-CoV-2 Persistence and Cardiovascular Sequelae in the Post-COVID Era: A Public Health Microbiology Perspective on Sudden Cardiac Death and Pulmonary Thromboembolism.Microorganisms · 2026Review
- LL-37: Biological Mechanisms and Emerging Therapeutic Applications in Intestinal Disease.Immunity, inflammation and disease · 2026Review
- A paper-based immunoassay with signal amplification for the sensitive detection of nucleocapsid protein toward the diagnosis of long COVID.The Analyst · 2026Article
- A Double-Edged Sword: Extracellular Serine Proteases as Facilitators of Infection and Mediators of Immunity.Molecules (Basel, Switzerland) · 2026Review
- SARS-CoV-2 peptide fragments selectively dysregulate specific immune cell populations via Gaussian curvature targeting.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Whole-Blood Cellular Responses: A Promising Indicator of SARS-CoV-2 Immunity Compared to Serology.Journal of clinical medicine · 2025Article
- Review
- Sequence Programmable Order-Disorder Transitions in Supramolecular Assembly of Peptide Nanofibers.Journal of the American Chemical Society · 2025Article
- Drp1 Proteins Released from Hydrolysis-Driven Scaffold Disassembly Trigger Nucleotide-Dependent Membrane Remodeling to Promote Scission.Journal of the American Chemical Society · 2025Article
- Machine-learning analysis identifies "elite" viral controllers with increased survival and homeostatic responses in critical COVID-19.Clinical and translational medicine · 2025Article
- Dynamic Cellular Proteome Remodeling during SARS-CoV-2 Infection. Identification of Plasma Protein Readouts.Journal of proteome research · 2025Article
- Viral sepsis: diagnosis, clinical features, pathogenesis, and clinical considerations.Military Medical Research · 2024Review
- The Intestine in Acute and Long COVID: Pathophysiological Insights and Key Lessons.The Yale journal of biology and medicine · 2024Review
- The Proteolytic Activity of Neutrophil-Derived Serine Proteases Bound to the Cell Surface Arming Lung Epithelial Cells for Viral Defense.Molecules (Basel, Switzerland) · 2024Article
- SARS-CoV2 infection in whole lung primarily targets macrophages that display subset-specific responses.Cellular and molecular life sciences : CMLS · 2024Article
- State-of-the-Art Molecular Biophysics in Russia.International journal of molecular sciences · 2024Article
- Long Covid: Hormone Imbalances and/or Rather Complex Immune Dysregulations?Journal of the Endocrine Society · 2024Article
- LL-37: Structures, Antimicrobial Activity, and Influence on Amyloid-Related Diseases.Biomolecules · 2024Review
- Changes in total charge on spike protein of SARS-CoV-2 in emerging lineages.Bioinformatics advances · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
35 authors.
Funding
Abstract
It is unclear how severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection leads to the strong but ineffective inflammatory response that characterizes severe Coronavirus disease 2019 (COVID-19), with amplified immune activation in diverse cell types, including cells without angiotensin-converting enzyme 2 receptors necessary for infection. Proteolytic degradation of SARS-CoV-2 virions is a milestone in host viral clearance, but the impact of remnant viral peptide fragments from high viral loads is not known. Here, we examine the inflammatory capacity of fragmented viral components from the perspective of supramolecular self-organization in the infected host environment. Interestingly, a machine learning analysis to SARS-CoV-2 proteome reveals sequence motifs that mimic host antimicrobial peptides (xenoAMPs), especially highly cationic human cathelicidin LL-37 capable of augmenting inflammation. Such xenoAMPs are strongly enriched in SARS-CoV-2 relative to low-pathogenicity coronaviruses. Moreover, xenoAMPs from SARS-CoV-2 but not low-pathogenicity homologs assemble double-stranded RNA (dsRNA) into nanocrystalline complexes with lattice constants commensurate with the steric size of Toll-like receptor (TLR)-3 and therefore capable of multivalent binding. Such complexes amplify cytokine secretion in diverse uninfected cell types in culture (epithelial cells, endothelial cells, keratinocytes, monocytes, and macrophages), similar to cathelicidin's role in rheumatoid arthritis and lupus. The induced transcriptome matches well with the global gene expression pattern in COVID-19, despite using <0.3% of the viral proteome. Delivery of these complexes to uninfected mice boosts plasma interleukin-6 and CXCL1 levels as observed in COVID-19 patients.
Indexed as
Identifiers
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.