[Bouhhhhhh ! ] Sars-Cov 2 Is Airway HIV

[S.Seneff]

https://www.medrxiv.org/content/10.1101/2020.03.27.20045427v1.full.pdf

While lymphocytopenia is a common characteristic of patients infected by the novel severe acute
respiratory syndrome coronavirus 2 (SARS-CoV-2), the mechanisms responsible for this depletion
are unclear. Through careful inspection of the spleens and lymph nodes (LNs) from six cases with
postmortem examinations, we observed that SARS-CoV-2 could directly infect secondary lymphoid
organs to induce cell death. Immunohistochemistry demonstrated ACE2 (angiotensin-converting
enzyme 2), the potential receptor of SARS-CoV-2, expresses on tissue-resident CD169+
macrophages in spleens and LNs. Immunofluorescent staining confirmed that viral nucleocaspid
protein (NP) can be found in ACE2+
cells, CD169+
macrophages, but not in CD3+
T cells or B220+
B cells in spleens and LNs. SARS-CoV-2 infection induces severe tissue damage including lymph
follicle depletion, splenic nodule atrophy, histiocyte hyperplasia and lymphocyte reductions.
Moreover, in situ TUNEL staining illustrated that viral infection leads to severe lymphocyte
apoptosis, which might be mediated by viral antigens inducing Fas upregulation. Furthermore,
SARS-CoV-2 also triggers macrophages to produce IL-6, a proinflammatory cytokine that directly
promotes lymphocyte necrosis. Collectively, these results demonstrate that SARS-CoV-2 directly
neutralizes human spleens and LNs through infecting tissue- resident CD169+
macrophages.

 

[SOMO]

Out of all the interleukins I think IL-6 is the one most often being branded as the most inflammatory, so it is the worst of the worst.

Aspirin reduces IL-6 slightly.

Effects of aspirin on serum C-reactive protein and interleukin-6 levels in patients with type 2 diabetes without cardiovascular disease: a randomiz... - PubMed - NCBI

Aspirin reduced IL-6 with 0.7 +/- 0.5 pg/ml, whereas use of placebo resulted in a mean increase of 0.2 +/- 0.8 pg/ml (P = 0.302). There were no significant differences in effects on CRP and IL-6 between 100 and 300 mg aspirin.

IMO even 300mg of Aspirin is a very small amount since the standard pill is 325mg. Increasing the dosage may have more significant effects on IL-6.

Pro- and Anti-Inflammatory Cytokines in Chronic Pediatric Dialysis Patients: Effect of Aspirin

Serum IL-6 concentration decreased with aspirin treatment but not significantly (P = 0.1). Serum IL-1β concentration remained unchanged, and IL-4 and IL-10 concentrations remained stable throughout aspirin treatment. The effect of aspirin treatment on serum cytokine concentrations was similar for HD and PD patients. In HD patients, IL-6, IL-8, and TNF-α remained suppressed 1 mo after discontinuation of aspirin. It is concluded that proinflammatory cytokines are elevated in pediatric HD and PD patients without counterbalance from anti-inflammatory cytokines, and aspirin therapy attenuates inflammation.

"Collectively, these results demonstrate that SARS-CoV-2 directly
neutralizes human spleens and LNs through infecting tissue- resident CD169+
macrophages."

That line sounds like nonsense because if Macrophages are present in a cell, there is ALREADY inflammation/infection there. Saying that the damage is being caused because the macrophages are infected with a virus is like saying the car was damaged by a cracked windshield instead of asking - what caused the windshield to crack?

 

[LeeLemonoil]

Remember that IL-6 is also essential part of a functioning immune response. Everyone infected with SarsCov2 and has no or light symptoms - a successful immune response - expresses the stuff.
Anyway:

Inhibiting Interleukin-6 (IL-6): The Key To Health - SelfHack

Top Ways to Inhibit IL-6

• Spices: Bay leaves [63], Black pepper [63], Nutmeg [63], Oregano [63], Sage [63]
• Resistant starch [64]
• Zinc [65]
• Magnesium [66]
• Probiotics: B. infantis [67], S. boulardii [68], L. casei [69], L. Salivarius [70]
• Trehalose [71, 72]
• Jasmine Tea/EGCG[73]
• Vitamin D3 [74]
• PQQ [75]
• Andrographis/Andrographolide [76] – Out of 20 plants tested, Andrographis inhibited IL-6 the most and was more potent than dexamethasone. (IC50= .74mcg/ml)
• Black Cumin Seed Oil/Thymoquinone [77]
• Curcumin [78, 79]
• Licorice [80]
• Fish oil/DHA [81]
• Fisetin [82]
• Cinnamon [63] /Sodium Benzoate
• Molecular hydrogen machine [83]
• Aspirin [84]
• Boswellia [85]
• Lithium [86]
• Hydroxytyrosol [87]
• Apigenin [63]
• Luteolin [88]
• Quercetin [63]
• Resveratrol (500 mg, with 5 g leucine) [79, 89]
• Red Yeast Rice/Lovastatin [90]

 

[S.Seneff]

Interleukin-6 in COVID-19: A Systematic Review and Meta-Analysis
Eric Anthony Coomes, View ORCID ProfileHourmazd Haghbayan
doi: Interleukin-6 in COVID-19: A Systematic Review and Meta-Analysis
This article is a preprint and has not been peer-reviewed [what does this mean?]. It reports new medical research that has yet to be evaluated and so should not be used to guide clinical practice.

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Abstract
Purpose: Coronaviruses may activate dysregulated host immune responses. As exploratory studies have suggested that interleukin-6 (IL-6) levels are elevated in cases of complicated COVID-19 and that the anti-IL-6 biologic tocilizumab may be beneficial, we undertook a systematic review and meta-analysis to assess the evidence in this field. Methods: We systematically searched MEDLINE and EMBASE for studies investigating the immunological response in COVID-19 or its treatment with tocilizumab; additional grey literature searches were undertaken. Meta-analysis was undertaken using random effects models. Results: Eight published studies, three pre-prints, and five registered trials were eligible. Meta-analysis of mean IL-6 concentrations demonstrated 2.9-fold higher levels in patients with complicated COVID-19 compared with patients with non-complicated disease (six studies; n=1302; 95%CI, 1.17-7.19; I2=100%). A single non-randomized, single-arm study assessed tocilizumab in patients with severe COVID-19, demonstrating decreased oxygen requirements, resolution of radiographic abnormalities, and clinical improvement. No adverse events or deaths were observed. Conclusions: In patients with COVID-19, IL-6 levels are significantly elevated and associated with adverse clinical outcomes. While inhibition of IL-6 with tocilizumab appears to be efficacious and safe in preliminary investigation, the results of several ongoing clinical trials should be awaited to better define the role of tocilizumab in COVID-19 prior to routine clinical application.

 

[S.Seneff]

Interferon-a2b treatment for COVID-19
Qiong Zhou, Xiao-Shan Wei, Xuan Xiang, Xu Wang, Zi-Hao Wang, Virginia Chen, Casey P Shannon, Scott J Tebbutt, Tobias R Kollmann, Eleanor N Fish
doi: https://doi.org/10.1101/2020.04.06.20042580
This article is a preprint and has not been peer-reviewed [what does this mean?]. It reports new medical research that has yet to be evaluated and so should not be used to guide clinical practice.

Abstract
Summary Background The global pandemic of COVID-19 cases caused by infection with SARS-CoV-2 is ongoing. We describe here the clinical course of COVID-19 in a cohort of confirmed cases in Wuhan, China, treated with the repurposed potential experimental therapeutics IFN-α2b, arbidol or a combination of IFN-α2b plus arbidol. Methods 77 adults with confirmed COVID-19 were treated with either nebulized IFN-α2b (5mU,b.i.d.), arbidol (200mg dispersible tablet, t.i.d.) or a combination of IFN-α2b plus arbidol. Serial SARS-CoV-2 testing along with hematological measurements, including cell counts and blood biochemistry, serum cytokine levels, temperature and blood oxygen saturation levels were recorded for each patient during their hospital stay. Findings Treatment with IFN-α2b with or without arbidol significantly reduced the duration of detectable virus in the upper respiratory tract and in parallel reduced duration of elevated blood levels for the inflammatory markers IL-6 and CRP. Interpretation IFN-α2b should be investigated as therapy in COVID-19 cases.



Interleukin-6 blockade for severe COVID-19
Mathilde ROUMIER, Romain PAULE, Matthieu GROH, Alexandre VALLEE, Felix ACKERMANN
doi: https://doi.org/10.1101/2020.04.20.20061861
This article is a preprint and has not been certified by peer review [what does this mean?]. It reports new medical research that has yet to be evaluated and so should not be used to guide clinical practice.

Abstract
In the context of COVID-19 pandemic and growing tensions worldwide regarding healthcare facilities, there is an urgent need for effective treatments likely to reduce the crunch of ICU beds. Following the assumption by Mehta and colleagues who exhorted physicians to screen patients with severe COVID-19 for hyperinflammation and investigate immunomodulatory drugs in this setting, we relate our short-term - yet promising - experience regarding IL6 blockade with tocilizumab in 30 selected patients of less than 80 years of age, >5 days of prior disease duration, severe (i.e. requiring strictly over 6L/min of oxygen therapy) rapidly deteriorating (i.e. increase by more than 3L/min of oxygen flow within the previous 12 hours) COVID-19-related pneumonia. By comparison with a control group of patients (matched for age, gender and disease severity using the inverse probability of treatment weighted methodology) that did not receive tocilizumab. We demonstrate that, in highly selected patients, IL6 blockade could curb the "cytokine storm", prevent ICU admission and the requirement for mechanical ventilation. Notwithstanding the shortcomings of this retrospective small sample-size study, we believe that these preliminary findings support the fostering of research efforts in the fight against COVID-19-induced inflammation, especially before patients require admission to the ICU.

 

[johnwester130]

wow

thougts on pirfenidone?