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To: CatHerd
said, "P. Yoelli is the bridge for malaria between mice and humans"
via mosquito
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0167178

said, "While P. vivax can go cerebral, it is fairly rare (where you live)"
https://pubmed.ncbi.nlm.nih.gov/31533821/

You said in the next line you said, "Malaria parasites (genes) are also nowhere"

I'm going to stop here. First we have to work out the vectors of malaria and the genes that are in covid. Before we move on to these next issues.
You seem to be stuck on the first points. Without understanding the premise you can't continue.

This report some of it was copied and pasted from Fauci's Emails. It seems to be where covid originally came from with a couple changes I've noticed. (coivd now has Plasmodium Yoelii and STAT1 from another paper(I've not shown.) VSV-G was likely incorporated into HIV virions and not picked up by Perez paper (my speculation.) This paper gives the steps on how to produce what is mostly now covid.
Compare this report to the findings of Jean-Claude Perez paper i gave earlier.
https://www.pnas.org/content/102/33/11876
60 posted on 08/10/2021 1:13:44 PM PDT by Steve Van Doorn (*in my best Eric Cartman voice* 'I love you, guys')
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To: Steve Van Doorn

Steve: “said, “P. Yoelli is the bridge for malaria between mice and humans”
via mosquito
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0167178

Me: Where, oh where, is there any proof P.Yoelli is a “bridge for malaria between mice and humans” in this paper about animal models for studying malaria transmission by South American mosquitoes? It is not there.

Can you cite one case of a human syffering from P. Yoelli? No, you can’t, any more than you can back up your claim that P. Yoelli causes Vivax malaria, which is totally absurd, as by definition, P. vivax causes it.

Steve: “said, “While P. vivax can go cerebral, it is fairly rare (where you live)”
https://pubmed.ncbi.nlm.nih.gov/31533821/

Me: You added the “where you live” part. Actually, it’s nonexistent where I live now (USA). The link you provided says vivax is recognized as “a major cause of severe and cerebral malaria” in areas where vivax predominates. Note *severe* and cerebral (severe does not always mean cerebral). This is only to be expected. For example, if 80% percent of cases are vivax, and 5% are severe, then it would be “a major cause” even if 15% are falciparum and 20% of those are severe.

The fact remains that falciparum is much more likely to go cerebral than vivax. Look it up. You will find it stated over and over and over.

I still don’t get why you think P. Yoelli causes vivax. Can you please explain?
Steve: “You said in the next line you said, “Malaria parasites (genes) are also nowhere”

Me: You added the genes part. I would not be be surprised if the virus shared one or more genes with plasmodium species (or lettuce or house cats or even possums). All living things share many genes (and viruses, too, even though they are not considered living things really). But to cause cerebral malaria, as you claim, you need the actual parasites.

Steve: “I’m going to stop here. First we have to work out the vectors of malaria and the genes that are in covid. Before we move on to these next issues.
You seem to be stuck on the first points. Without understanding the premise you can’t continue.”

Me: We know the vector for malaria. It’s mozzies. Covid is not a vector-borne disease. It is spread from human to human via respiratory droplets.

Now for your Perez “report”. Have a look at this:

- - -
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7033698/#!po=22.7273

“Sequences that completely match the insertion 3 and 4 sequences were not found in any HIV-1 sequences. This clearly shows that these insertion sequences are widely present in living organisms including viruses, but not HIV-1 specific. All these regions in HIV-1 envelope glycoprotein are highly variable with many large insertions and deletions, indicating that they are not essential for biological functions of HIV-1 envelope glycoprotein.

(snip)

Second, these insertions are present not only in 2019-nCoV viruses but also in three betaCoV sequences from bats: two (ZC45 and ZXC21) from Zhejiang deposited in GenBank in 2018 and RaTG13 from Yunnan obtained in 2013 [8]. The RaTG13 is much more similar to 2019-nCoV than both ZC45 and ZXC21 (Figure 1A). The similarity of the spike protein between RaTG13 and 2019-nCoV is 97.7%.”
- - -

Personally, I suspect SARS-COV-2 came from the Wuhan lab. It may or may not have been a product of the gain-of-function research being carried out there. I would not be surprised if it is. That said, you do need to understand that just because SARS-COV-2 might have some genes in common with other viruses (like HIV) or even protazoa (like malaria parasites) — and even insects and mammals — that does not mean it can cause AIDS or malaria in humans (or cause them to grow tails or whatever). See here:

https://science.howstuffworks.com/life/genetic/people-bananas-share-dna.htm

Just because humans have a whole bunch of genes in common with banana trees does not mean we can sprout banana stalks out of our heads.

Finally, if the SARS-COV-2 virus really does happen to have a gene in common with P. Yoelli, that hardly means it can magically produce P. vivax parasites!

You apparently have the bizarre notion that SARS-COV-2 can cause cerebral malaria, and therefore Decadron should not be used to treat Covid patients. Do you actually believe SARS-COV-2 can somehow release malaria parasites into the blood of Covid patients? Seriously? And if this miraculous thing can actually happen, why has no one noticed them in the blood drawn from Covid patients?

You have accused doctors of killing patients (including one of our fellow Freepers) by giving them Decadron because it is contraindicated in malaria. I’m sorry, but this is nuts.


63 posted on 08/10/2021 6:33:15 PM PDT by CatHerd (Not a newbie - lost my password)
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