DR. FAUCI BACKED CONTROVERSIAL WUHAN LAB WITH MILLIONS OF U.S. DOLLARS FOR RISKY CORONAVIRUS RESEARC

I did make a thread about it. But I'm mentioning it in this thread as well. There is clear hypocrisy at work here. Those throwing around the "conspiracy theorist" label are themselves the biggest "conspiracy theorists" around.

 

I'm not giving up, please hurt me, but do it nicely or I will sue.

 

List those conspiracy theories please

 

Is that a rhombus I see in your pocket? Get down on the ground now!

 

Yes Mamm, I will do so.

 

Stop resisting arrest!

 

I'm not resisting, you're not complying.

 

I already named the biggest one of all time: Russian collusion.

A totally outlandish conspiracy theory for which no evidence ever existed.

Arrogant "liberals" and neocons went around proclaiming the truth of this asinine theory for years.

When it comes to peddling dubious narratives, "liberals" are the biggest "conspiracy theorists" around. Nobody even comes close.

 

Never watched CNN in my life.
So you couldn't refer to me.

Now I know you just make stuff up.

 

The vast majority of COVID in the USA came from Europe.

Epidemiologists have traced he strains of this virus. On west coast states, they found strains that came directly from China. No state east of the Rocky Mountains has detectable numbers of cases that came from the west. They came from Europe.

Forty percent of the cases in WA came from the east coast states that received their strains from Europe - not China direct. States east of the Rockies got their dose from Europe, NOT China direct.

At the shutdown with Europe, there was essentially zero planning. So, the thousands coming from Europe over the next days each stood in tightly packed security crowds for hours in various US airports - the perfect environment for viruses. Security was supposedly responsible for screening, but they were totally overwhelmed.

https://theintercept.com/2020/04/12...s-of-coronavirus-from-europe-than-from-china/

And, actions at our borders is only one of the several highly important failures that has gotten us to where we are.

Pointing to the shutdown of travel from China is a red herring.

 

I would be interested in you sharing the particulars of why you have this opinion. The nuts and bolts. Some of us are into that part of the pandemic.

 

If you have specific questions, I would be happy to answer them.

 

Everything I’ve studied on the subject specific to C19 claims certainty that it has no engineered components. I have not been able to find actual research not behind pay walls so if you have links I’d appreciate that.

To be clear, I’m not making a case for engineered C19, I’m just probing the weaknesses of the argument it isn’t.

Specifically, the claim it isn’t engineered is predicated on comparison to known profiles of corona viruses. This is an assumption not taking into account the possibility of information in actual existence we aren’t privy to.

Also, the theory an engineered virus would necessarily be based on an existing known pathogenic model is an assumption. A logical assumption only if we are arrogant enough to believe we have all the information and abilities a potential engineer would.

Next, the cleavage site of C19 is said to resemble that of avian the flu virus. This is attributed to convergence by default it seems but I can’t find any information on whether the similarity is only phenotypic or very similar in genotype as well. If I was making a judgement on origins I would want that information.

Again, I’m not advocating for belief this thing is engineered. I’ve just been around the block enough times with viruses and other conditions/diseases in animals to know making assumptions and never re-questioning them almost always causes you to miss something important you would have caught keeping a more open mind.

 

Sure thing. I'll get you some quotes and links normally behind pay-walls and a description from my research why it's not engineered. I'll do this this evening EST.

I will tell you the evidence is extensive based upon natural selection and evolution in general.

 

Thanks. I am fascinated by this bugger. If there is an intermediate host and it could be identified our knowledge would increase as well. It’s frustrating having to basically depend on China for or access to all that part of the equation.

 

Do you mean the Dr. Fauci with ties to the Clinton Foundation? That Dr. Fauci?

 

Trump is also affiliated with the Clinton Foundation, a former repeated Democrat, and still involved in non GOP political interests.

 

If you "have no opinion one way or the other" one wonders why you posted information designed to vilify Fauci? You certainty don't sound amused. You sound determined to undermine the science.

 

Part 1

Here are some preliminary quotes, links and scientific findings I want to share with you now:

Not behind a paywall: https://www.nature.com/articles/s41591-020-0820-9

Above is an excellent, but long read, and it is only a primer, so please feel free to ask any specific questions on that research as it pertains to the discussion at hand.

Here is a highlight quote below, but before I paste it, notice it states "it is improbable SARS-COV-2 emerged through laboratory manipulation of a related SARS-COV- like coronavirus." The context here is from a study published back in March and at the time this study was an early insight, so the researchers were not going to guarantee that the virus not being man-made, but their use of improbable means highly unlikely based upon specific genetic and amino acid analysis. Epitopes (amino acid residues) are even more telling than nucleotide changes (base pair mutations within nuclear material: RNA often in viruses, but DNA as well).

Quote:

"It is improbable that SARS-CoV-2 emerged through laboratory manipulation of a related SARS-CoV-like coronavirus. As noted above, the RBD of SARS-CoV-2 is optimized for binding to human ACE2 with an efficient solution different from those previously predicted7,11. Furthermore, if genetic manipulation had been performed, one of the several reverse-genetic systems available for betacoronaviruses would probably have been used19. However, the genetic data irrefutably show that SARS-CoV-2 is not derived from any previously used virus backbone20. Instead, we propose two scenarios that can plausibly explain the origin of SARS-CoV-2: (i) natural selection in an animal host before zoonotic transfer; and (ii) natural selection in humans following zoonotic transfer. We also discuss whether selection during passage could have given rise to SARS-CoV-2.

1. Natural selection in an animal host before zoonotic transfer
As many early cases of COVID-19 were linked to the Huanan market in Wuhan1,2, it is possible that an animal source was present at this location. Given the similarity of SARS-CoV-2 to bat SARS-CoV-like coronaviruses2, it is likely that bats serve as reservoir hosts for its progenitor. Although RaTG13, sampled from a Rhinolophus affinis bat1, is ~96% identical overall to SARS-CoV-2, its spike diverges in the RBD, which suggests that it may not bind efficiently to human ACE27 (Fig. 1a).

Malayan pangolins (Manis javanica) illegally imported into Guangdong province contain coronaviruses similar to SARS-CoV-221. Although the RaTG13 bat virus remains the closest to SARS-CoV-2 across the genome1, some pangolin coronaviruses exhibit strong similarity to SARS-CoV-2 in the RBD, including all six key RBD residues21 (Fig. 1). This clearly shows that the SARS-CoV-2 spike protein optimized for binding to human-like ACE2 is the result of natural selection.

Neither the bat betacoronaviruses nor the pangolin betacoronaviruses sampled thus far have polybasic cleavage sites. Although no animal coronavirus has been identified that is sufficiently similar to have served as the direct progenitor of SARS-CoV-2, the diversity of coronaviruses in bats and other species is massively undersampled. Mutations, insertions and deletions can occur near the S1–S2 junction of coronaviruses22, which shows that the polybasic cleavage site can arise by a natural evolutionary process. For a precursor virus to acquire both the polybasic cleavage site and mutations in the spike protein suitable for binding to human ACE2, an animal host would probably have to have a high population density (to allow natural selection to proceed efficiently) and an ACE2-encoding gene that is similar to the human ortholog."

Here is more contextual commentary and responses from the researchers as well:

https://www.sciencedaily.com/releases/2020/03/200317175442.htm

 

Part 2:

Recent research found in my University Library database:

(English) By: Malik YA, The Malaysian journal of pathology [Malays J Pathol], ISSN: 0126-8635, 2020 Apr; Vol. 42 (1), pp. 3-11; Publisher: Academy of Medicine of Malyasia, College of Pathologists; PMID: 32342926;
were identified beginning with the discovery of SARS-CoV in 2002. With the recent detection of SARS-CoV-2, there are now seven human coronaviruses. Those that cause mild diseases are the 229E, OC43, NL63 and HKU1, and the pathogenic species are SARS-CoV, MERS-CoV and SARS-CoV-2 Coronaviruses (order Nidovirales, family Coronaviridae, and subfamily Orthocoronavirinae) are spherical (125nm diameter), and enveloped with club-shaped spikes on the surface giving the appearance of a solar corona. Within the helically symmetrical nucleocapsid is the large positive sense, single stranded RNA. Of the four coronavirus genera (α,β,γ,δ), human coronaviruses (HCoVs) are classified under α-CoV (HCoV-229E and NL63) and β-CoV (MERS-CoV, SARS-CoV, HCoVOC43 and HCoV-HKU1). SARS-CoV-2 is a β-CoV and shows fairly close relatedness with two bat-derived CoV-like coronaviruses, bat-SL-CoVZC45 and bat-SL-CoVZXC21. Even so, its genome is similar to that of the typical CoVs. SARS-CoV and MERS-CoV originated in bats, and it appears to be so for SARS-CoV-2 as well. The possibility of an intermediate host facilitating the emergence of the virus in humans has already been shown with civet cats acting as intermediate hosts for SARS-CoVs, and dromedary camels for MERS-CoV. Human-to-human transmission is primarily achieved through close contact of respiratory droplets, direct contact with the infected individuals, or by contact with contaminated objects and surfaces. The coronaviral genome contains four major structural proteins: the spike (S), membrane (M), envelope (E) and the nucleocapsid (N) protein, all of which are encoded within the 3' end of the genome. The S protein mediates attachment of the virus to the host cell surface receptors resulting in fusion and subsequent viral entry. The M protein is the most abundant protein and defines the shape of the viral envelope. The E protein is the smallest of the major structural proteins and participates in viral assembly and budding. The N protein is the only one that binds to the RNA genome and is also involved in viral assembly and budding. Replication of coronaviruses begin with attachment and entry. Attachment of the virus to the host cell is initiated by interactions between the S protein and its specific receptor. Following receptor binding, the virus enters host cell cytosol via cleavage of S protein by a protease enzyme, followed by fusion of the viral and cellular membranes. The next step is the translation of the replicase gene from the virion genomic RNA and then translation and assembly of the viral replicase complexes. Following replication and subgenomic RNA synthesis, encapsidation occurs resulting in the formation of the mature virus. Following assembly, virions are transported to the cell surface in vesicles and released by exocytosis., Database: MEDLINE Complete PubMed

Subjects: Betacoronavirus genetics; Betacoronavirus pathogenicity; Coronavirus classification; Coronavirus physiology; Genome, Viral

 

Part 3:

CoV-2 Yasmin A. MALIK Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia Abstract Zoonotic coronaviruses were discovered in the 1960s. Since then pathogenic human coronaviruses were identified beginning with the discovery of SARS-CoV in 2002. With the recent detection of SARS-CoV-2, there are now seven human coronaviruses. Those that cause mild diseases are the 229E, OC43, NL63 and HKU1, and the pathogenic species are SARS-CoV, MERS-CoV and SARS-CoV-2 Coronaviruses (order Nidovirales, family Coronaviridae, and subfamily Orthocoronavirinae) are spherical (125nm diameter), and enveloped with club-shaped spikes on the surface giving the appearance of a solar corona. Within the helically symmetrical nucleocapsid is the large positive sense, single stranded RNA. Of the four coronavirus genera (a,b,g,d), human coronaviruses (HCoVs) are classified under a-CoV (HCoV-229E and NL63) and b-CoV (MERS-CoV, SARS-CoV, HCoVOC43 and HCoV-HKU1). SARS-CoV-2 is a b-CoV and shows fairly close relatedness with two bat-derived CoV-like coronaviruses, bat-SL-CoVZC45 and bat-SL-CoVZXC21. Even so, its genome is similar to that of the typical CoVs. SARS-CoV and MERS-CoV originated in bats, and it appears to be so for SARS-CoV-2 as well. The possibility of an intermediate host facilitating the emergence of the virus in humans has already been shown with civet cats acting as intermediate hosts for SARS-CoVs, and dromedary camels for MERS-CoV. Human-to-human transmission is primarily achieved through close contact of respiratory droplets, direct contact with the infected individuals, or by contact with contaminated objects and surfaces. The coronaviral genome contains four major structural proteins: the spike (S), membrane (M), envelope (E) and the nucleocapsid (N) protein, all of which are encoded within the 3’ end of the genome. The S protein mediates attachment of the virus to the host cell surface receptors resulting in fusion and subsequent viral entry. The M protein is the most abundant protein and defines the shape of the viral envelope. The E protein is the smallest of the major structural proteins and participates in viral assembly and budding. The N protein is the only one that binds to the RNA genome and is also involved in viral assembly and budding. Replication of coronaviruses begin with attachment and entry. Attachment of the virus to the host cell is initiated by interactions between the S protein and its specific receptor. Following receptor binding, the virus enters host cell cytosol via cleavage of S protein by a protease enzyme, followed by fusion of the viral and cellular membranes. The next step is the translation of the replicase gene from the virion genomic RNA and then translation and assembly of the viral replicase complexes. Following replication and subgenomic RNA synthesis, encapsidation occurs resulting in the formation of the mature virus. Following assembly, virions are transported to the cell surface in vesicles and released by exocytosis. Keywords: Coronavirus, SARS-CoV-2, classification, genetic characteristics, replication Address for correspondence: Yasmin A. Malik. Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. Email: yasmin0220@gmail.com REVIEW ARTICLE INTRODUCTION Before the SARS-CoV outbreak in 2002, two human coronaviruses, namely HCoV-229E and HCoV-OC43, were often seen as just one of the causes of the common cold. With the subsequent emergence of MERS-CoV in 2012 and the current COVID-19, understanding of the properties of coronavirus is needed to help determine the characteristics of SARS-Cov-2."

 

Part 4:
RESEARCH ARTICLE Detection of novel coronaviruses in bats in Myanmar Marc T. ValituttoID1 *, Ohnmar Aung1 , Kyaw Yan Naing Tun1 , Megan E. Vodzak1¤ , Dawn Zimmerman1 , Jennifer H. YuID1 , Ye Tun Win2 , Min Thein Maw2 , Wai Zin Thein2 , Htay Htay Win2 , Jasjeet Dhanota3 , Victoria Ontiveros3 , Brett Smith3 , Alexandre TremeauBrevard3 , Tracey Goldstein3 , Christine K. Johnson3 , Suzan Murray1 , Jonna Mazet3 1 Global Health Program, Smithsonian’s National Zoological Park and Conservation Biology Institute, Washington, District of Columbia, United States of America, 2 Livestock Breeding and Veterinary Department, Ministry of Agriculture, Livestock and Irrigation, Naypyitaw, Myanmar, 3 One Health Institute, School of Veterinary Medicine, University of California, Davis, California, United States of America ¤ Current address: Vanderbilt Vaccine Center, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America * ValituttoM@si.edu


"Abstract The recent emergence of bat-borne zoonotic viruses warrants vigilant surveillance in their natural hosts. Of particular concern is the family of coronaviruses, which includes the causative agents of severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), and most recently, Coronavirus Disease 2019 (COVID-19), an epidemic of acute respiratory illness originating from Wuhan, China in December 2019. Viral detection, discovery, and surveillance activities were undertaken in Myanmar to identify viruses in animals at high risk contact interfaces with people. Free-ranging bats were captured, and rectal and oral swabs and guano samples collected for coronaviral screening using broadly reactive consensus conventional polymerase chain reaction. Sequences from positives were compared to known coronaviruses. Three novel alphacoronaviruses, three novel betacoronaviruses, and one known alphacoronavirus previously identified in other southeast Asian countries were detected for the first time in bats in Myanmar. Ongoing land use change remains a prominent driver of zoonotic disease emergence in Myanmar, bringing humans into ever closer contact with wildlife, and justifying continued surveillance and vigilance at broad scales."

 

Discussion and research perspective:

In the earliest studies as to the structure and origins of the cause of COVID-19, SARS-CoV-2, and related subtypes, there was little known about the structure and function of the virion that separated it from other corona viruses that preceded it. The analysis then, was to not just look at what it shared in common with other viruses, but by what distinguished it as well, for better understanding of its origins, functions in a host, potential treatment options, and threat levels.

While early research produced no evidence that the virus was man-made, and there was evidence to the contrary, this did not preclude it being let loose from a lab, (though there was no structural evidence to support this assertion) and it was also shown highly improbable that the virus was man-made, the researchers worded their conclusions very conservatively and carefully to not allow assumptions to dominate their early findings. However, more structural and pathogenic studies have been performed and in line with how viruses evolve, so while this virus is novel in certain characteristics it has no markers of being a hybrid of viruses from a lab reservoir and it does not demonstrate characteristics of a man-made virus as the articles above explain.

 

As an aside:

https://www.researchgate.net/community/COVID-19

However, I am not placing scientific credibility or my faith in a "universal vaccine" either. This is an important distinction, and one that needs to be discussed.

Vaccines that can help? yes... medications on and off label, that clinical trials show true effectiveness? yes...

True antigenic or epitope matching? Nope.

Here, Fauci and Gates et., al are incorrect. This might mean that over time when masks become less prevalent and social distancing too, becomes less necessary we will have some spikes and dangers. This is where it gets tricky--how to balance the risks, since we see natural herd immunity will not get it done completely or quickly, but it is not possible to have a universal vaccine; perhaps a decent vaccine for the most dangerous epitopes but this takes even longer than 18 months; we do need to be more cautious with coughs, sneezes, washing hands, and social distancing, but we also need to balance what is realistic.

I am sure it might be surprising to some that I deviate from Fauci on this, but I understand why he thinks the vaccine route is best, and perhaps across the globe it is but, his statement: "universal vaccine" is impossible.

 

This all matches up with what I’ve reviewed previously. I have to reiterate though that these are all assumptions. For example, just because we can demonstrate RBD development allowing binding in humans through natural selection in pangolins has occurred doesn’t preclude using that trait in recombination to develop a new virus. Not to me anyway. I can’t accept the ability to demonstrate a thing can happen a certain way proves that it did. Like I said, that viewpoint has come back to bite me me before. I’m not saying this theory on Cov-2 evolution is incorrect, Im just not ready to stop considering other options on the simple evidence it “could” have happened this way.

I do appreciate the information you provided. Some was from sources I haven’t run across. I’ve enjoyed reading it and we don’t disagree on substance anywhere I can see.

Do you think pangolins were an intermediate host? That theory is floated but nobody wants to commit either way. Also, do you know if isolates taken from other infected species such as the infamous tiger had point mutations or maybe even recombinant additions allowing such cross species infections? Early on the idea of additional intermediate hosts was pretty much dismissed so I quit paying much attention to that side of the equation.