ReviewBiomedicines2026
Spike Protein at the Crossroads of Long-COVID and Vaccine-Induced Immune Thrombotic Thrombocytopenia Syndromes: A Cardio-Hematological Perspective.
Review in Biomedicines, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike (S) protein is central to viral infectivity, host-pathogen interactions, and immune recognition. Beyond its indispensable role in viral entry, accumulating experimental and clinical evidence indicates that spike protein may exert pleiotropic biological effects involving endothelial, cardiovascular, hematological, neurological, and immunological pathways. During natural infection, these effects occur in the context of active viral replication, additional viral antigens, and systemic inflammation, whereas vaccination induces a fundamentally different, transient exposure to a prefusion-stabilized spike antigen without viral propagation. In this review, we critically examine the molecular and clinicopathological properties of the SARS-CoV-2 spike protein and the biological differences between infection-derived and vaccine-derived spike exposure. Particular emphasis is placed on endothelial dysfunction, platelet and complement activation, immune-thrombosis, persistent viral antigens and tissue reservoirs in Long-COVID, and the distinct anti-PF4-mediated pathophysiology of vaccine-induced immune thrombotic thrombocytopenia (VITT). Emerging evidence suggests that persistent or dysregulated spike-related antigen exposure may contribute to chronic multisystem manifestations in a subset of individuals following SARS-CoV-2 infection; however, evidence linking persistent vaccine-derived spike to chronic clinical syndromes remains substantially more limited and does not currently establish causality. Integrating these observations, we propose the 'Long-Spike' hypothesis as a hypothesis-generating conceptual framework rather than a defined clinical syndrome. Further prospective studies integrating ultrasensitive antigen detection, tissue-based analyses, immunophenotyping, and cardiovascular and hematological biomarkers are required to determine the clinical relevance and causal significance of persistent spike-related antigens.
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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.