SARS-CoV-2 changes long-term macrophage response, the mysterious case of the French flu
And another case of how useless mRNA is
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Mild COVID-19 imprints a long-term inflammatory eicosanoid- and chemokine memory in monocyte-derived macrophages
I found this paper fascinating and pertinent to some of my ideas I shared, specially among the “persistent low grade inflammation”, and this is a real explanation on why some people get excessive immune response from “mild” breakthroughs.
Macrophages are cells from the innate immune system, called effector cells, which literally means they exert a effect on other cells, and the immune system, by secreting (producing) pro-inflammatory, and anti-microbial mediators (mediators are other proteins that help to fight invaders, in a very crude way).
Authors found out that fatty acid metabolism is higher, and so is eicosanoids (explanation below), among other powerful metabolites (in some places in the literature they consider it a hormone, it’s a paracrine effect (it affects ALL nearby cells).
And even people recovered from mild infection had higher response to the Spike protein.
Eicosanoids are bioactive metabolites of polyunsaturated fatty acids (PUFAs) with key roles in infection and inflammation8. Eicosanoids are formed from arachidonic acid (AA) through different enzymatic pathways, including the cyclooxygenase (COX) pathway, synthesizing prostanoids and the 5-lipoxygenase (5-LOX) pathway, generating leukotrienes (LTs). LTs are potent granulocyte-chemotactic metabolites which cause bronchoconstriction, vascular leakage, and airway remodeling. Resident and recruited macrophages in the lung produce high levels of cysteinyl LTs (cysLTs) and leukotriene B4 (LTB4), thereby promoting granulocyte infiltration, airway inflammation and tissue remodeling
Thus, despite mild acute disease in the investigated cohort, MDM exhibited a persistent inflammatory imprint, which was associated with increased symptom burdens and aberrant LPS responses at 3-5 months post infection
While macrophages substantially lack the receptors used by the virus to enter cells (even though by now we are aware it can use a lot of others), they reacted to Spikes from both Elder SARS (the first), and SARS-CoV-2. There is a small argument among some researchers on what the virus can do to macrophages.
Perhaps this is one of the mechanisms and pathway used, for what I have been seeing for the last 6 months. Heightened allergic responses to this viral infection, and weird immune damage.
While I would prefer a broader study, using different receptors (specially the ones explored by other research teams), this is a very pertinent paper, which finally demonstrates one of my points, that the infection, and specially breakthrough will may cause a change in immune response for weeks, and it is immune suppressive, which will clearly shift, and feed any subclinical disease the person has lying around, or is genetically predisposed.
This would be also one of the reasons a decent portion of the vaccinated population get sicker, not only after a breakthrough infection, but getting one, and a booster. You are literally eliciting a cellular response that is jet fuel to a napalm fire.
The real question is, when that fire becomes white phosphorus, and it never goes out, until it burns your immune system completely ?
The persistent upregulation of pro-inflammatory eicosanoids in post COVID-19 macrophages may have multiple consequences for subsequent immune responses, e.g. during bacterial or viral infection or in patients suffering from chronic inflammatory diseases such as asthma, thus requiring future investigation.
This entire paragraph resonates with quite a number of other virus posts I have. And this wouldn’t be me, if I didn’t do this.
Antagonizing arachidonic acid-derived eicosanoids reduces inflammatory Th17 and Th1 cell-mediated inflammation and colitis severity
One of the 2021 myths, that the vaccines reduced viral load. Well, they do, for a amazing 30 days, next 30 goes down, nonexistent afterwards. Add this, to the colossal mountain of evidence on how the mRNA vaccine is utter useless. (They are outright dangerous in my opinion)
SARS-CoV-2 spike L452R mutation increases Omicron variant fusogenicity and infectivity as well as host glycolysis
I found this paper rather curious, and decide to share, the lack of one specific mutation changes the pathogenic profile in a substantial manner. And it is one you should be on the lookout for, as we previously saw, recombination does exist, and it is happening.
If any subsequent Omicron variant acquires this mutation, it will be rather bad, specially among the vaccinated, if it acquires other mutations and more immune evasion and antibody resistance, for acquired immunity too. High glycolysis enables it fast, well, everything.
I have a few other papers to share, but I think the most is already big enough for now, will save for the next one.
While the coronavirus epidemic takes up in the world, another disease continues its expansion in the hexagon. The past week was marked by a "strong increase in flu (of the) influenza" in France, summarizes this Wednesday Public Health France in its weekly balance sheet. The agency notes that now "all metropolitan areas (are) in epidemic, except Corsica.
This includes Île-de-France while it, struck early by the end-of-2021 epidemic, had experienced a lull at the beginning of the year and was no longer considered in the epidemic phase. She is ironed this week. Outside the metropolis, Guyana is also struck by the influenza epidemic, but other departments are spared.
The less infected and less immunized French
This flight of influenza is unusually late. In recent years, the peak of the epidemic - measured by the consultation rate in relation to the number of inhabitants - had instead in February. The winter of 2020-2021 was particular, because of the containment measures taken against COVID. They had, by extension, allowed to block the circulation of many other microbes, like the flu virus
A follower on Twitter send me the French news. If you want to make sense, you should read this series of post. Start here for the direct Flu reference.
More of these will start to happen, and out of season, it is NOT merely viral interference, this is Toll Like Receptor dysfunction, and immune suppression from other viral infections, like SARS-CoV-2. Keep your immune system always prime.
Thankfully, this isn’t bird flu.
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