Publications

This paper proposes “Spikeopathy” as a testable framework to explain a subset of Long COVID and post–SARS-CoV-2 conditions by focusing on the persistent presence and compartmentalization of spike protein rather than symptoms alone.

It argues that spike protein may persist beyond acute infection in distinct biological compartments—free in serum, sequestered within peripheral blood mononuclear cells (PBMCs), or packaged into extracellular vesicles (EVs)—with each location driving different pathological mechanisms and symptom clusters, such as systemic inflammation, immune dysregulation, neurocognitive impairment, dysautonomia, and microvascular dysfunction.

The paper emphasizes that spike-related pathology does not require continuous high-level plasma detection, allowing for low-abundance or tissue-protected reservoirs that evade standard assays. It outlines a biomarker-driven research and diagnostic strategy to stratify patients into mechanistically distinct subtypes and guide more precise investigation.

The report describes two individuals suffering prolonged post-COVID symptoms associated with persistent SARS-CoV-2 spike protein presence despite a range of conventional treatments.

In Patient X, high intracellular spike protein levels and cognitive difficulties persisted two years after infection. After initiating daily oral therapy with Vedicinals-9, intracellular spike levels dropped substantially over time and neurological symptoms improved. Patient Y also showed reduced exosomal spike burden and some symptomatic relief.

The authors propose that the combined natural compounds in Vedicinals-9 may act synergistically to enhance clearance of persistent spike protein and resolve downstream pathophysiological contributors, while emphasizing the need for controlled clinical trials.

This article explores emerging evidence that autoantibodies targeting human muscarinic cholinergic receptors may play a meaningful role in the pathophysiology of long COVID, particularly neurological and autonomic symptoms.

These anti-CHRM autoantibodies may disrupt cholinergic signaling pathways involved in cognition, autonomic balance, and broader physiological regulation. The paper argues that neutralizing or inhibiting these autoantibodies could represent a promising therapeutic direction.

This in-vitro study evaluated a phytoceutical cocktail in LPS-stimulated RAW264.7 macrophages and found significant reductions in nitric oxide, reactive oxygen species, and inflammatory signaling.

The findings support a synergistic anti-inflammatory and antioxidant effect of the combined plant compounds and provide mechanistic support for broader translational and clinical investigation.

This review frames long COVID as a complex, multi-system syndrome involving persistent viral components, immune dysregulation, chronic inflammation, endothelial dysfunction, and impaired viral clearance.

It argues for a shift away from symptom-only classification toward mechanism-driven diagnostics, biomarker development, and individualized treatment strategies targeting immune modulation, viral persistence, and systemic repair.

This retrospective study found that early antibiotic use during acute COVID-19 was associated with shorter recovery time, better oxygen saturation, and fewer prolonged post-COVID symptoms, regardless of vaccination status.

The authors suggest that early antibiotics may influence disease progression through anti-inflammatory, microbiome-modulating, or indirect antiviral effects, while also noting that the findings are observational and require prospective validation.

This study examines sequence and structural homology between SARS-CoV-2 spike protein and human muscarinic acetylcholine receptors as a potential basis for molecular mimicry in post-acute sequelae of COVID-19.

The proposed framework offers a mechanistic explanation for dysautonomia, fatigue, cognitive impairment, sleep disturbance, and cardiovascular instability through cross-reactive antibody responses that may disrupt cholinergic signaling in multiple tissues.

This in-vitro study found that VEDICINALS®9 inhibited proliferation and migration in A549 human lung adenocarcinoma cells and modulated a wide range of cancer-related proteins.

The findings suggest multi-target activity across pathways associated with growth, invasion, survival, and angiogenesis, supporting further investigation of the formulation in cancer research models.

This perspective highlights the nasal cavity and cribriform region as a biologically important route for SARS-CoV-2 access to the central nervous system.

It argues that intranasal therapeutic strategies may help reduce respiratory disease burden while also limiting neuroinvasive complications associated with NeuroCOVID.

This randomized multi-center exploratory study evaluated VEDICINALS-9 as an adjunct to standard care in mild to moderate COVID-19.

The authors reported earlier RT-PCR negativity, reductions in inflammatory biomarkers, and faster symptom recovery in the supplemented group, supporting further clinical study of the formulation as an adjunctive strategy.

This publication reviews organ-level effects associated with Vedicinals-9, with emphasis on cardioprotection, endothelial integrity, redox support, and inflammatory modulation.

Rather than positioning the formulation as a single-target intervention, the paper presents it as a systems-level supportive strategy with potential relevance to cardiovascular preservation under inflammatory stress.

This paper reviews immune alterations associated with both SARS-CoV-2 infection and COVID-19 vaccination, focusing on lymphopenia and autoimmune phenomena.

It emphasizes the importance of understanding susceptibility, immune recovery trajectories, and long-term immune remodeling in the setting of chronic inflammation and post-acute sequelae.

This review surveys reported neurological adverse events after COVID-19 vaccination and discusses mechanisms such as molecular mimicry, neuroinflammation, endothelial dysfunction, and blood–brain barrier disturbance.

It emphasizes early recognition, individualized assessment, and continued post-vaccination surveillance to better understand and manage rare but clinically significant neurological effects.

This systematic review synthesizes persistent physical and neurological symptom patterns in adults with Long-COVID, including fatigue, dyspnea, muscle weakness, brain fog, headache, and sleep disturbance.

It underscores the heterogeneous and multisystem nature of post-acute sequelae and highlights the need for multidisciplinary evaluation and targeted recovery strategies.

This paper explores the coexistence of lymphocytopenia and autoimmune-like responses in COVID-19, framing the disease as one of immune disorganization.

It reviews restorative treatment concepts aimed at immune rebalance rather than simple suppression, including strategies that address oxidative stress, inflammatory signaling, and lymphocyte function.

This review analyzes overlapping mechanisms driving neurological deficits in acute COVID-19 and Long-COVID, including neuroinflammation, endothelial injury, mitochondrial dysfunction, hypoxia, and autoimmunity.

It argues for individualized, systems-level treatment strategies that address vascular, immune, and neurocognitive dysfunction together rather than in isolation.

This paper proposes a mechanistic framework in which persistent spike production and tissue saturation drive a senescence-associated cascade in Long COVID.

It distinguishes early spike-linked pathology from later senescence-dominant disease states and offers a structured model for extracellular vesicle profiling, biomarker development, and senescence-targeted therapeutic investigation.

This publication presents a four-pathway framework explaining elevated circulating spike levels since 2024 and their relationship to accelerated Long COVID pathology.

It connects antibody escape, impaired neutralization, increased viral reservoir formation, tissue senescence cascades, and fibrinolysis-resistant microclot formation into a unified model for worsening symptom severity and progressive tissue burden.

This research proposal explores a structural hypothesis for why severe COVID-19 outcomes appeared to decline after Omicron emerged, despite high transmission. The authors focus on whether systematic deletions in surface-exposed N-terminal domain loops of the spike protein may have removed putative allergenic determinants present in earlier SARS-CoV-2 variants.

The paper compares ancestral and Omicron spike NTD loop regions, including H69–V70, V143–Y144–Y145, and N211, and proposes that these regions may have contributed to hypersensitivity-driven inflammatory patterns observed in some pre-Omicron infections.

The authors emphasize that this is a testable hypothesis rather than a definitive conclusion, calling for peptide allergenicity assays, mast-cell activation studies, patient immunophenotyping, and structural-functional comparisons between ancestral and Omicron spike constructs.