Publications

Spikeopathy—Spike Protein-Associated Pathobiology: A Series I: Definition and Scope

Authors: Abdul Mannan Baig; Beate Jaeger; Brigitte König; Joachim Gerlach; Philip Mavberg; Sandy Rosko; Ivan Belynov; Usman Ali.

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 rigorous, biomarker-driven research and diagnostic strategy to stratify patients into mechanistically distinct subtypes, enabling more precise investigation and targeted interventions, while explicitly distinguishing this framework from broader post-viral syndromes and avoiding premature disease labeling.

Reduction of Persistent Spike Protein and Improvement in COVID-19 Symptoms Following Therapy with Vedicinals-9 (Case Report)

Authors: Joachim Gerlach; Philip Mavberg; Brigitte König; Abdul Mannan Baig; Beate Jaeger; Anne Mucke; Inbar A. Tofan.

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 (188 pg/2.5 × 10⁶ PBMCs) and cognitive difficulties persisted two years after infection. After initiating daily oral therapy with Vedicinals-9, a tailored natural compound formulation, intracellular spike levels dropped dramatically—90% within seven weeks and further by 12 weeks—accompanied by notable improvement in neurological symptoms such as concentration ability. Patient Y, who experienced fatigue, exercise intolerance, and sleep disturbances, showed similarly reduced spike protein in exosomes and some symptomatic relief during ongoing Vedicinals-9 therapy, suggesting potential benefit beyond standard care.

The authors propose that the combined natural compounds in Vedicinals-9 may act synergistically to enhance cellular clearance of persistent spike protein and resolve microthrombi, addressing underlying pathophysiological contributors to Long COVID. They highlight significant laboratory and clinical improvements in both cases but note limitations inherent in a two-case report and emphasize the need for controlled clinical trials to confirm efficacy and clarify mechanisms of action.

Strategic Inhibition of CHRM Autoantibodies: Molecular Insights and Therapeutic Potentials in Long COVID

Authors: Joachim Gerlach; Abdul Mannan Baig; Sandy Roska.

The article explores emerging evidence that autoantibodies targeting human muscarinic cholinergic receptors (CHRMs)—a subset of G-protein-coupled receptors (GPCRs)—play a significant role in the pathophysiology of long COVID, particularly its neurological and autonomic symptoms. These anti-CHRM autoantibodies (AAbs) appear to arise after SARS-CoV-2 infection and can interact with neural and non-neural cells, potentially disrupting cholinergic signaling pathways that regulate cognition, autonomic balance, and other functions. Although the precise origins and mechanisms of these autoantibodies remain incompletely understood, early findings suggest correlations between specific AAb profiles and neurological dysfunction in long COVID, highlighting them as contributors to patient symptom burden beyond what traditional biomarkers explain.

Building on these molecular insights, the authors argue for strategies to neutralize or inhibit CHRM autoantibodies as a promising therapeutic direction for long COVID.

Potent phytoceuticals cocktail exhibits anti-inflammatory and antioxidant activity on LPS-triggered RAW264.7 macrophages in vitro

Authors: Gabrielle De Rubis; Keshav Raj Paudel; Sofia Kokkinis; Tammam El-Sherkawi; Jessica Katrine Datsyuk; Prakash Salunke; Joachim Gerlach; Kamal Dua.

The study evaluated a phytoceutical cocktail for its anti-inflammatory and antioxidant effects in LPS-stimulated RAW264.7 macrophages, a standard in-vitro inflammation model. LPS exposure normally induces high levels of nitric oxide (NO), reactive oxygen species (ROS), and pro-inflammatory signaling. Treatment with the phytoceutical blend significantly reduced NO and ROS production, indicating suppression of inflammatory and oxidative stress responses. The cocktail also modulated key inflammatory and antioxidant pathways at the gene and protein level. These findings suggest a synergistic effect of combined plant compounds rather than single-agent activity. The results support the concept that multi-component phytoceuticals can restore immune balance under inflammatory stress. While limited to an in-vitro model, the study provides a mechanistic foundation for further translational and clinical investigation.

Unraveling the enigma of long COVID: novel aspects in pathogenesis, diagnosis, and treatment protocols

Authors: Joachim Gerlach; Abdul Mannan Baig; Sandy Rosko; Beate Jaeger; Hans Rausch.

The review frames long COVID (PASC) as a complex, multi-system condition characterized by persistent or new symptoms lasting months after acute SARS-CoV-2 infection, now recognized as a genuine biomedical syndrome rather than a psychosomatic or transient state. It proposes that long COVID arises from interacting mechanisms, including persistent viral components or antigenemia, immune dysregulation, chronic inflammation, endothelial and vascular dysfunction, and host genetic susceptibility that may impair viral clearance. The authors highlight limitations of current symptom-based diagnosis and argue for integrative diagnostic approaches capable of detecting ongoing viral, immunologic, or metabolic abnormalities. Treatment strategies are described as largely empirical and fragmented, underscoring the need for mechanism-driven, personalized protocols targeting immune modulation, viral persistence, and systemic repair. Overall, the paper calls for a paradigm shift toward comprehensive pathophysiological models, improved biomarkers, and well-designed clinical trials to move long COVID care beyond symptom management toward causal intervention.

A retrospective cohort study on early antibiotic use in vaccinated and unvaccinated COVID-19 patients

Authors: Carlo Brogna; Luigi Montano; Maria Elisabetta Zanolin; Domenico Rocco Bisaccia; Gianluca Ciammetti; Valentina Viduto; Mark Fabrowski; Abdul Mannan Baig; Joachim Gerlach; Iapicca Gennar; Elio Bignardi; Barbara Brogna; Aquilino Frongillo; Simone Cristoni; Marina Piscopo.

The retrospective study examined COVID-19 patients who received early antibiotic treatment during the acute phase of infection and found that those treated promptly experienced shorter recovery times, better oxygen saturation, and fewer prolonged post-COVID symptoms, regardless of vaccination status. Benefits were most evident when antibiotics were started early, while comorbidities were associated with longer illness duration.

The authors suggest that early antibiotics may influence disease progression through anti-inflammatory, microbiome-modulating, or indirect antiviral effects, but emphasize that the findings are observational. They caution that prospective clinical trials are needed to confirm these results and to balance potential benefits against concerns such as antibiotic resistance and appropriate clinical use.

Sequence similarities in SARS-CoV-2 Spike Protein and Human Muscarinic receptors as the basis of Autoimmunity and Symptomology in Post-Acute Sequelae COVID-19

Authors: Sandy Rosko; Abdul Mannan Baig; Beate Jaeger; Joachim Gerlach.

The study examines sequence and structural similarities between the SARS-CoV-2 spike protein and human muscarinic acetylcholine receptors (CHRMs) as a potential mechanistic basis for autoimmune phenomena observed in post-acute sequelae of COVID-19 (PASC). Using bioinformatic analyses, the authors identify regions of homology that may promote molecular mimicry, whereby antibodies generated against spike protein cross-react with CHRM subtypes expressed in neural, cardiac, gastrointestinal, and immune tissues. Such cross-reactivity could disrupt normal cholinergic signaling, which plays a critical role in autonomic regulation, cognition, heart rate control, and inflammatory modulation. This framework provides a plausible explanation for common long COVID symptoms, including dysautonomia, fatigue, cognitive impairment, sleep disturbance, and cardiovascular instability.

In vitro anti-cancer activity of a polyherbal preparation, VEDICINALS®9, against A549 human lung adenocarcinoma cells

Authors: Keshav Raj Paudel; Rashi Rajput; Gabriele De Rubis; Venkata Sita Rama Raju Allam; Kylie Anne Williams; Sachin Kumar Singh; Gaurav Gupta; Prakash Salunke; Phil Hansbro; Joachim Gerlach; Kamal Dua.

The study evaluated the in vitro anti-cancer activity of the polyherbal formulation VEDICINALS®9 against A549 human lung adenocarcinoma cells, a commonly used model for non-small cell lung cancer. At a concentration of 0.2% (v/v), VEDICINALS®9 significantly inhibited cancer cell proliferation and migration, as demonstrated through cell viability, wound-healing, and transwell migration assays. Protein expression analysis revealed broad modulation of cancer-related pathways, including downregulation of multiple proteins associated with tumor growth, survival, invasion, and angiogenesis—such as Axl, basic FGF, survivin, progranulin, enolase-2, cathepsins B and D, BCL-x, amphiregulin, CapG, Dkk-1, and u-plasminogen activator—alongside upregulation of tumor-suppressive factors including p53 and endostatin. Collectively, these findings suggest that VEDICINALS®9 exerts multi-targeted anti-cancer effects in vitro by suppressing proliferative and migratory signaling while enhancing tumor-inhibitory and anti-angiogenic responses, supporting its potential relevance for further investigation in lung cancer research.

Intranasal Route: A Nasocerebral Approach against SARS-CoV-2 in NeuroCOVID

Authors: Joachim Gerlach; Abdul Mannan Baig.

The nasal cavity, richly connected to the brain via the olfactory nerve and cribriform plate, serves as an entry point for SARS-CoV-2 into the central nervous system, potentially contributing to neurological symptoms seen in NeuroCOVID. Targeting the virus at this intranasal interface—before it can invade deeper neural tissues—offers a strategic therapeutic and preventative approach. By focusing on blocking viral replication, reducing local viral load, and interrupting transport across the neural mucosa, intranasal interventions could mitigate both respiratory disease and the neurological complications associated with COVID-19. This perspective highlights the biological basis for intranasal delivery as a route to combat SARS-CoV-2 infection and reduce neuroinvasion, underscoring the need to explore therapies that act directly at this mucosal gateway.

Management of mild to moderate COVID-19 patients supplemented with “Vedicinals-9” as an adjuvant phyto-nutraceutical to prevent disease progression and improve clinical conditions: a randomized, multi-centered, exploratory study

Authors: Yogendra Kumar Choudhary; Joachim Gerlach; Prakash Salunke.

The randomized, open-label, multi-center clinical study evaluated VEDICINALS-9 (VD9) as an adjunct phyto-nutraceutical to standard care in 124 mild to moderate COVID-19 patients aged 18–60 to determine whether it could prevent disease progression and improve clinical outcomes. Patients received either standard care alone or standard care plus VD9 daily for 14 days. Results showed that significantly more patients in the VD9 group became SARS-CoV-2 RT-PCR negative earlier (29% by day 4 vs. 1.6%), with a greater reduction in inflammatory biomarkers such as CRP and IL-6 at multiple time points and a faster decline in viral load compared to standard care alone. CD4+ and CD8+ T cell counts increased in both groups, and VD9 was associated with improvements in antibody levels and other biomarkers like ferritin and D-dimer. Time to recovery of symptoms like sore throat was shorter in the VD9 group, and a higher proportion were discharged within 4–7 days. No adverse events were reported, suggesting VD9 was safe and may synergistically enhance viral clearance, modulate inflammation, and support recovery when added to routine COVID-19 treatment.

Series of Organ Effects of Vedicinals-9: Vedicinals-9 and Cardioprotection

Authors: Joachim Gerlach; Pralhad Wangikar; Abdul Mannan Baig; Prakash Salunke.

This publication reviews a series of organ-level effects associated with Vedicinals-9, with a particular focus on cardioprotection and systemic support during inflammatory stress states such as viral illness. The authors describe how the polyherbal formulation exerts multi-organ protective effects through antioxidant activity, modulation of inflammatory signaling, and support of endothelial and mitochondrial function. In cardiac contexts, Vedicinals-9 is shown to influence pathways linked to oxidative stress reduction, cellular survival, and vascular integrity, which are critical factors in preventing inflammation-driven myocardial injury. Rather than acting through a single target, the formulation appears to work via network pharmacology, influencing immune, metabolic, and redox balance across organs including the heart, lungs, liver, and kidneys. Overall, the paper positions Vedicinals-9 as a systems-level supportive intervention with potential relevance for reducing organ stress and preserving cardiovascular function during systemic inflammatory or infectious challenges, while emphasizing the need for further controlled clinical validation.

Effects of COVID-19 and vaccination on the human immune system: cases of lymphopenia and autoimmunity

Authors: Joachim Gerlach; Abdul Mannan Baig.

This paper examines how both SARS-CoV-2 infection and COVID-19 vaccination can alter immune system dynamics, with particular attention to reported cases of lymphopenia and autoimmune phenomena. The authors describe how acute infection commonly induces lymphocyte depletion—affecting CD4+, CD8+, B cells, and NK cells—through mechanisms involving inflammatory cytokines, immune exhaustion, and altered hematopoiesis, with lingering immune dysregulation observed in some individuals after recovery. The review also discusses post-vaccination immune responses, noting that while vaccines are designed to stimulate protective immunity, a subset of cases has reported transient lymphopenia, immune imbalance, or autoimmune-like manifestations, potentially linked to molecular mimicry, bystander activation, or heightened innate immune signaling. Overall, the article highlights the need to better understand individual susceptibility, immune recovery trajectories, and long-term immune remodeling following both infection and vaccination, especially in the context of chronic inflammation, autoimmunity, and post-acute COVID-related syndromes.

COVID-19 Post Vaccination Neuronal Adverse Events: Probable Mechanisms and Treatment Possibilities

Authors: Joachim Gerlach; Rachel Jessey; Abdul Mannan Baig; Prakash Salunke.

This review examines reported neurological adverse events following COVID-19 vaccination, exploring plausible biological mechanisms and potential management considerations. The authors outline a spectrum of post-vaccination neurological manifestations—including headaches, neuropathies, demyelinating disorders, encephalitis, seizures, and movement abnormalities—and discuss how these events may arise from immune-mediated mechanisms rather than direct neurotoxicity. Proposed pathways include molecular mimicry between spike protein epitopes and neural antigens, aberrant innate immune activation, cytokine-driven neuroinflammation, microvascular or endothelial dysfunction, and dysregulation of the blood–brain barrier. The paper also considers the role of individual susceptibility factors such as pre-existing autoimmunity, inflammatory burden, and immune priming. Finally, it reviews treatment possibilities focused on immune modulation, anti-inflammatory strategies, and supportive neurological care, emphasizing the importance of early recognition, personalized risk assessment, and continued post-vaccination surveillance to better understand and manage these rare but clinically significant events.

Long-COVID and its Physical and Neurological Symptoms in Adults: A Systematic Review

Authors: Joachim Gerlach; Sameera Rizvi; Abdul Mannan Baig; Shahia Pardhan.

This systematic review synthesizes available evidence on Long-COVID and its persistent physical and neurological symptoms in adults, highlighting the broad, multisystem nature of post-acute sequelae following SARS-CoV-2 infection. Across multiple studies, the most frequently reported ongoing symptoms included fatigue, dyspnea, muscle weakness, chest pain, and exercise intolerance, alongside prominent neurological and neurocognitive complaints such as brain fog, memory impairment, headache, sleep disturbances, dizziness, anosmia, anxiety, and depression. The review notes that these symptoms can persist for months after acute infection, even in individuals who initially experienced mild disease, suggesting mechanisms beyond direct viral damage, including chronic inflammation, immune dysregulation, endothelial dysfunction, autonomic imbalance, and neuroinflammation. Overall, the findings emphasize that Long-COVID represents a complex, heterogeneous condition with significant functional and quality-of-life impacts, underscoring the need for multidisciplinary evaluation, longitudinal monitoring, and targeted strategies to address both physical and neurological dimensions of post-COVID recovery.

The immune paradox of SARS-CoV-2: Lymphocytopenia and autoimmunity evoking features in COVID-19 and possible treatment modalities

Authors: Joachim Gerlach; Mark Fabrowski; Abdul Mannan Baig; Valentina Viduto.

This paper explores the “immune paradox” of SARS-CoV-2, in which COVID-19 simultaneously induces lymphocytopenia (depletion and dysfunction of immune cells) and autoimmune-like responses, contributing to disease severity and prolonged sequelae. The authors describe how acute infection is associated with marked reductions in CD4⁺ and CD8⁺ T cells, B cells, and NK cells, driven by cytokine excess, immune exhaustion, apoptosis, and bone marrow suppression, while paradoxically promoting autoantibody production and aberrant immune activation. Proposed mechanisms include molecular mimicry between viral antigens and host tissues, dysregulated innate immune signaling, persistent antigenic stimulation, and failure of immune resolution pathways. The review also discusses possible treatment modalities aimed at restoring immune balance rather than simple suppression, including immune modulation, anti-inflammatory strategies, antioxidant support, and interventions designed to normalize lymphocyte function and prevent chronic autoimmunity. Overall, the article frames COVID-19 as a condition of immune disorganization, where loss of immune competence and inappropriate immune activation coexist and shape both acute disease and long-term outcomes.

Underlying Causes and Treatment Modalities for Neurological Deficits in COVID-19 and Long-COVID

Authors: Joachim Gerlach; Nigel Greig; Abdul Mannan Baig; Prakash Salunke.

This review analyzes the underlying causes of neurological deficits observed in both acute COVID-19 and Long-COVID, outlining how SARS-CoV-2 can affect the nervous system through multiple, overlapping mechanisms. The authors describe contributions from neuroinflammation, immune dysregulation, endothelial and microvascular injury, blood–brain barrier disruption, hypoxia, mitochondrial dysfunction, and autoimmune processes, rather than direct viral invasion alone. Persistent neurological symptoms—such as cognitive impairment, brain fog, headaches, neuropathies, dizziness, mood disorders, and autonomic dysfunction—are linked to chronic inflammatory signaling, microcirculatory disturbances, and maladaptive immune responses that may continue long after viral clearance. The paper also reviews treatment modalities focused on restoring immune balance, reducing inflammation and oxidative stress, supporting vascular and mitochondrial health, and addressing autonomic and neurocognitive dysfunction through multidisciplinary and individualized approaches. Overall, the review positions COVID-related neurological deficits as a systems-level disorder requiring integrative strategies rather than symptom-specific interventions alone.

Persistent Spike Protein Production and Progressive Tissue Saturation in Long COVID: Novel Hypothesis for a Senescence Cascade

Authors: Joachim Gerlach; Abdul Mannan Baig; Beate Jaeger; Brigitte König; Kevin McCairn; Charles Rixey; Philip Mavberg; Phillip Triantos; Ursula Ehrhorn; Sandy Rosko; Usman Ali.

This paper advances a mechanistic framework for Long COVID centered on persistent spike protein production and progressive tissue saturation. Drawing from longitudinal diagnostic observations and published literature, the authors propose that a small population of spike-producing or spike-retaining cells may continuously replenish circulating spike protein in free and extracellular vesicle–associated forms.

The manuscript outlines a testable “senescence cascade” model in which persistent spike exposure drives irreversible cellular senescence and a senescence-associated secretory phenotype (SASP), amplifying inflammation and tissue dysfunction beyond the original antigen source. The framework distinguishes between early spike-linked pathology and later senescence-dominant disease states, offering structured hypotheses for biomarker development, extracellular vesicle profiling, spike sequencing, and senescence-targeted therapeutic investigation.

Antibody Escape and the Drastic Elevation of Circulating Spike Protein Since 2024: A Mechanistic Framework for Accelerated Long COVID Pathology

Authors: Joachim Gerlach; Abdul Mannan Baig; Beate Jaeger; Brigitte König; Kevin McCairn; Charles Rixey; Philip Mavberg; Phillip Triantos; Ursula Ehrhorn; Dietmar Schuermann; Sandy Rosko; Usman Ali.

This publication presents a four-pathway mechanistic framework explaining the marked rise in circulating spike protein levels observed since 2024 and its relationship to accelerated Long COVID pathology. The authors propose that near-complete antibody escape in recent SARS-CoV-2 variants—combined with immune imprinting and IgG4 class switching—has created conditions in which spike protein persists in circulation despite high antibody titers.

The paper outlines how impaired neutralization during acute infection increases viral reservoir formation, how structural mismatch reduces effective spike clearance, how persistent spike exposure promotes tissue senescence cascades, and how unbound spike drives fibrinolysis-resistant microclot formation. Together, these converging mechanisms provide a unified model for elevated spike burden, progressive tissue saturation, microvascular dysfunction, and worsening symptom severity in Long COVID.