Medic Debate

Recent studies have shown a correlation between COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, and the distinct, exaggerated immune response titled "cytokine storm". This immune response leads to excessive production and accumulation of reactive oxygen species (ROS) that cause clinical signs characteristic of COVID-19 such as decreased oxygen saturation, alteration of hemoglobin properties, decreased nitric oxide (NO) bioavailability, vasoconstriction, elevated cytokines, cardiac and/or renal injury, enhanced D-dimer, leukocytosis, and an increased neutrophil to lymphocyte ratio. Particularly, neutrophil myeloperoxidase (MPO) is thought to be especially abundant and, as a result, contributes substantially to oxidative stress and the pathophysiology of COVID-19. Conversely, melatonin, a potent MPO inhibitor, has been noted for its anti-inflammatory, anti-oxidative, anti-apoptotic, and neuroprotective actions. Melatonin has been proposed as a safe therapeutic agent for COVID-19 recently, having been given with a US Food and Drug Administration emergency authorized cocktail, REGEN-COV2, for management of COVID-19 progression. This review distinctly highlights both how the destructive interactions of HOCl with tetrapyrrole rings may contribute to oxygen deficiency and hypoxia, vitamin B12 deficiency, NO deficiency, increased oxidative stress, and sleep disturbance, as well as how melatonin acts to prevent these events, thereby improving COVID-19 prognosis.

In Gibraltar, a peninsula in Spain, almost 99% of the population is fully vaccinated – that’s according to info provided by Google.Since that time, new COVID cases per day have increased more than 2500%

A previously symptomless 86-year-old man received the first dose of the BNT162b2 mRNA COVID-19 vaccine. He died 4 weeks later from acute renal and respiratory failure. Although he did not present with any COVID-19-specific symptoms, he tested positive for SARS-CoV-2 before he died. Spike protein (S1) antigen-binding showed significant levels for immunoglobulin (Ig) G, while nucleocapsid IgG/IgM was not elicited. Acute bronchopneumonia and tubular failure were assigned as the cause of death at autopsy; however, we did not observe any characteristic morphological features of COVID-19. Postmortem molecular mapping by real-time polymerase chain reaction revealed relevant SARS-CoV-2 cycle threshold values in all organs examined (oropharynx, olfactory mucosa, trachea, lungs, heart, kidney and cerebrum) except for the liver and olfactory bulb. These results might suggest that the first vaccination induces immunogenicity but not sterile immunity.

The recent report of Lenze and colleagues (Lenze et al. 2020) indicates that the selective serotonin reuptake inhibitor (SSRI) fluvoxamine might reduce the rate of clinical deterioration in outpatients with symptomatic COVID-19. Though limited by small sample sizes (n’s of 72 and 80) and brief duration, largescale follow-up studies appear definitely warranted. The authors’ stated rationale for testing fluvoxamine is its agonistic effects at the sigma-1 receptor (S1R), as stimulation of the S1R receptor is reported to reduce damaging effects of the inflammatory response.

Results: Of 152 patients who were randomized (mean [SD] age, 46 [13] years; 109 [72%] women), 115 (76%) completed the trial. Clinical deterioration occurred in 0 of 80 patients in the fluvoxamine group and in 6 of 72 patients in the placebo group (absolute difference, 8.7% [95% CI, 1.8%-16.4%] from survival analysis; log-rank P = .009). The fluvoxamine group had 1 serious adverse event and 11 other adverse events, whereas the placebo group had 6 serious adverse events and 12 other adverse events.

Conclusions and relevance: In this preliminary study of adult outpatients with symptomatic COVID-19, patients treated with fluvoxamine, compared with placebo, had a lower likelihood of clinical deterioration over 15 days. However, the study is limited by a small sample size and short follow-up duration, and determination of clinical efficacy would require larger randomized trials with more definitive outcome measures.

The Wuhan coronavirus (Covid-19) "vaccine" push in Israel is failing to "save lives" as hordes of jabbed people all throughout the promised land are dropping dead from getting their genes modified. According to data collected by journalist Alex Berenson, Trump Vaccines are failing to protect against not only mild infection with the Chinese Virus but also severe infection. "That's a theory," Berenson tweeted about the government claim that Fauci Flu shots somehow prevent serious infection, adding that "the clinical trials didn't (and couldn't) prove it." Government data out of Israel shows that 81 percent of all new Chinese Virus deaths and 65 percent of all "severe" and "critical" hospitalizations are occurring in people who received the shots.

The trial (ClinicalTrial.gov NCT04388514) was conducted in four different Italian centers (April-October 2020). Patients were treated according to best available standard of care (SoC) therapy, with or without O3-autohemotherapy (O3-AHT).

Results: A total of 92 patients were enrolled: SoC + O3-AHT (48 patients) were compared to the SoC treatment (44 patients). The two groups differed in steroids therapy administration (72.7% in SoC arm vs. 50.0% in O3-AHT arm; p = 0.044). Steroid therapy was routinely started when it was subsequently deemed as effective for the treatment of COVID-19 disease. No significant differences in mortality rates, length of hospital stay, mechanical ventilation requirement and ICU admission were observed. Clinical improvement in patients with pneumonia was assessed according to a specifically designed score (decrease in SIMEU class, improvement in radiology imaging, improvement in PaO2/FiO2, reduction in LDH and requirement of oxygen therapy ≤ 5 days). Score assessment was performed on day-3 (T3) and day-7 (TEnd) of O3-AHT treatment. A significant increase in the score was reported at TEnd, in the O3-AHT treatment arm (0 [0-1] in the SoC arm vs. 2 [1-3] the O3-AHT arm; p = 0.018). No adverse events related O3-AHT treatment was observed.

Conclusion: In mild-to-moderate pneumonia due to SARS-CoV-2, adjuvant oxygen/ozone therapy did not show any effect on mortality, or mechanical intubation but show a clinical improvement a day 7 from randomization in a composite clinical endpoint. Larger Randomized prospective studies alone or in combination with steroids are needed to confirm our results.

The incidence of adverse reactions of inactivated virus vaccines, RNA vaccines, and adenovirus vector vaccines was higher than that of placebo. Common adverse reactions included pain, swelling, and fever at the injection site.

Conclusion: From the perspective of effectiveness, RNA vaccine > adenovirus vector vaccine > inactivated virus vaccine. From the perspective of safety, the incidence of adverse reactions of the three vaccines is higher than that of a placebo, and the incidence of adverse reactions of the adenovirus vector vaccine is higher.

7094 articles were identified initially and 43 were retrieved for more detailed evaluation. 5 randomized, double-blind, placebo-controlled trials were selected. A total of 1604 subjects with either vaccines or placebo infections were included in the meta-analysis within the scope of these articles. According to the results, there is an increase in total adverse events for subjects with either low (95% CI : 1.90-4.29) or high ( CI : 2.65-5.63) dose vaccination. The adverse effects of COVID-19 vaccine are mainly local ones including pain, itching, and redness, and no significant difference was identified in the systemic reactions. All adverse effects were transient and resolved within a few days. Moreover, the neutralizing and IgG antibody levels post different dose vaccinations were all significantly increased at day 14/21 ( P = 0.0004 and P = 0.0003, respectively) and day 28/35 ( P < 0.00001) in vaccine groups compared to placebo controls. Besides, the levels of neutralizing and IgG antibodies were also elevated significantly at from day 14 to 35, versus day 0 (All P < 0.001). In conclusion, our analysis suggests that the current COVID-19 vaccine candidates are safe, tolerated, and immunogenic, which provides important information for further development, evaluation, and clinical application of COVID-19 vaccine.

This document was labelled as "game Set and Match" by my friend, professor Niels Harrit from Copenhagen, who also documented the presence of rests of explosives in the rubble of WTC after the 9/11 "attack"

The National Institute of Health’s grant AI23946-08 issued to Dr. Ralph Baric at the University of North Carolina at Chapel Hill (officially classified as affiliated with Dr. Anthony Fauci’s NIAID by at least 2003) began the work on synthetically altering the Coronaviridae (the coronavirus family) for the express purpose of general research, pathogenic enhancement, detection, manipulation, and potential therapeutic interventions targeting the same. As early as May 21, 2000, Dr. Baric and UNC sought to patent critical sections of the coronavirus family for their commercial benefit.1 In one of the several papers derived from work sponsored by this grant, Dr. Baric published what he reported to be the full length cDNA of SARS CoV in which it was clearly stated that SAR CoV was based on a composite of DNA segments. “Using a panel of contiguous cDNAs that span the entire genome, we have assembled a full-length cDNA of the SARS-CoV Urbani strain, and have rescued molecularly cloned SARS viruses (infectious clone SARS-CoV) that contained the expected marker mutations inserted into the component clones.”2 On April 19, 2002 – the Spring before the first SARS outbreak in Asia – Christopher M. Curtis, Boyd Yount, and Ralph Baric filed an application for U.S. Patent 7,279,372 for a method of producing recombinant coronavirus. In the first public record of the claims, they sought to patent a means of producing, “an infectious, replication defective, coronavirus.” This work was supported by the NIH grant referenced above and GM63228. In short, the U.S. Department of Health and Human Services was involved in the funding of amplifying the infectious nature of coronavirus between 1999 and 2002 before SARS was ever detected in humans. 

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Klaas Proesmans came to our seminar in Mexico that teaches the use of chlorine dioxide to cure diseases. He arrived here in Mexico about two months before the actual clinical trial of the four days that was from the 11th to the 16th of December, 2012, in Uganda. He said to me at that time that he really didn’t think chlorine dioxide worked to cure diseases but he felt it was his job to prove it one way or the other. At the time of this clinical trial many diseases were treated, but the disease of interest was malaria. And 154 cases of malaria were given doses of MMS which, of course, was chlorine dioxide. 143 cases were free of malaria within 24 hours of taking the dose, with only 11 cases requiring a second dose. This was all recorded on DVD and on paper with signatures of doctors and technicians. There was no chance of mistake. One hundred and fifty-four cases of malaria were made well. 

Expression of CCR5 and its cognate ligands have been implicated in COVID-19 pathogenesis, consequently therapeutics directed against CCR5 are being investigated. Here, we explored the role of CCR5 and its ligands across the immunologic spectrum of COVID-19. We used a bioinformatics approach to predict and model the immunologic phases of COVID so that effective treatment strategies can be devised and monitored. We investigated 224 individuals including healthy controls and patients spanning the COVID-19 disease continuum. We assessed the plasma and isolated peripheral blood mononuclear cells (PBMCs) from 29 healthy controls, 26 Mild-Moderate COVID-19 individuals, 48 Severe COVID-19 individuals, and 121 individuals with post-acute sequelae of COVID-19 (PASC) symptoms. Immune subset profiling and a 14-plex cytokine panel were run on all patients from each group. B-cells were significantly elevated compared to healthy control individuals (P<0.001) as was the CD14+, CD16+, CCR5+ monocytic subset (P<0.001). CD4 and CD8 positive T-cells expressing PD-1 as well as T-regulatory cells were significantly lower than healthy controls (P<0.001 and P=0.01 respectively). CCL5/RANTES, IL-2, IL-4, CCL3, IL-6, IL-10, IFN-γ, and VEGF were all significantly elevated compared to healthy controls (all P<0.001). Conversely GM-CSF and CCL4 were in significantly lower levels than healthy controls (P=0.01).