Thoughts on Hong Kong Virologist Warning

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  • Wed, Jul 22, 2020 - 06:38am

    #11
    stevedaly

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    Bioweapon or GOF run wild?

We all resist change.  Just can’t accept such a monster weapon could ever be created.  Do we begin to have to face a new reality?

  • Wed, Jul 22, 2020 - 10:47am

    #12
    VOGUY

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    Thoughts on Hong Kong Virologist Warning

THIS IS WHY I decided to join PEAK.  There is simply outstanding people that are educated on important matters and care enough to tell the truth.  I know Dr. Mayer is not going to check back, but for the sake of all who have read his thoughts, I say THANK YOU.  God is amazing and His creation of the human body is mind-blowing.

  • Wed, Jul 22, 2020 - 11:01am

    #13
    VOGUY

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    Thoughts on Hong Kong Virologist Warning

Good question stevedaly – we are in troubling days indeed.  May God grant each one on here wisdom as we navigate the days ahead and my His Kindness come to all.

  • Thu, Jul 23, 2020 - 09:43am

    #14
    tbp

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    Reply To: Thoughts on Hong Kong Virologist Warning

@Dr. Jurgen Mayer

That is what we are dealing with right now, super cancer in the form of a deadly pandemic virus. So this virus, it is not what you think it is. This is not the flu, this is likely going to turn out to be worse than cancer. Why? We have already established that hCoV-2019 has at least 6 routes of attack and is using your own immune system against us. This is why patients are presenting with such varying symptoms. This virus can and will attack every organ in the host and cause long-term medical conditions. Please keep in mind that “recovered patients” simply refer to someone that did not die from this virus.

But many people experience it asymptomatically — seemingly over 50%. And children experience pretty much no effects. It must have to do with immunocompetence, which will be influenced primarily by:

– lack of nutrient deficiencies (building blocks sufficiency)
– lack of toxins exposure
– lack of comorbidities

And even with some of that (maybe not severe vitamin D deficiency), if given effective treatments early — such as HCQ+zinc, CDS (as a ROS like endogenous hydrogen peroxide released by WBCs that then turns into usable oxygen), NAC (or prevention of glutathione depletion), vitamin C (or just preventing its depletion which happens fast if sepsis [an inflammatory immune response that can lead to the dreaded cytokine storm] occurs), maybe artemisinin, used intelligently in combination with corticosteroids and/or anticoagulants as needed — people do seem to recover quite well… although it’s true there are some (many?) people who can’t seem to get rid of it after months (IME from talking to people on /r/COVIDpositive in many cases they’re using only 1000IU/day vitamin D, but in some cases it’s definitely not persistent vitamin D deficiency).

Note that “cases” are rising because testing is increasing. The death rate however has dropped tremendously, even by using only dexamethasone/corticosteroids, convalescent plasma, and remdesivir, and not intubating patients upon respiratory symptoms. No vitamin D, HCQ+zinc, vitamin C, NAC, B3, selenium, much less CDS, or anything that works well with no side-effects… just their Big Pharma approved treatments… yet even so, the mortality rate has decreased by like 40x.

The 6 routes of attack aren’t the same though — so far it looks like only ACE2 (CD143) cause major problems, because it’s expressed on cells that have the RNA translation machinery needed to replicate. CD147-expressing cells don’t have it, correct?

The attack on BiP/GRP78 remains of unclear use/effect/power (as you said it’s the “master chaperone of unfolded proteins, me thinks protein rerouting is occurring and potentially hijacked cleaving during healthy protein folding”), correct?

ADAM17 even less clear that it can cause any harm, right?

CD4 docking/hijacking potency and thus harm is also unclear, correct?

Furin as a route of attack is part of the ACE2 route of attack, no?

It seems a bit more likely that the virus escaped from the WIV, rather than deliberately released, so its targeting of non-ACE2 receptors would likely be experimental and undeveloped, especially given that the previous hCoVs were already known to successfully infect and harm via ACE2.

  • Thu, Jul 23, 2020 - 07:01pm

    #15
    Dr. Jurgen Mayer

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    Reply To: Thoughts on Hong Kong Virologist Warning

Thanks for the DM, your replies are always a pleasure to read as they are collected and thorough. I think we can all appreciate that. I need to learn how to craft replies like everyone else where you are properly quoting me. At any rate, let’s begin!

But many people experience it asymptomatically — seemingly over 50%.

There are two possibilities here, either the virus is not very dangerous and it has virtually no impact on most people OR most of the tests are false-positives. As scientists, we know how deadly the virus actually is. So the most logical conclusion here is there are an overwhelming amount of false positives coming out. As you are likely aware, even cursory research will concur that virtually all testing devices are quite faulty. If asymptomatic patients exist it is likely because they have built up antibodies to coronaviruses as they were likely previously exposed. This would be from either the two betacoronaviruses causing the common cold, hCoV-OC43 or hCoV-HKU1 or the two alphacoronaviruses causing the common cold, hCoV-229E or hCoV-NL63 or SARS-CoV, MERS-CoV. Without antibodies or some type of successful immediate (preventive) immune response, if a patient is asymptomatic they either received a very small viral load, have a very healthy immune system that could fend off a small viral load, or have natural built-up immunities. The average individual is not particularly healthy. If they were infected with a large dose of this virus, it is highly improbable that the patient would not develop any symptoms. That is simply illogical. What if I were to suggest the global mortality was 7 million with a case count of no less than 50 million? It is a fact that both the current case count and mortality numbers are exceptionally wrong. This skewed data says 4% of confirmed cases have died. What if this number was 14%? I think you are SIGNIFICANTLY downplaying the actual extent of this pandemic and are taking the reported data at face value, which is a serious mistake. Spain, as an example, simply stopped reporting deaths in June after recording 680 daily deaths. Did the virus just go away? Perhaps China shared “magic” with Spain.

 

The 6 routes of attack aren’t the same though — so far it looks like only ACE2 (CD143) cause major problems, because it’s expressed on cells that have the RNA translation machinery needed to replicate. CD147-expressing cells don’t have it, correct?

This is not accurate. There are a host of publications citing illness from non CD143 routes. If SARS-CoV and SARS-CoV-2 are both dockings with ACE2 then we would expect similar symptoms. Granted this novel virus docking is significantly stronger but we are seeing exceptionally different problems compared with SARS-CoV, which indicates there are many other routes that are causing illnesses. Dr. Martenson appears to have covered the CD147 route today. The implications of this hijack are far deeper and we currently do not have enough data.

 

The attack on BiP/GRP78 remains of unclear use/effect/power (as you said it’s the “master chaperone of unfolded proteins, me thinks protein rerouting is occurring and potentially hijacked cleaving during healthy protein folding”), correct?

There has not been nearly enough research on GRP78 but this route should be of significance. Think of this as an important secondary route if somehow CD143 became “unavailable”. Here is the latest update that I could locate for you. “The latest findings propose that GRP78 is cell surface‐localized, where it performs physiological roles to adjust signaling and cellular homeostasis. It is, using the structural alignments method, determined that Region IV of the S protein is the main driving force for GRP78 binding. This bond may represent one of the ways the virus takes to enter the host cell by increasing the percentage of GRP78 protein linked to the elderly and people with chronic diseases and tumors. It was revealed that GRP78 is capable of facilitating surface attachment of Middle East respiratory syndrome coronavirus (MERS‐CoV) and bat coronavirus HKU9 (bCoV‐HKU9) to host cell. In SARS‐CoV‐infected cells, GRP78 is induced. Studies on the expression of this GRP78 and its polymorphisms and their role in determining the susceptibility and resistance to coronaviruses are very limited; however, it may be responsible for increasing the rate of infection and death. Therefore, it may be applied to produce an anticorrelation drug against COVID‐19. Also, antagonism of GR78 may lead to a therapeutic for COVID‐19.”

 

ADAM17 even less clear that it can cause any harm, right?

ADAM17 is of critical importance to the virus. One of the main mechanisms for ARDS is the development of a cytokine storm, including high levels of IL-6 and TNF-alpha. ACE2 can be clipped from the surface of cells by proteases including ADAM17, and this appears to increase viral infection. ADAM17 also mediates the release of TNF-alpha and IL-6 receptor. ACE2 can be shed by two proteases, ADAM17 and TMPRSS2. TMPRSS2-cleaved ACE2 allows hCoV-2 cell entry, whereas ADAM17-cleaved ACE2 offers protection to organs. hCoV-2 infection-caused ACE2 dysfunction worsens COVID-19 and could initiate multi-organ failure. Here, we will explain the role of ACE2 in the pathogenesis of severe and critical conditions of COVID-19 and discuss auspicious strategies for controlling the disease.

https://academic.oup.com/ndt/article/35/6/1071/5820263 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7290508/

 

CD4 docking/hijacking potency and thus harm is also unclear, correct?

Harm is very clear. HIV patients with compromised CD4 are at exceptional risk for this route of attack. Dr. Martenson covered this today when discussing CD209 (DC-SIGN) as an impact on the immune system is being greatly expressed by the virus and there quite a lot of research data to back that up.

 

Furin as a route of attack is part of the ACE2 route of attack, no?

No, during RNA package assembly the virion is calling for proteolytic cleavage at the S1/S2 subunit in the Spike protein and is oddly requesting that human Furin (protease) cleave the unit. Without this cleavage site, the virus would be somewhat useless, regardless of what it wanted to bind to. Furin is supercharging the virus for replication. There are 6 key amino acids in the RBD that are enabling the virus for high binding efficiency. Happy to elaborate on this in more detail if needed. For absolute clarification, the ORF1a contains two proteases that it uses for enzyme recycling when tossing peptide residues. This virion is tricking Furin in the host body to work on its behalf to enact a proteolytic cleavage. Furin has no relationship to the virus itself. So MY question is, if this has somehow targeted Furin for cleavage, has it possibly tricked Furin into doing anything else? That is unknown.

 

 

It seems a bit more likely that the virus escaped from the WIV, rather than deliberately released, so its targeting of non-ACE2 receptors would likely be experimental and undeveloped, especially given that the previous hCoVs were already known to successfully infect and harm via ACE2.

 

Natural or not, intentional release in China would be national suicide. The country was heading towards a mild recession and will surely now face a massive depression. The part where you say the targeting of non-ACE2 receptors would be undeveloped is spot on! Somehow this virus came out of the box having mastered all of these tricks. How is that possible? We have no answer for that. We have no idea where this virus came from. I urge you to consider that this virus may not have originated in China. Perhaps it came from another nation? Wuhan is simply the first place it was reported. Here is a great thought experiment.

 

Rewind to October 2019 and let’s arbitrarily lock down the borders of China and USA. Domestic flights are fine but international travel, exports/imports are blocked. Next, we release hCoV-2019 in both nations at exactly the same time. Given that it is autumn in the USA, how long does it take for the US to figure out there is a novel virus? How long does it take for China to figure out there is a novel virus? Because China was able to figure that out VERY fast. Why? Because of their extensive history with SARS. Most of the Doctors and Scientists in China dealt with SARS and would be quick to notice something similar spring up. On top of this, China has a culture that is conditioned to wear masks and take preventative measures. The USA on the other hand has (more or less) no history with SARS or coronavirus outbreaks and no cultural background of protective measures such as wearing masks. I believe in our hypothetical scenario that it would take the USA no less than 3 months to actually identify the virus, sequence it, and begin to send out alerts. Within 6 months the pathogen is out of control as the country struggles to arrange preventative health measures for its citizens. In China, the government simply lock down a city, weld everyone in their homes and walk away ☹ My larger point here is that if this pathogen originated in the USA, virtually no one would have noticed it and it could have been brought directly to Wuhan during the 2019 CISM Military Games. I think this is more probable because countless people in the USA reported having the worst flu of their lives and noticed something exceptionally strange going around. Perhaps that just means the outbreak did happen in Wuhan first and the outbreak in the states simply went unnoticed for many months. Who knows. Either way, I support an accidental release theory, be it natural or manmade.

  • Thu, Jul 23, 2020 - 09:42pm

    #16
    2retired

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    Thoughts on Hong Kong Virologist Warning

Reading a story line of apocalypse is captivating, but there are some potentially good thoughts to chew on. German and Swedish  cohorts that seem resistant to this virus have been reported at 60-80%. An explanation maybe (in some population groups) that there is enough cross recognition of parts of the virus to mitigate development of the disease state. It would also suggest that herd immunity/resistance could be reached with a very low % sero- positive for antibodies. It would also give an explanation for the curve of infections tailing off so quickly. Alternate explanations for variation between counties mortality rates seem more likely with the lack of correlations between lockdowns and beneficial effects.

Ep89 Viral Impacts Explained – The PANDA Pandemic Data & Analytics Group

I still don’t want to get it, and think the overwhelming evidence and circumstances surrounding its early days in Wuhan, point to the virology lab origin

  • Fri, Jul 24, 2020 - 06:12am

    #17
    Copper’s Hu-mom

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    Thoughts on Hong Kong Virologist Warning

That is a very interesting thought experiment.  I am one who had an unusual, more virulent virus in December 2019 that caused me to miss more work than I had ever missed before. It did not act like a flu, which usually manifests in a severe headache for me.  However, no one else in my family became ill, as one might expect them to.  Is anyone studying the possibilities that you raise, Dr. Mayer?

  • Fri, Jul 24, 2020 - 07:39am

    #18
    tbp

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    Thoughts on Hong Kong Virologist Warning

Thanks for the DM, your replies are always a pleasure to read as they are collected and thorough. I think we can all appreciate that. I need to learn how to craft replies like everyone else where you are properly quoting me. At any rate, let’s begin!

Thanks for the reply; I think the same of you! The “blockquote” button is 4 buttons to the right of the Italics button.

There are two possibilities here, either the virus is not very dangerous and it has virtually no impact on most people OR most of the tests are false-positives. As scientists, we know how deadly the virus actually is.

But it’s also clear that people with low vitamin D can easily die from it, but people with D levels above 40ng/ml always have much better outcomes. The “official story” (a lie, really) is that sufficiency is above 30ng/ml or so. Yet even 40ng/ml is actually quite low vitamin D — ideal is 60-80ng/ml.

So the most logical conclusion here is there are an overwhelming amount of false positives coming out. As you are likely aware, even cursory research will concur that virtually all testing devices are quite faulty.

Yeah, and the creator of PCR, Kary Mullis, always said it was never designed for diagnosis, only for DNA amplification. I’ve been leaning towards the “few false positives” side of the fence, because I figure more scientists of various stripes would’ve figured it out and be pointing it out, since governments around the world are using PCR testing to take away people’s freedom. In your understanding, when a swab of throat/lung tissue is taken, and lipid layers are dissolved and free genomic sequences are picked up and then amplified (duplicated) using rtPCR, how are they then compared to existing database sequences — is there room for confusion with other hCoVs? Could SARS-CoV-2/2019-nCoV be confused with the somewhat virulent hCoV-OC43 or hCoV-229E during the comparison phase of PCR testing?

If asymptomatic patients exist it is likely because they have built up antibodies to coronaviruses as they were likely previously exposed. This would be from either the two betacoronaviruses causing the common cold, hCoV-OC43 or hCoV-HKU1 or the two alphacoronaviruses causing the common cold, hCoV-229E or hCoV-NL63 or SARS-CoV, MERS-CoV. Without antibodies or some type of successful immediate (preventive) immune response, if a patient is asymptomatic they either received a very small viral load, have a very healthy immune system that could fend off a small viral load, or have natural built-up immunities. The average individual is not particularly healthy. If they were infected with a large dose of this virus, it is highly improbable that the patient would not develop any symptoms. That is simply illogical.

Well, a higher viral load may confer an advantage to the virus, but even in small amounts, if the defence is weak enough, it should be able to start replicating and multiplying exponentially. I have no reason to think I don’t get exposed every year to the flu just as much as other people, yet I haven’t had flu symptoms for more than 15 years. That’s because I’m not in that average of unhealthy individuals, because I’ve studied what it means to be healthy from independent sources not affiliated with official government/international “health authorities” and their myriad parroters/believers of falsehoods/lies.

What if I were to suggest the global mortality was 7 million with a case count of no less than 50 million? It is a fact that both the current case count and mortality numbers are exceptionally wrong. This skewed data says 4% of confirmed cases have died. What if this number was 14%? I think you are SIGNIFICANTLY downplaying the actual extent of this pandemic and are taking the reported data at face value, which is a serious mistake.

I’ve been more of the thought that there are tons of asymtomatics that would test positive, but I can’t discard what you’re saying about large numbers of false positives, which would fit more with SARS1 and MERS mortality rates… although effective treatments were even less certain back then… With vitamin D sufficiency (or better yet optimal 60-80ng/ml) + early HCQ+zinc + vitamin C + NAC + B3 + magnesium (+ maybe benzo or cannabis or taurine or amantadine [also a Cathepsin L inhibitor] to reduce stress), in other words if they didn’t suppress the best treatments, I’m pretty sure the CFR/IFR would be far lower. For elderly and those with weakened immune systems due to comorbidities, if the above isn’t enough, CDS and/or convalescent plasma would seem appropriate, along with corticosteroids and/or anticoagulants when appropriate, and I think that’d would save most people (although sequelae could range from mild to very bad).

There’s also these that can be used to interfere with the virus at different stages:

– monolaurin (inactivates lipid-coated viruses)
– auranofin (amount of virus within cells dropped by 85% by 24h, and 95% by 48h)
– camostat (a potent TMPRSS2 inhibitor)
– hesperidin (a Spike-ACE2 attachment inhibitor)
– ivermectin (inhibits IMPa/ß1-mediated nuclear import of viral proteins)
– artemisinin (another one with a reactive peroxide group with a vast array of medicinal applications, from malaria to cancer to neurodegenerative diseases — the president of Burundi may have been assassinated for promoting this for SC2 as a warning to other African leaders)

Spain, as an example, simply stopped reporting deaths in June after recording 680 daily deaths. Did the virus just go away? Perhaps China shared “magic” with Spain.

I happen to live there; yeah, they stopped reporting because everyone could see Spain was the worst managed country in Europe and the worst in the world if going by deaths per million and not counting the smallest countries (like San Marino and Andorra) and not counting Belgium (which counted all deaths of any cause as Covid, like some US states under Deep State control). They were also already massively undercounting deaths in elderly care residences, and in fact continue today to deliberately try to kill off as many old people as possible to lessen SS burden so they can improve their vote buying money prospects in the yet-to-be-realized State budget. They are a criminal gang composed of the worst elements in the socialist party (very much like the DNC in the US, maybe like Germany’s SPD squared or cubed if the comparison is even valid) + the communist party + separatist/supremacistic regional parties + Basque ex-terrorist party… so it’s not suprising that any “official” data coming from Spain has the same credibility as that coming out of China.

OK so some of the damage may be inflicted via the other targets (CD147, BiP/GRP78, ADAM17, CD4), but we just don’t have enough data to understand exactly how. But the mortality rate is still lower than it was for SARS1 and MERS, yet the same PCR tests were also used to detect those, right?

ADAM17 is of critical importance to the virus. One of the main mechanisms for ARDS is the development of a cytokine storm, including high levels of IL-6 and TNF-alpha. ACE2 can be clipped from the surface of cells by proteases including ADAM17, and this appears to increase viral infection. ADAM17 also mediates the release of TNF-alpha and IL-6 receptor. ACE2 can be shed by two proteases, ADAM17 and TMPRSS2. TMPRSS2-cleaved ACE2 allows hCoV-2 cell entry, whereas ADAM17-cleaved ACE2 offers protection to organs.

Wait, so TMPRSS2 cleaves ACE2 also, in addition to the Spike protein (into S1 and S2 subunits)?

So what does ADAM17 do in benefit to the virus, or what does the virus do to ADAM17 that benefits it?

No, during RNA package assembly the virion is calling for proteolytic cleavage at the S1/S2 subunit in the Spike protein and is oddly requesting that human Furin (protease) cleave the unit. Without this cleavage site, the virus would be somewhat useless, regardless of what it wanted to bind to. Furin is supercharging the virus for replication. There are 6 key amino acids in the RBD that are enabling the virus for high binding efficiency. Happy to elaborate on this in more detail if needed. For absolute clarification, the ORF1a contains two proteases that it uses for enzyme recycling when tossing peptide residues. This virion is tricking Furin in the host body to work on its behalf to enact a proteolytic cleavage. Furin has no relationship to the virus itself. So MY question is, if this has somehow targeted Furin for cleavage, has it possibly tricked Furin into doing anything else? That is unknown.

Right, but furin cleavage is also used by other viruses such as HIV, influenza, dengue fever, and several filoviruses including ebola and marburg virus, so there’s nothing new in that, right? In addition to furin, it also requires TMPRSS2 cleavage, and then Cathepsin L (an endosomal cysteine protease) has to mediate the cleavage of the S1 subunit of the Spike protein to induce virion-cell membrane fusion… which, when you combine all 3 protease modification requirements, does seem strange/unusual/suspicious — how probable in your estimation would it be for that to occur naturally/zoonotically?

Natural or not, intentional release in China would be national suicide. The country was heading towards a mild recession and will surely not face a massive depression. The part where you say the targeting of non-ACE2 receptors would be undeveloped is spot on! Somehow this virus came out of the box having mastered all of these tricks. How is that possible? We have no answer for that. We have no idea where this virus came from. I urge you to consider that this virus may not have originated in China. Perhaps it came from another nation? Wuhan is simply the first place it was reported. Here is a great thought experiment.

Rewind to October 2019 and let’s arbitrarily lock down the borders of China and USA. Domestic flights are fine but international travel, exports/imports are blocked. Next, we release hCoV-2019 in both nations at exactly the same time. Given that it is autumn in the USA, how long does it take for the US to figure out there is a novel virus? How long does it take for China to figure out there is a novel virus? Because China was able to figure that out VERY fast. Why? Because of their extensive history with SARS. Most of the Doctors and Scientists in China dealt with SARS and would be quick to notice something similar spring up. On top of this, China has a culture that is conditioned to wear masks and take preventative measures. The USA on the other hand has (more or less) no history with SARS or coronavirus outbreaks and no cultural background of protective measures such as wearing masks. I believe in our hypothetical scenario that it would take the USA no less than 3 months to actually identify the virus, sequence it, and begin to send out alerts. Within 6 months the pathogen is out of control as the country struggles to arrange preventative health measures for its citizens. In China, the government simply lock down a city, weld everyone in their homes and walk away ☹ My larger point here is that if this pathogen originated in the USA, virtually no one would have noticed it and it could have been brought directly to Wuhan during the 2019 CISM Military Games. I think this is more probable because countless people in the USA reported having the worst flu of their lives and noticed something exceptionally strange going around. Perhaps that just means the outbreak did happen in Wuhan first and the outbreak in the states simply went unnoticed for many months. Who knows. Either way, I support an accidental release theory, be it natural or manmade.

Yeah, whether originating from China or elsewhere, it’s the international gain-of-function brigade who would be responsible, as even if it came out of the WIV, the funding came from NIH/Fauci and the global health mafia that are now working hard to use the virus to enslave us under a medical police state paradigm where we no longer own our own bodies. CCP is unquestionably responsible for covering up the outbreak though, telling its WHO puppet Dr. Tedros that there was no evidence of human-to-human transmission, while killing/disappearing their scientist whistleblowers, etc.

  • Fri, Jul 24, 2020 - 07:45am

    #19
    Chris Martenson

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    Re: Dr Mayer – Thoughts on Hong Kong Virologist Warning

There is a scientific theory out there that some patients will begin to test false-positive for HIV and or present with HIV-like symptoms. This is because the virus has the “car keys” to the specific (and only) protein that the HIV virus targets. To be crystal clear, I am not stating or suggesting that anyone could develop HIV from the hCoV-2019 virus. I am talking about false-positive testing as well as “similar” symptoms due to becoming immunocompromised.

Dr. Mayer – another awesome post.  Thank you.

I don’t know if you saw it, but in yesterday’s youtube video I pulled up a few anecdotes (cases, actually) of people whose EBV was detrimentally reactivated due to exposure to SARS2.

I have zero anecdotes but I’m concerned about CMV as well.  I’m sure there are many others, possibly HIV as well.

I’m keenly interested in this:

Our plague targets ACE2 (CD143), Basigin (CD147), BiP (GRP78), Furin (PACE), ADAM17, CD4, Cathepsin L, and likely many others that we are not yet aware of.

How is this even possible?  Could standard GoF research accidentally create such a beast?  I am unfamiliar with how serial passaging or whatever techniques were employed, could result in such a diverse line of attacks.

So I guess I am wondering if this isn’t just the outcome that happens when you insert a polybasic furin cleavage site in just the right spot?

Otherwise I am stumped by how such a thing could have even come about, ‘accidentally’ via GoF or otherwise.

  • Fri, Jul 24, 2020 - 06:38pm

    #20
    Dr. Jurgen Mayer

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    tbp

I think you are not seeing the bigger picture of mortality. SARS mortality should also not be trusted. If China is not being transparent about their cases now, why then do you believe they were being transparent with SARS-CoV? So you are building on a foundation of sand and not realizing that the data you are working with cannot be trusted. What was the actual CFR of SARS-CoV? We have absolutely no clue because, if you look back in history, China initially covered up the SARS outbreak. Shocking, right?

The lack of honest reporting coming out of Spain should have you realize that Spain is not unique in this approach. Turkmenistan claims there are zero cases yet has filed a national public health emergency..that claim has the WHO concerned about what may actually be happening. So we can debate if the actual confirmed cases are higher or less but we need to firmly understand is the mortality count is not only exceptionally low but cannot be trusted when we factually know that countries like North Korea, Turkmenistan, China, and Spain have stopped reporting mortality. Do you see what I mean? Your data is all wrong, so you are reaching the wrong conclusions. Was the CFR of SARS-CoV worse than this? Absolutely not! Why? The numbers you see before you are all lies. That needs to become obvious in order to you to see the bigger picture. Even my government in Germany is lying about the situation. We have a fantastic health care system but there are many cases and deaths that are not being reported. 93% recovery of all patients?

But it’s also clear that people with low vitamin D can easily die from it, but people with D levels above 40ng/ml always have much better outcomes. The “official story” (a lie, really) is that sufficiency is above 30ng/ml or so. Yet even 40ng/ml is actually quite low vitamin D — ideal is 60-80ng/ml.

Can we combat the virus? Absolutely! Can we prepare our bodies to significantly limit the impact? Absolutely! Will billions of humans do that? No, and perhaps many billions are not in the position to do such a thing. I highly doubt the citizens in the slums of Dhaka, Bangladesh have the ability to purchase the right balance of vitamins to strengthen their immune system prior to infection. So there is no doubt here that we can combat this virus. But there are over 7 billion people out there and at least 1 billion were already starving to death and living in poverty. So, the bigger picture, this is a problem.

how are they then compared to existing database sequences — is there room for confusion with other hCoVs? Could SARS-CoV-2/2019-nCoV be confused with the somewhat virulent hCoV-OC43 or hCoV-229E during the comparison phase of PCR testing?

This is a very smart and important question. But you asking it makes me think you do not understand Open Reading Frames and their relationship here. So let us first start with that explanation and then return to your question.

The virion is coded assembly instructions, just as you would put together a dresser. The very first area of the virion is called an Open Reading Frame. Within this are a very long series of nucleotide chains. The virion reads 3 nucleic acids at a time, this grouping is called a codon. The very first part of the initial Open Reading Frame, which would be referred to as ORF1a. Within the beginning, there is a specific codon that calls for assembly START transmission. AUG is almost always the START codon that initiates the assembly for mRNA virions. Then it reads out its program like a computer code and UNPACKS various parts to ASSEMBLE its structure IN ORDER. So let’s dive into that order! ORF1a unpacks/assembles two built-in proteases for enzyme processing (garbage disposal of wasted amino acid residues). Once these are assembled we eventually reach a STOP codon which ends the reading/assembly of ORF1a. We then START reading ORF1b and this area is exceptionally important. Right after reading begins, there is a ribosomal shift in order to activate the assembly of the RNA dependent RNA polymerase (RdRp). Sort of think of this as your national ID number. The government would use that number to quickly match you in a database. RdRp is the commander of viral replication and transcription and also contains the central Helix, which controls viral replication. A bunch of other, less important things happen after this assembly and then we reach an N-terminus of ORF1b. START begins for assembly of the Spike protein, then STOP. START of the Envelope protein, etc. Then reaches the STOP N-terminus of the entire package. I marked up a diagram that should be super helpful for everyone.

As the program is read out (codons), these NA are converted to amino acids and the amino acids are GLUED together by something called a peptide residue, which forms a peptide bond, but that hole leads us way into biochemistry!

SO, with that lesson in molecular biochemistry out of the way let’s proceed to your question

how are they then compared to existing database sequences — is there room for confusion with other hCoVs? Could SARS-CoV-2/2019-nCoV be confused with the somewhat virulent hCoV-OC43 or hCoV-229E during the comparison phase of PCR testing?

 

We mainly run PCR tests for RdRp analysis from position 15,361-15,460 within ORF1b in the nucleotide chain. We can then easily convert NA to AA and have an RdRp read-out. We use FASTA format to upload our RdRp chain and have that search databases for similar results. For example, this is how I confirmed the identity of 4991 was actually RaTG13. I reviewed the 4991 RdRp then ran an alignment against the RdRp of RaTG13 and found a 100% match. Ok, but why do we search for RdRp? Why not search for part of the Spike protein? The RdRp is far more important than the Spike protein. Without viral replication and assembly, the Spike protein never gets assembled in the virion in the first place. This means that RdRp will exist for virtually every RNA virus in the world, whereas a Spike protein will not. We also use PCR testing for a specific region of the (E) Envelope protein when we believe we are dealing with an enveloped mRNA virus. If I take a random RdRp sequence from Bat guano and run that through the databases I can quickly see what family of viruses we might be dealing with. But there is the problem with RdRp reading, you are only getting part of the story. Most of the betacoronavirus ORF1ab are quite similar and the RdRp are even more similar. Why? Because this is shared assembly from a common ancient ancestor. The way in which a virus will “call” to replicate is nearly identical. The way in which the virus replicates can be exceptionally different. Very fine distinction there. I can tell 100 students to write an essay. My instructions to all 100 different students are identical but their essays will all be different. I need you to think of a pregnancy test that provides a 78% result. A woman takes the test 10 times and it is positive 7/10 times. You and I think she is probably pregnant but we have doubts due to the accuracy of the test. Do you know how we can verify that she is pregnant? We take her to the Doctor to verify pregnancy. That is the difference between taking a crappy PCR test for a possible RdRp match and having us Scientists sequence the entire genome of a virus sample from your cells. That PCR test can only see if you might be positive for a coronavirus. It could be this coronavirus. It could see OC43 as a close enough match and say you are positive. But having your genome sample in a lab, we can tell the exact strain family (clade) you have and denote every single mutation in every protein of that virus. While there are 15 million “confirmed cases”, there are only around 100,000 sequenced genomes from patients. That means that we, as Doctors, have confirmed only 0.6% of the global “confirmed cases”.

That is part of what I am doing every day. I am reviewing new patient data and reviewing the provided genome to determine exact mutations. This helps us track various mutations in the virus and we can use that data to help determine when the patient was likely infected.

Read this when you have time – https://www.who.int/docs/default-source/coronaviruse/protocol-v2-1.pdf?sfvrsn=a9ef618c_2

 

OK so some of the damage may be inflicted via the other targets (CD147, BiP/GRP78, ADAM17, CD4), but we just don’t have enough data to understand exactly how. But the mortality rate is still lower than it was for SARS1 and MERS, yet the same PCR tests were also used to detect those, right?

SARS-CoV had a much smaller sample size and was predominately clustered in China, which suppressed data. So you are comparing one coverup to another. In both cases, the numbers you are seeing are not correct. Nonetheless, we absolutely do not have enough data to determine the impact of these other infection routes. That being said, I would mostly be in the dark even if breakthroughs happened tomorrow. I rely on Dr. Martenson and others to provide their expertise on these subjects. I study the virus itself, so I am buried in amino acids and biochemistry. So you should defer to others for answers about the infection routes and what impact that has on the body.

Wait, so TMPRSS2 cleaves ACE2 also, in addition to the Spike protein (into S1 and S2 subunits)?

You are confusing ACE2 and the virus. hACE2 has a cleavage site that can (it is not required) be activated, whereas the Spike protein of the novel virus has a cleavage site that requires cleavage. Two different things. TMPRSS2 is typically the preferred protease for hACE2 cleavage, however, sometimes it chooses to use ADAM17. Whereas the novel coronavirus prefers Furin. So there is no overlap here. Two different conversations. Scientists are suggesting that the virus has somehow hijacked ADAM17 and makes it select for cleavage priority over TMPRSS2, forcing cleavage of hACE2, this, in turn, weakens the structure of hACE2 and as the virus docks to hACE2, that then facilitates the breakdown of the cell.

Right, but furin cleavage is also used by other viruses such as HIV, influenza, dengue fever, and several filoviruses including ebola and marburg virus, so there’s nothing new in that, right?

You are very correct, however, you failed to mention any other coronaviruses. This has never been seen in coronaviruses before. Do you know what most of the viruses you mentioned have in common? Their cleavage sites contain an RxRR motif, which makes the virus 1,000x+ more virulent within the host. Whereas the also rare, RxxR motif would make the virus, let’s say 200x+ more virulent. Let’s review the list of these cleavage site motifs from every known virus and see what we find:

HIV (REKR), Influenza H5 (RKKR), Avian H5N1 (RKKR), hCMV (RTKR), MERS-CoV (RSCR)

hRSV (RKRR), Yellow Fever (RSRR), Zika (RSRR), Ebola (RTRR), hCoV-2019 (RRAR), hCoV-HKU1 (RKRR), hCoV-OC43 (RRSR)

So we have 4 (beta)coronaviruses in this list, let’s explore them.

MERS-CoV uses TMPRSS2 for cleavage at its S1/S2 site. “Cleavage of the S protein in the Golgi apparatus of infected cells has been proposed to be essential for subsequent MERS-S activation by TMPRSS2 or furin during entry into target cells because it may endow the S protein with sufficient structural flexibility to engage these proteases for processing16” – Source

hCoV-OC38 has a very cool mutated cleavage site and uses a variety of proteases for cleavage and does not appear to have a preference. Furin is used for cleavage but that is not the same as saying Furin is selected for cleavage, which is the case for hCoV-2019 – Source

hCoV-HKU1 does prefer Furin and this has been seen that when Furin is inhibited, the cleave does not happen and the virion (during assembly and before folding) will fail in assembly and BREAK before folding into a protein. Inhibition of Furin in this sense has not been thoroughly tested by Pathologists or Immunologists but given that HKU1 prefers Furin, this should be an area of significant study.

 

Hopefully, I have been able to paint a picture where the preference of Furin for cleavage is novel on a coronavirus not associated with the common cold and more specifically that the cleavage site contains a very important RxRR motif that is seen in viruses that express rapid replication within hosts.

 

In addition to furin, it also requires TMPRSS2 cleavage, and then Cathepsin L (an endosomal cysteine protease) has to mediate the cleavage of the S1 subunit of the Spike protein to induce virion-cell membrane fusion… which, when you combine all 3 protease modification requirements, does seem strange/unusual/suspicious

Just a misunderstanding here as TMPRSS2 and Cathepsin are involved in hACE2 and have nothing to do with proteases related to hCoV-2019.

 

how probable in your estimation would it be for that to occur naturally/zoonotically?

I can make strong arguments for both and provide the detailed science for both outcomes. Given the existence of a few specific beta coronaviruses, it seems highly probable that this was zoonotic. Bat RmYN02/2019 also helps explain the existence of our polybasic furin cleavage site. In my professional opinion, I would say it is 85% probable to have been of zoonotic origin. I can explain virtually every aspect of the genome but cannot explain its ability to instantly use so many host receptors. That is why this is so novel. Nonetheless, the fact that we have not positively identified either the primary or secondary hosts after 9+ months is exceptionally troubling.

 

Thanks for reading

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