So a healthy immune system could also allow for a more severe reaction….almost be a liability? Depends on your interpretation of a healthy immune system. For some not so clear reason some people’s immune systems make the wrong decision and make some types of IgG which enhance damaging and lethal responses (neutralizing IgG is beneficial) , burning down the house to get rid of the rats, sort of like an allergic response does but only by analogy. One caveat to this assessment, it could change as more data becomes available. One firm conclusion: the virus is here to stay even if it becomes hidden as we have seen with dog coronaviruses.
John when you say it could become hidden? Does that mean it would be harmless or dormant or only attack certain people with specific immune issues? Dormant may not be best description. It will not be harmless unless it self attenuates which may take years or never. What I mean is that in some it finds a safe place to reproduce and shed periodically like GI or nasal tract and the immune system does not see it, or overreacts or suppresses it in cycles. This is probably what cold coronaviruses already do in humans. Seen in infectious peritonitis coronavirus in cats where 100% in a cattery infected but only a few die periodically. Some say from mutations but more likely because this is how coronaviruses adapt to continue. Here to stay. Hope for a good vaccine.
So what are your recommendations if you have it? So far we have been told – increase vitamins C, D3, Zinc & probiotic? Well good health and anything that reduces inflammation is good. These will not prevent infection and susceptibility to a storm. They may slightly improve chances of survival. Decreasing chances of exposure, reducing the dose of virus in a given exposure and your genetics are the strongest prognosticators. Perhaps some prior exposure to the other human coronaviruses. Need a good vaccine. Until then masks, social distance and good hygiene. The virus is very efficient at infection but not so good at long distance or persistent environmental infection. People close together putting out a lot of viruses in a small space bad; outdoors, sunshine and space good. Sorry only very high heat kills it (130F/30+min). Not seasonal. Probiotics may improve the microbiome increasing mucosal immunity (IgA).https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7375307/pdf/main.pdf
In less then 4 weeks we will be back in school, what to do? Yeah. It is a big unknown. I feel for all the parents and teachers. It is true that children 9 and under rarely show symptoms (or infection?) but older they progressively respond more like adults with age. It is a game of numbers: more susceptible, more exposures, the rarer becomes more common. More possible silent superspreaders. But this is an experiment and we might get lucky. Yes it is a gamble like numbers.
So we might fare a little better if we have it once already?There is some evidence and speculation by medics that some cross protection comes from the other human coronaviruses. Regardless of what you hear about antibody levels, full recovery from COVID is only possible if there is an adequate immune response. Historically these viruses have induced immunity for a year or longer (in animals and perhaps humans with cold CoV), if they don’t mutate which is not that common, and repeated exposure to low numbers of virus reinforces this immunity resulting in mild or inapparent infection. However this may not completely eliminate carriers.
So those of us who suffer from cytokines storms are more susceptible?Could be. Why steroids might be handy or more specific inhibitors preferred.
Steroid inhalers effective? Has helped in some clinical settings.
What’s you thought on the zinc, z pack & hydroxy?Zinc is a purported nonspecific immune booster; z pack is an antibiotic treating only secondary bacterial infections, not viruses, but a side effect is as an anti inflammatory; hydroxychloroquine is a nonspecific anti inflammatory but has some bad side effects on the heart (some but not all people, risk benefit problem). Again limited help by anti inflammatory actions but with risks.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7375307/pdf/main.pdf
If have O blood type are you less likely to get it?No there is no difference with blood type. O folks are no better off. Look closer at results/conclusions: “On univariate analysis, there was no association between blood type and any of the peak inflammatory markers nor between blood type and any of the clinical outcomes of severity.”https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7354354/pdf/277_2020_Article_4169.pdf
Does MMR vaccine protect against COVID-19?It might work to protect those under nine because they have fewer ACE2 receptors but older people who have had measles, mumps and rubella and should have life long immunity are getting infected and dying. Again, this is only cross immunity; not the strongest. Older people have too many ACE2 receptors, a decline in immunity and underlying conditions (like me Type 2 diabetes). Maybe a super immunization like with shingles vaccine (4x the usual antigen level) but for measles and rubella might work. However a specific vaccine would be better. It’s all in the numbers: level of exposure (viral dose) vs level of immunity.
If u get the virus….have the disease, then test negative…….then retest some time later, Say couple days or weeks later and test positive ……DID u ever really clear the disease? Did u clear the disease and now dead viral products (residual particles) are causing u to be falsely positive? Did u catch it again Or never really cleared it despite showing negative? Or were u falsely showing negative? Or don’t know? Or are the tests inaccurate whether falsely + or -? I don’t think it is likely that one gets a new infection 2 or more times in the same season. Although antibody titers drop quickly in 2-3 months, data suggests T cell and B cell memory cell immunity is more substantial and enduring. PCR is only as good as the sample so garbage in garbage out: false negatives and missed infections. Timing is also important: when did infection start and what stage are you in—miss shedding virus. Sequestered infection in nasal sinuses and in GI so shedding of virus intermittently and residual RNA not from viable virus. This is why we always used 3 orthogonal techniques to identify viable agent: PCR, antigen/antibody and culture and isolation. False negatives worse than false positives. Can get equivocal results for any test for variety of reasons, positive one time negative another and back again. Coronavirus carrier states are common in animal coronaviruses and extended chronic infection at low viral load has been observed in humans.
Is it possible that SARS-2Cov is actually SARS-1Cov – in the sense that SARS-Cov1 is still hiding in an animal reservoir and just got reintroduced to human kind at some point and just mutated in a different direction, so to speak? So, SARS-3Cov may one day make its appearance when again, the host animal is again perturbed by mankind and makes a jump and again, goes through it mutations/iterations until it’s prime time for its human host? SARS2 is related to SARS1 only in sharing the ACE2 receptor and a few common genetic features but is a direct bat virus. CoV-2 belongs to the Betacoronavirus genus, which includes Bat SARS-like coronavirus, SARS-CoV, and MERS-CoV. Phylogenetic tree analysis of the novel coronavirus showed that SARS-CoV-2 belongs, together with SARS-CoV and Bat SARS-like coronavirus, to a different clade from MERS-CoV, and it is more phylogenetically related to Bat SARS-like coronaviruses (isolated in China from horseshoe bats between 2015 and 2018) than to SARS-CoV.
Are you worried about any of the vaccine technology moving forward? I would assume targeting the “spike protein” is something the body does when it’s infected with SARS-2Cov.
I would not expect that our body possess an endogenous “spike” or “spike-like” protein that would compromise people at a later time, like in the event another likeness were to arise, be it infectious or genetic in nature. Is that a safe assumption?No, only other viruses are likely to have such a protein. The only similarity would be a natural protein ligand of ACE2 receptors and/or of furin, the protease that leads to freeing up the fusion protein of the virus so it can enter the host cell. Some of furin’s substrates are: proparathyroid hormone, transforming growth factor beta 1 precursor, proalbumin, pro-beta-secretase, membrane type-1 matrix metalloproteinase, beta subunit of pro-nerve growth factor and von Willebrand factor. ACE2 is also a protease with a variety of substrates of which the biologically active peptides that ACE2 cleaves, the most relevant are apelin-13 and Angiotensin II. Apelin-13 is an active peptide that significantly improves serum insulin reduction and reduces hyperglycemia. Long-term apelin treatment significantly increases pancreatic islet beta cells. These facts may explain how binding to the receptor by the virus may inhibit its action and, therefore, exacerbate diabetes. It is doubtful that the anti-virus antibody or T cell receptors would crossreact with these natural ligands. The body does not make receptors just for viruses; they appropriate ones that already exist for normal physiological functions. The immune system most often can distinguish the difference between a virus and a natural ligand. The real problem would be if the vaccine triggered the wrong branch of the immune system, a systemic ant-parasite response, which would yield a generalized allergic-like response, cytokine storm.
So, you essentially would still have to depend on the immune system to be stimulated by those viral “mutants” that were not neutralized by the monoclonal antibody treatment and also run the risk of those mutants being passed onto another person, infecting them and thus leaving the monoclonal antibody treatment ineffective in their treatment and care? A “cocktail” approach – as you highlighted with HIV would prove more comprehensive in terms of treatment. Remdesivir does not appear to have that much efficacy – based off some recent studies I read – against SARS-2Cov. It’s not the “miracle drug” that people were hoping it would be. It takes a long time to find/synthesize/test, etc a small molecule to be a good drug target for any pathogen. And, a cocktail would require two/three drug candidates or even antibodies for treatment. That’s a long time in terms of research? Don’t confuse treatment with immunity. The cocktail for CoV was referring to a mixture of different antibodies and perhaps T cell immunity which is what one expects with the proper mix of antigens in the vaccine. Whether talking about drugs, antibodies or antibiotics, it is harder for a microbe to mutate past multiple antimicrobial agents than one. People who are immunized are very unlikely to produce a monoclonal antibody but some may want to use one as a therapeutic. So far mutants observed have not shown escape from an animal or person’s immunity. SARS is too stable a bug for that. But if therapies are mono then the selection pressure will force selection like antibiotics and Remdesivir will do. I agree it is not a very effective drug.
Can this process be made inert to be used on Humans as a Decontamination tool ????? Yes on skin but not inhaled. See the picture of it being applied to a finger. The plasma quickly inactivates with distance from the source. Therefore, only direct breathing of it near the source may prove toxic. Nano plasma produced on surfaces of nanoparticles is widespread but instantaneous and very short-lived because it is produced by pulsed microwaves; it represents a potential undefined hazard because of possible inhalation of the nanoparticles and internal activation to produce plasma.
Why wasn’t the stability of mRNA vaccines brought up at the beginning? User friendly capabilities? Yeah, how many doctors offices have such freezers? None! And yes, how not to break the cold chain of transport? Who is going to QA/QC that process? This is a ridiculous example of advanced biotechnology leading medical practicability: a demanding cold chain difficult to achieve even in the US and advanced countries but impossible in developing countries, much less creating a problem to drive the expected cost through the roof. Why didn’t they pursue DNA vaccines which are far more stable? And if someone had picked up and developed our nanobe vaccine delivery concept, stability at room temperature for at least 4 years. https://www.laboratoryequipment.com/569702-Hurdle-1-Develop-COVID-19-Vaccine-Hurdle-2-Deliver-it-at-Ultra-low-Temperatures/ US pharmaceutical interests push ahead at any cost without thinking about accessibility of their products because in the US they can charge anything traffic will bear and damned those who can’t afford it or are uninsured.
What is the possibility of an autoimmune problem with the “nano lipid” vehicle that is equipped with a T cell specific protein to Target the T cells? Is it possible that due to the lipophilic nature of the Nanolipid it could just non-specifically stick to the membrane of another cell and fuse and unload the mRNA cargo? Basically setting it up for protein synthesis and presenting the spike protein on the surface of that non-T cell ? Since such “nano lipids” are so small and lipophilic… is it possible it could cross the blood brain barrier?
Those possibilities are remote. To pass through the blood brain barrier the nanoparticles would have to be placed high in the nasal cavity. Lipids alone are not sufficient to cross the blood brain barrier. Again autoimmunity also requires some host genetic predisposition. Remember the immune system normally attacks virus in other cell types other than T cells, even killing the cells harboring virus as by NK cells and cytotoxic T cells as well as antibody dependent cell cytotoxicity.
Could the animal wormer Ivermectin be used to treat COVID-19 ? Activity against SARS-CoV-2 of the animal wormer ivermectin has been greatly exaggerated. Although in cell culture and some experimental animals, RNA antiviral effects have been reported in last 50 years, they are only effective in the initial phase of infection and fade rapidly https://www.nature.com/articles/s41429-020-0336-z.pdf. Doses for COVID, based on cell culture studies, would have to approach 1000 times animal therapeutic doses. Also it would have to be used during the asymptomatic phase before virus numbers outran the binding/inhibition. Although used widely clinically in animals there have been no reported antiviral effects of note, intentionally or accidentally.
Do you have an opinion as to the likelihood that SARS-CoV-2 may have come out of a lab as opposed to solely being a zoonotic virus? It has all the characteristics of an animal virus “lost” in an aberrant human host. The “lab” connection at Wuhan is purely incidental. Even if lab personnel were infected, it is now impossible (because of bungling and long delaying the attribution investigation) to determine if they got it from specimens collected from bats or other wild or domestic animals (therefore, possibly personnel’s carrying it to outside the lab) or from frequenting the local live (wild) animal and fish market. When a virus is in both places at origin, it confounds the investigation. My experience with wild animal markets in Asia and Eastern Europe, convinces me it is the most likely source (like SARS-1), not some nefarious lab fantasy. There are data that the virus (a 99% genetic match) was found in Southeast Asia early in its emergence. My blog discusses this as it has evolved over the pandemic in excruciating detail.
Does the route of administration increase the likelihood that the adenovirus–based vaccines will cause thrombosis? Adenovirus vectors causing clotting if accidentally injected into a blood vessel rather than intramuscularly? Seriously doubt this. It is very hard to make an IV injection by accident and the reactions take up to 2 weeks. It is from the formation of platelet auto-antibody and activation of complement pathway of clotting that thrombosis appears first followed by thrombocytopenia, depletion of platelets. An IV material is long gone before this happens. SARS-CoV-2 infection itself. not just adenovirus, profoundly affects clotting (95 times more likely with SARS-CoV-2 infection than general population and 10 times more likely from infection than vaccination).
Should people with rheumatoid arthritis or other autoimmune disease receive COVID vaccine or 3rd boosters?
I am not sure of the justification for not getting a COVID vaccine booster. Rheumatoid arthritis is not an IgE (histamine; anaphylaxis) mediated disease but IgG and IgM mediated. It involves an antibody to an antibody, in turn, to an unknown antigen (not spike protein of a CoV). It is an autoantibody against the Fc portion of IgG .
Rheumatoid factor can also be a cryoglobulin (antibody that precipitates when a blood sample is cooled); it can be either type 2 (monoclonal IgM to polyclonal IgG) or type 3 (polyclonal IgM to polyclonal IgG) cryoglobulin. On rare occasion, it can be an autoantibody against other types of Ig even IgE. The virus is more likely to induce autoimmunity than the vaccine. Although predominantly IgM, rheumatoid factor can be other isotypes of antibody even IgE, but not a acute allergic reaction.
“ The American College of Rheumatology stresses the importance of anyone with RA becoming fully vaccinated against COVID-19, as people with RA may have a greater risk of severe COVID-19, hospitalization, and worse outcomes than the general population.”
Global Biosurveillance 