Settling the Biological Virus Debate

[Poor Richard Saunders]

I suspect the issue is that Dr. Mark Bailey didn't start with the beginning of the paragraph of the analysis he was quoting. I downloaded a copy of the actual analysis and will quote the complete paragraph below, bolding the first sentence:

**
At this point, the contig with the identification k141_27232, with which 1,407,705 sequences are associated, and thus about 5% of the remaining 26,108,482 sequences, should be discussed in detail. Alignment with the nucleotide database on 05/12/2021 showed a high match (98.85%) with "Homo sapiens RNA, 45S pre- ribosomal N4 (RNA45SN4), ribosomal RNA" (GenBank: NR_146117.1, dated 04/07/2020). This observation contradicts the claim in [1] that ribosomal RNA depletion was performed and human sequence reads were filtered using the human reference genome (human release 32, GRCh38.p13). Of particular note here is the fact that the sequence NR_146117.1 was not published until after the publication of the SRR10971381 sequence library considered here.
**

Source:
https://brandfolder.com/s/3z266k74ppmnwkvfrxs6jjc

It seems that the mathematician is saying that this 98.85% match was for a specific contig with the id of K141_27232.

Let's examine this in detail and see how disingenuous Dr Bailey is.
Why would Bailey leave off the sentence that shows that only 5% of theremaining sequences showed a 98.55 match? That would mean that of those remaining sequences less than 5% showed a match to homo sapiens RNA.
But even that is still misleading. When we look at the paper put on the internet by a mathematician the refused to give his name we find something else.
After filtering the
paired-end reads, 26,108,482 of the original total of 56,565,928 reads remained, with
a length of about 150 bp.
The mathematician used less than 50% of the original reads because he restricted himself to only using reads of 150bp. That seems a bit odd. Why would you claim you can't replicate something when use less than 50% of the data.
.4615 x .05 x .985 = 2.27

So the reality is that about 2.27% of the reads MAY have a match with homo sapien RNA. (It's actually quite a bit less as I will show.) The mathematician seems to fail to include the error in his claim that he insists exists in all reads.

So let's recap.
Dr Bailey cherry picks some sentences out of a paper by an anonymous author and we are expected to believe him.

1
Title
Structural analysis of sequence data in virology
An elementary approach using SARS-CoV-2 as an example
Author
By a mathematician from Hamburg, who would like to remain unknown

The anonymous mathematician then filters the data to eliminate over half of it.

To prepare the paired-end reads for the actual assembly step with Megahit
(v.1.2.9) [20], we used the FASTQ preprocessor fastp (v.0.23.1) [21]. After filtering the
paired-end reads, 26,108,482 of the original total of 56,565,928 reads remained, with
a length of about 150 bp.

By filtering the data the mathematician comes up with significantly fewer contigs.
From the paper that did the original sequencing.
Megahit generated a total of 384,096 assembled contigs (size range of 200–30,474 nt), whereas Trinity generated 1,329,960 contigs with a size range of 201–11,760 nt.
https://www.nature.com/articles/s41586-020-2008-3#Sec1
From our anonymous mathematician:

We obtained 28,459 (200 nt - 29,802 nt) contigs, significantly less than described in
[1].

When you restrict your data, you would certainly be able to assemble fewer contigs. Something our anonymous mathematician seems unconcerned about.
But lets go back and look at that statement again that Dr Bailey decided to not include.

At this point, the contig with the identification k141_27232

Is that right? Is that really only ONE of the 28,459 possible contigs from our mathematician that has a 98.5% match?
That would mean that the error was not even 1%. It was 0.000035% of the possible combinations came up with a possible match to human RNA.
What is interesting is whether the other 28,458 came up with a 98% or higher match to the Wuhan sequence. We will never know because the anonymous mathematician doesn't tell us.
But he does tell us this.

We set all bases with a
quality lower than 20 to "N" (unknown). A quality of 20 means an error rate of 1% per
nucleotide, which can be considered sufficient in the context of our analyses.

So he allowed a 1% per nucleotide error and then tries to claim a single contig with more than 6,000 nucleotides should be accepted as proof of something? Not very good math on his part.

In conclusion, we have Baily cherry picking a statement from a mathematician that didn't use all the data. That is not evidence of anything other than fraud on the part of Baily.

 

[Truck Fump / h1b]

Let's examine this in detail and see how disingenuous Dr Bailey is.
Why would Bailey leave off the sentence that shows that only 5% of theremaining sequences showed a 98.55 match? That would mean that of those remaining sequences less than 5% showed a match to homo sapiens RNA.
But even that is still misleading. When we look at the paper put on the internet by a mathematician the refused to give his name we find something else.
After filtering the
paired-end reads, 26,108,482 of the original total of 56,565,928 reads remained, with
a length of about 150 bp.
The mathematician used less than 50% of the original reads because he restricted himself to only using reads of 150bp. That seems a bit odd. Why would you claim you can't replicate something when use less than 50% of the data.
.4615 x .05 x .985 = 2.27

So the reality is that about 2.27% of the reads MAY have a match with homo sapien RNA. (It's actually quite a bit less as I will show.) The mathematician seems to fail to include the error in his claim that he insists exists in all reads.

So let's recap.
Dr Bailey cherry picks some sentences out of a paper by an anonymous author and we are expected to believe him.


The anonymous mathematician then filters the data to eliminate over half of it.

By filtering the data the mathematician comes up with significantly fewer contigs.
From the paper that did the original sequencing.
Megahit generated a total of 384,096 assembled contigs (size range of 200–30,474 nt), whereas Trinity generated 1,329,960 contigs with a size range of 201–11,760 nt.
https://www.nature.com/articles/s41586-020-2008-3#Sec1
From our anonymous mathematician:

When you restrict your data, you would certainly be able to assemble fewer contigs. Something our anonymous mathematician seems unconcerned about.
But lets go back and look at that statement again that Dr Bailey decided to not include.

Is that right? Is that really only ONE of the 28,459 possible contigs from our mathematician that has a 98.5% match?
That would mean that the error was not even 1%. It was 0.000035% of the possible combinations came up with a possible match to human RNA.
What is interesting is whether the other 28,458 came up with a 98% or higher match to the Wuhan sequence. We will never know because the anonymous mathematician doesn't tell us.
But he does tell us this.

So he allowed a 1% per nucleotide error and then tries to claim a single contig with more than 6,000 nucleotides should be accepted as proof of something? Not very good math on his part.

In conclusion, we have Baily cherry picking a statement from a mathematician that didn't use all the data. That is not evidence of anything other than fraud on the part of Baily.

EMF harm is the main point here.

would you agree?

 

[Poor Richard Saunders]

First of all, polio's decline started well before Salk's polio vaccine was introduced:

**
Diagram 2
Polio death rates began to decline long before major
inoculation campaigns were started

View attachment 24624

From 1923 to 1953, long before large-scale polio vaccinations began to be carried out in the mid-1950s, mortalities attributed to polio had already decreased substantially: in the USA by 47 percent; in Great Britain by 55 percent; in other European countries, the statistics are comparable.
**

Source:
Engelbrecht, Torsten; Köhnlein, Claus; Bailey, Samantha; Scoglio, Stefano. Virus Mania (p. 73). Books on Demand. Kindle Edition.

Secondly, while I agree that DDT did not decrease during your time frame, exposure to it after 1954 did, and fairly dramatically too. There's also the fact that pesticide production in general dropped off dramatically after 1954 as well. Again from Virus Mania:

**
Diagram 3 Polio cases and DDT production in the USA, 1940-1970
View attachment 24625

A look at statistics shows that the polio epidemic in the United States of America reached its peak in 1952, and from then on rapidly declined. We have seen that this cannot be explained by the Salk-inoculation, since this was first introduced in 1955. There is a most striking parallel between polio development and the utilization of cide historian Pete Daniel goes a step further in saying that “[the officials in charge] knew better, but the bureaucratic imperative to protect pesticides led the division into territory alien to honesty.”392

It would be years before the US government held a hearing on DDT and even longer until they finally prohibited it in 1972. Unfortunately, the government discussions were not widely reported, so the general public remained unaware of the connection between polio (in humans!) and pesticides, or other non-viral factors. To achieve this, in the beginning of the 1950’s, ten years before Carson’s Silent Spring, someone would have had to have written a bestseller which described the repercussions of DDT (and other toxins) in humans. Unfortunately, this was not the case; and even later on such a book has not appeared.

Diagram 4 Polio cases and pesticide production in the USA, 1940-1970

View attachment 24626
**

Source:
Engelbrecht, Torsten; Köhnlein, Claus; Bailey, Samantha; Scoglio, Stefano. Virus Mania (pp. 84-85). Books on Demand. Kindle Edition.


Some more interesting info I just found:

**
Listed below are public health statistics (U.S. Public Health Reports) from the four states which adopted compulsory vaccination, and the figures from Los Angeles, California (similar results in other states available from books listed at the back of this booklet):

TENNESSEE

1958: 119 cases of polio before compulsory shots

1959: 386 cases of polio after compulsory shots

OHIO

1958: 17 cases of polio before compulsory shots

1959: 52 cases of polio after compulsory shots

CONNECTICUT

1958: 45 cases of polio before compulsory shots

1959: 123 cases of polio after compulsory shots

NORTH CAROLINA

1958: 78 cases of polio before compulsory shots

1959: 313 cases of polio after compulsory shots


LOS ANGELES

1958: 89 cases of polio before shots

1959: 190 cases of polio after shots
**

Source:
Vaccines: The Biggest Medical Fraud in History (History of Vaccination Book 26) | Amazon.com

Don't you just love to pick cherries?
(Include links to your sources. I realize you don't want to because it shows how your evidence is not really evidence but you are required to include links if you quote them.)

1.) Death rates from Polio are meaningless since if one person gets it and one person dies then the death rate is 100% Meanwhile if 50,000 get polio and are paralyzed and no one dies the death rate is zero. The biggest problem from polio was not deaths but paralysis. The vaccine didn't affect death rates. It prevented people from getting polio. Treatment also improved which would prevent death.
https://ourworldindata.org/grapher/...nd-deaths-in-the-united-states-since-1910.svg

2.) This chart and information directly contradicts you since it points out that polio PEAKED in 1952. It is also impossible to read and without a source I can't point out how DDT peaked in the 60's long after Polio was almost non existent.

3.) Most people had their children vaccinated for polio before 1958. According to the CDC, by September of 1957, more than 50% of the children from the ages 5-15 had received 3 doses of the polio vaccine.
https://stacks.cdc.gov/view/cdc/73807
Comparing 1958 to 1959 is cherry picking 2 years that are meaningless in the time frame. Not only that you are selectively picking areas that had outbreaks. Cherry picking of the worst kind.

 

[Poor Richard Saunders]

True, but we both agree that EMFs play a large role in the disease.



Only that he adds a step, the activation of the alleged flu virus, whereas I don't feel there is any evidence that the flu virus exists, which means that EMFs would be the sole cause.



Again, only partially true, as we both agree that EMFs play a large role in causing the flu.

He doesn't argue that EMFs cause the flu. He argues that EMFs activate the virus. The VIRUS causes the flu when it is activated.

Yes, that is our major disagreement.



Naturally, as I don't believe that contagious viruses exist.



No, I'm not "bastardizing his argument", I'm pointing out the evidence he's brought to the table that EMFs play a large role in the causation of the flu.

You are bastardizing his argument. He says EMFs activate a virus. The virus causes the flu according to Firstenberg.

No, I've never made such an argument.

Yes, you did.

You know I no longer believe that biological viruses exist, so I clearly don't agree with any of this.



I have never made such a claim. The claim I've made is that I don't believe they exist because of the lack of solid evidence that they exist.

It would appear you think logic no longer exists as well.
If viruses exist then they clearly have many hosts that would allow them to reproduce.
Claiming they can't reproduce is a circular argument on your part.
You - Viruses can't exist because they can't reproduce.
You - They can't reproduce because they don't exist.

Can you give me an example?



Definitely not.



According to Wikipedia, rabies is usually transmitted via a bite:
**
The virus is usually present in the nerves and saliva of a symptomatic rabid animal.[47][48] The route of infection is usually, but not always, by a bite.
**

Source:
https://en.wikipedia.org/wiki/Rabies

Sounds contagious to me.



Again, sounds contagious to me.

So if someone is contagious it means they might bite you? ROFLMAO.
Sorry, but you don't get to redefine words.
Here this seems to about your level :
https://kidshealth.org/en/teens/contagious.html
Infectious diseases that spread from person to person are said to be contagious.
When you require biting to infect, then it is not contagious.

 

[Poor Richard Saunders]

Always snipping bits of sentences giving the wrong impression.


.

I wonder why you don't apply this to Baily whom you keep quoting and yourself who you have also taking to quoting.

 

[Poor Richard Saunders]

I
Later on, I came to believe that it would be best to stick with the mainstream definition of viruses, which stipulates that they -are- contagious, which would make uncontagious viruses an oxymoron.

This is the definition of virus:
an infective agent that typically consists of a nucleic acid molecule in a protein coat, is too small to be seen by light microscopy, and is able to multiply only within the living cells of a host.
"the hepatitis B virus"
Nothing in that definition that stipulates it is contagious.

con·ta·gious
(of a disease) spread from one person or organism to another by direct or indirect contact.

You can spend all the direct and indirect contact you want with a dog that has rabies. It won't infect you since rabies is not contagious.

You seem to think if you make shit up then it becomes true. That isn't how the real world works. If you make shit up, then people think you are an idiot or a troll.

 

[Scott]

I suspect the issue is that Dr. Mark Bailey didn't start with the beginning of the paragraph of the analysis he was quoting. I downloaded a copy of the actual analysis and will quote the complete paragraph below, bolding the first sentence:

**
At this point, the contig with the identification k141_27232, with which 1,407,705 sequences are associated, and thus about 5% of the remaining 26,108,482 sequences, should be discussed in detail. Alignment with the nucleotide database on 05/12/2021 showed a high match (98.85%) with "Homo sapiens RNA, 45S pre- ribosomal N4 (RNA45SN4), ribosomal RNA" (GenBank: NR_146117.1, dated 04/07/2020). This observation contradicts the claim in [1] that ribosomal RNA depletion was performed and human sequence reads were filtered using the human reference genome (human release 32, GRCh38.p13). Of particular note here is the fact that the sequence NR_146117.1 was not published until after the publication of the SRR10971381 sequence library considered here.
**

Source:
https://brandfolder.com/s/3z266k74ppmnwkvfrxs6jjc

It seems that the mathematician is saying that this 98.85% match was for a specific contig with the id of K141_27232.

Let's examine this in detail and see how disingenuous Dr Bailey is.
Why would Bailey leave off the sentence that shows that only 5% of the remaining sequences showed a 98.55 match?

First of all, that's not actually what the paper said. Quoting what the mathematician's analysis actually said, bolding the parts you skipped over that I think are crucially important:
**
At this point, the contig with the identification k141_27232, with which 1,407,705 sequences are associated, and thus about 5% of the remaining 26,108,482 sequences, should be discussed in detail. Alignment with the nucleotide database on 05/12/2021 showed a high match (98.85%) with "Homo sapiens RNA, 45S pre- ribosomal N4 (RNA45SN4), ribosomal RNA" (GenBank: NR_146117.1, dated 04/07/2020).
**

The point is that this remaining 5% of the sequences, comprising a total of 1,407,705 sequences, all belongs to a single contig, with the identification of k141_27232. It strongly suggests that this contig, far from being viral in nature, was actually -human- in nature. The mathematician even goes so far as to name the specific human component that it has such a high match with:
**
"Homo sapiens RNA, 45S pre- ribosomal N4 (RNA45SN4), ribosomal RNA" (GenBank: NR_146117.1, dated 04/07/2020).

There is one other point that I think is worth noting. To be fair to the authors of the alleged discovery of Cov 2, they wouldn't have known about this ribosomal RNA, because it hadn't yet been discovered yet:

**
Of particular note here is the fact that the sequence NR_146117.1 was not published until after the publication of the SRR10971381 sequence library considered here.
**

SRR10971381 was the original rna sequence for Cov 2, while NR_146117.1 is the ribosomal RNA of the contig with the million plus reads (aka the 5% of what remained after fastp removed a little over half of all the sequences).

But even that is still misleading. When we look at the paper put on the internet by a mathematician the refused to give his name we find something else.
After filtering the paired-end reads, 26,108,482 of the original total of 56,565,928 reads remained, with a length of about 150 bp.
The mathematician used less than 50% of the original reads because he restricted himself to only using reads of 150bp. That seems a bit odd.

He did, but the irony here is that this mathematician was apparently following the -original- protocol used by those who allegedly discovered Cov 2 to begin with (aka "the authors") and like you, he finds this to be problematic. I think quoting the entire paragraph from which you got your quote is in order:

**
Renewed de novo assembly of published sequence data

To repeat the de novo assembly, we downloaded the original sequence data (SRR10971381) from 27/01/2020 on 11/30/2021 using the SRA tools [19] from the Internet. To prepare the paired-end reads for the actual assembly step with Megahit (v.1.2.9) [20], we used the FASTQ preprocessor fastp (v.0.23.1) [21]. After filtering the paired-end reads, 26,108,482 of the original total of 56,565,928 reads remained, with a length of about 150 bp. A large proportion of the sequences, presumably a majority of those of human origin were overwritten by the authors with "N" for unknown and therefore filtered out by fastp. This is to be regarded as problematic in the sense of scientificity, since not all steps can be retraced or reproduced. For the elaborate contig generation from the remaining short sequence reads, we used Megahit (v.1.2.9) using the default setting.
**

Source:
https://brandfolder.com/s/3z266k74ppmnwkvfrxs6jjc

The mathematician then gets into what could not be reproduced:
**
We obtained 28,459 (200 nt - 29,802 nt) contigs, significantly less than described in [1]. Deviating from the representations in [1], the longest contig we assembled comprised only 29,802 nt, 672 nt less than the longest contig with 30,474 nt, which according to [1] comprised almost the entire viral genome. Our longest contig showed a perfect match with the MN908947.3 sequence at a length of 29,801 nt (Tables and Figures, Tables 1, 2). Thus, we could not reproduce the longest contig of 30,474 nt, which is so important for scientific verification. Consequently, the published sequence data cannot be the original reads used for assembly.
**

 

[Poor Richard Saunders]

First of all, that's not actually what the paper said. Quoting what the mathematician's analysis actually said, bolding the parts you skipped over that I think are crucially important:
**
At this point, the contig with the identification k141_27232, with which 1,407,705 sequences are associated, and thus about 5% of the remaining 26,108,482 sequences, should be discussed in detail. Alignment with the nucleotide database on 05/12/2021 showed a high match (98.85%) with "Homo sapiens RNA, 45S pre- ribosomal N4 (RNA45SN4), ribosomal RNA" (GenBank: NR_146117.1, dated 04/07/2020).
**

The point is that this remaining 5% of the sequences, comprising a total of 1,407,705 sequences, all belongs to a single contig, with the identification of k141_27232. It strongly suggests that this contig, far from being viral in nature, was actually -human- in nature. The mathematician even goes so far as to name the specific human component that it has such a high match with:
**
"Homo sapiens RNA, 45S pre- ribosomal N4 (RNA45SN4), ribosomal RNA" (GenBank: NR_146117.1, dated 04/07/2020).

I didn't skip over anything. You don't seem to understand the process at all. Bailey misrepresents it and you are completely ignorant.

The mathematician claims that a single contig out of the 28,459 contigs he assembled showed a similarity to a human RNA. Each contig can use reads that were used in other contigs. All they are doing is assembling the reads in different ways.
That contig in question used only 5% of the total reads he had after he filtered out 55% of the reads so that particular contig used less than 2% of the reads. Because each contig can reuse reads used in other contigs, the number of reads in a specific contig is meaningless when it comes to finding the actual sequence of the virus.

What is important is how many contigs result in similar or identical results. If a contig is completely different from all the other ones then that is an outlier and not likely to be the sequence of the virus.
The anonymous mathematician, who for some reason doesn't want to put his name to this groundbreaking science, had 1 contig out of 28,459 contigs that could considered similar to human RNA.
That would mean that .0035% of the contigs from the mathematician had a possible match to a human RNA sequence. No reasonable mathematician would accept this as statistically significant.

There is one other point that I think is worth noting. To be fair to the authors of the alleged discovery of Cov 2, they wouldn't have known about this ribosomal RNA, because it hadn't yet been discovered yet:

**
Of particular note here is the fact that the sequence NR_146117.1 was not published until after the publication of the SRR10971381 sequence library considered here.
**

SRR10971381 was the original rna sequence for Cov 2, while NR_146117.1 is the ribosomal RNA of the contig with the million plus reads (aka the 5% of what remained after fastp removed a little over half of all the sequences).

Clearly you don't understand the process.

He did, but the irony here is that this mathematician was apparently following the -original- protocol used by those who allegedly discovered Cov 2 to begin with (aka "the authors") and like you, he finds this to be problematic. I think quoting the entire paragraph from which you got your quote is in order:

**
Renewed de novo assembly of published sequence data

To repeat the de novo assembly, we downloaded the original sequence data (SRR10971381) from 27/01/2020 on 11/30/2021 using the SRA tools [19] from the Internet. To prepare the paired-end reads for the actual assembly step with Megahit (v.1.2.9) [20], we used the FASTQ preprocessor fastp (v.0.23.1) [21]. After filtering the paired-end reads, 26,108,482 of the original total of 56,565,928 reads remained, with a length of about 150 bp. A large proportion of the sequences, presumably a majority of those of human origin were overwritten by the authors with "N" for unknown and therefore filtered out by fastp. This is to be regarded as problematic in the sense of scientificity, since not all steps can be retraced or reproduced. For the elaborate contig generation from the remaining short sequence reads, we used Megahit (v.1.2.9) using the default setting.
**

Source:
https://brandfolder.com/s/3z266k74ppmnwkvfrxs6jjc

The mathematician then gets into what could not be reproduced:
**
We obtained 28,459 (200 nt - 29,802 nt) contigs, significantly less than described in [1]. Deviating from the representations in [1], the longest contig we assembled comprised only 29,802 nt, 672 nt less than the longest contig with 30,474 nt, which according to [1] comprised almost the entire viral genome. Our longest contig showed a perfect match with the MN908947.3 sequence at a length of 29,801 nt (Tables and Figures, Tables 1, 2). Thus, we could not reproduce the longest contig of 30,474 nt, which is so important for scientific verification. Consequently, the published sequence data cannot be the original reads used for assembly.
**

The mathematician didn't follow the original protocol at all since the first thing he did was eliminate 55% of the reads.
So much nonsense from you.

 

[Truck Fump / h1b]

I didn't skip over anything. You don't seem to understand the process at all. Bailey misrepresents it and you are completely ignorant.

The mathematician claims that a single contig out of the 28,459 contigs he assembled showed a similarity to a human RNA. Each contig can use reads that were used in other contigs. All they are doing is assembling the reads in different ways.
That contig in question used only 5% of the total reads he had after he filtered out 55% of the reads so that particular contig used less than 2% of the reads. Because each contig can reuse reads used in other contigs, the number of reads in a specific contig is meaningless when it comes to finding the actual sequence of the virus.

What is important is how many contigs result in similar or identical results. If a contig is completely different from all the other ones then that is an outlier and not likely to be the sequence of the virus.
The anonymous mathematician, who for some reason doesn't want to put his name to this groundbreaking science, had 1 contig out of 28,459 contigs that could considered similar to human RNA.
That would mean that .0035% of the contigs from the mathematician had a possible match to a human RNA sequence. No reasonable mathematician would accept this as statistically significant.

Clearly you don't understand the process.


The mathematician didn't follow the original protocol at all since the first thing he did was eliminate 55% of the reads.
So much nonsense from you.

but at least you agree 5g is malicious and bad.

 

[Poor Richard Saunders]

but at least you agree 5g is malicious and bad.

Tin foil hat!! Make it!!!! Wear it!!!!!!

 

[Truck Fump / h1b]

Tin foil hat!! Make it!!!! Wear it!!!!!!

eat a fart cock.

 

[Scott]

First of all, polio's decline started well before Salk's polio vaccine was introduced:

**
Diagram 2
Polio death rates began to decline long before major
inoculation campaigns were started

View attachment 24624

From 1923 to 1953, long before large-scale polio vaccinations began to be carried out in the mid-1950s, mortalities attributed to polio had already decreased substantially: in the USA by 47 percent; in Great Britain by 55 percent; in other European countries, the statistics are comparable.
**

Source:
Engelbrecht, Torsten; Köhnlein, Claus; Bailey, Samantha; Scoglio, Stefano. Virus Mania (p. 73). Books on Demand. Kindle Edition.

Secondly, while I agree that DDT did not decrease during your time frame, exposure to it after 1954 did, and fairly dramatically too. There's also the fact that pesticide production in general dropped off dramatically after 1954 as well. Again from Virus Mania:

**
Diagram 3 Polio cases and DDT production in the USA, 1940-1970
View attachment 24625

A look at statistics shows that the polio epidemic in the United States of America reached its peak in 1952, and from then on rapidly declined. We have seen that this cannot be explained by the Salk-inoculation, since this was first introduced in 1955. There is a most striking parallel between polio development and the utilization of cide historian Pete Daniel goes a step further in saying that “[the officials in charge] knew better, but the bureaucratic imperative to protect pesticides led the division into territory alien to honesty.”392

It would be years before the US government held a hearing on DDT and even longer until they finally prohibited it in 1972. Unfortunately, the government discussions were not widely reported, so the general public remained unaware of the connection between polio (in humans!) and pesticides, or other non-viral factors. To achieve this, in the beginning of the 1950’s, ten years before Carson’s Silent Spring, someone would have had to have written a bestseller which described the repercussions of DDT (and other toxins) in humans. Unfortunately, this was not the case; and even later on such a book has not appeared.

Diagram 4 Polio cases and pesticide production in the USA, 1940-1970

View attachment 24626
**

Source:
Engelbrecht, Torsten; Köhnlein, Claus; Bailey, Samantha; Scoglio, Stefano. Virus Mania (pp. 84-85). Books on Demand. Kindle Edition.


Some more interesting info I just found:

**
Listed below are public health statistics (U.S. Public Health Reports) from the four states which adopted compulsory vaccination, and the figures from Los Angeles, California (similar results in other states available from books listed at the back of this booklet):

TENNESSEE

1958: 119 cases of polio before compulsory shots

1959: 386 cases of polio after compulsory shots

OHIO

1958: 17 cases of polio before compulsory shots

1959: 52 cases of polio after compulsory shots

CONNECTICUT

1958: 45 cases of polio before compulsory shots

1959: 123 cases of polio after compulsory shots

NORTH CAROLINA

1958: 78 cases of polio before compulsory shots

1959: 313 cases of polio after compulsory shots


LOS ANGELES

1958: 89 cases of polio before shots

1959: 190 cases of polio after shots
**

Source:
Vaccines: The Biggest Medical Fraud in History (History of Vaccination Book 26) | Amazon.com

Don't you just love to pick cherries?

What I picked were sources that I feel provide solid evidence for my beliefs in regards to biological viruses and vaccines.

(Include links to your sources. I realize you don't want to because it shows how your evidence is not really evidence but you are required to include links if you quote them.)

I included my source every single time. Had you truly been paying attention, you would have noted that my source was a book, Virus Mania, to be precise. You want to see the original source, you'll have to buy the book. I bought the kindle version, as is clear from my references.

1.) Death rates from Polio are meaningless since if one person gets it and one person dies then the death rate is 100% Meanwhile if 50,000 get polio and are paralyzed and no one dies the death rate is zero.

I would have preferred to see a graph that included actual numbers of deaths instead of just the percentage of deaths from polio, but to say that the percentage of people who had polio who died from it is meaningless is false. The death or mortality rate of Covid 19 is certainly tracked extensively:
https://www.worldometers.info/coronavirus/coronavirus-death-rate/

So the fact that the death rate was going down long before polio vaccines is a very important point, suggesting that the vaccines had nothing to do with polio not having as severe an effect on people.

The biggest problem from polio was not deaths but paralysis. The vaccine didn't affect death rates. It prevented people from getting polio.

Not according to to the states that adopted compulsory polio vaccinations, as I pointed out in my last post. For those who missed it:

**
Listed below are public health statistics (U.S. Public Health Reports) from the four states which adopted compulsory vaccination, and the figures from Los Angeles, California (similar results in other states available from books listed at the back of this booklet):

TENNESSEE

1958: 119 cases of polio before compulsory shots

1959: 386 cases of polio after compulsory shots

OHIO

1958: 17 cases of polio before compulsory shots

1959: 52 cases of polio after compulsory shots

CONNECTICUT

1958: 45 cases of polio before compulsory shots

1959: 123 cases of polio after compulsory shots

NORTH CAROLINA

1958: 78 cases of polio before compulsory shots

1959: 313 cases of polio after compulsory shots


LOS ANGELES

1958: 89 cases of polio before shots

1959: 190 cases of polio after shots
**

Source:
Vaccines: The Biggest Medical Fraud in History (History of Vaccination Book 26) | Amazon.com

Treatment also improved which would prevent death.https://ourworldindata.org/grapher/...nd-deaths-in-the-united-states-since-1910.svg

That chart actually makes the point of Virus Mania, namely that polio deaths peaked back in the 1910s or so.

2.) This chart and information directly contradicts you since it points out that polio PEAKED in 1952.

DDT exposure was around its highest at that time as well, as I pointed out in Diagram 3. Let's see if I can get it a bit bigger this time:

**

A look at statistics shows that the polio epidemic in the United States of America reached its peak in 1952, and from then on rapidly declined. We have seen that this cannot be explained by the Salk-inoculation, since this was first introduced in 1955. There is a most striking parallel between polio development and the utilization of [pesticides.] historian Pete Daniel goes a step further in saying that “[the officials in charge] knew better, but the bureaucratic imperative to protect pesticides led the division into territory alien to honesty.”392
**

There's also a direct correlation between total pesticide production and polio incidences:
**
It would be years before the US government held a hearing on DDT and even longer until they finally prohibited it in 1972. Unfortunately, the government discussions were not widely reported, so the general public remained unaware of the connection between polio (in humans!) and pesticides, or other non-viral factors. To achieve this, in the beginning of the 1950’s, ten years before Carson’s Silent Spring, someone would have had to have written a bestseller which described the repercussions of DDT (and other toxins) in humans. Unfortunately, this was not the case; and even later on such a book has not appeared.

Diagram 4 Polio cases and pesticide production in the USA, 1940-1970

**

The source for both of these diagrams and the text:
Engelbrecht, Torsten; Köhnlein, Claus; Bailey, Samantha; Scoglio, Stefano. Virus Mania (pp. 84-85). Books on Demand. Kindle Edition.

3.) Most people had their children vaccinated for polio before 1958. According to the CDC, by September of 1957, more than 50% of the children from the ages 5-15 had received 3 doses of the polio vaccine.
https://stacks.cdc.gov/view/cdc/73807
Comparing 1958 to 1959 is cherry picking 2 years that are meaningless in the time frame. Not only that you are selectively picking areas that had outbreaks. Cherry picking of the worst kind.

Don't you find it just a -tad- surprising the the places that had outbreaks were from the 4 states which adopted compulsory vaccination?

 

[Truck Fump / h1b]

my dad purposefully swam in a polio pool, giving no fucks.

no polio.

polio is a mental disease caused by 5g.

 

[Scott]

True, but we both agree that EMFs play a large role in the disease.

Only that he adds a step, the activation of the alleged flu virus, whereas I don't feel there is any evidence that the flu virus exists, which means that EMFs would be the sole cause.

Again, only partially true, as we both agree that EMFs play a large role in causing the flu.

He doesn't argue that EMFs cause the flu. He argues that EMFs activate the virus. The VIRUS causes the flu when it is activated.
You are bastardizing his argument. He says EMFs activate a virus. The virus causes the flu according to Firstenberg.

As you yourself admit, Firstenberg believes that the alleged flu virus is -activated- by EMFs. Without these EMFs, he doesn't believe said alleged virus would be harmful. Thus, the true cause would be the EMFs. Lest there be any doubt as to what he thinks the cause is, I'll requote what I quoted way back in Post #502:

**
Influenza Is an Electrical Disease

Suddenly and inexplicably, influenza, whose descriptions had remained consistent for thousands of years, changed its character in 1889. Flu had last seized most of England in November 1847, over half a century earlier. The last flu epidemic in the United States had raged in the winter of 1874–1875. Since ancient times, influenza had been known as a capricious, unpredictable disease, a wild animal that came from nowhere, terrorized whole populations at once without warning and without a schedule, and disappeared as suddenly and mysteriously as it had arrived, not to be seen again for years or decades. It behaved unlike any other illness, was thought not to be contagious, and received its name because its comings and goings were said to be governed by the “influence” of the stars.

View attachment 24572

But in 1889 influenza was tamed. From that year forward it would be present always, in every part of the world. It would vanish mysteriously as before, but it could be counted on to return, at more or less the same time, the following year. And it has never been absent since.

Like “anxiety disorder,” influenza is so common and so seemingly familiar that a thorough review of its history is necessary to unmask this stranger and convey the enormity of the public health disaster that occurred one hundred and thirty years ago. It’s not that we don’t know enough about the influenza virus. We know more than enough. The microscopic virus associated with this disease has been so exhaustively studied that scientists know more about its tiny life cycle than about any other single microorganism. But this has been a reason to ignore many unusual facts about this disease, including the fact that it is not contagious.

In 2001, Canadian astronomer Ken Tapping, together with two British Columbia physicians, were the latest scientists to confirm, yet again, that for at least the last three centuries influenza pandemics have been most likely to occur during peaks of solar magnetic activity—that is, at the height of each eleven-year sun cycle.

Such a trend is not the only aspect of this disease that has long puzzled virologists. In 1992, one of the world’s authorities on the epidemiology of influenza, R. Edgar Hope-Simpson, published a book in which he reviewed the essential known facts and pointed out that they did not support a mode of transmission by direct human-to-human contact. Hope-Simpson had been perplexed by influenza for a long time, in fact ever since he had treated its victims as a young general practitioner in Dorset, England, during the 1932–1933 epidemic—the very epidemic during which the virus that is associated with the disease in humans was first isolated. But during his 71-year career Hope-Simpson’s questions were never answered. “The sudden explosion of information about the nature of the virus and its antigenic reactions in the human host,” he wrote in 1992, had only “added to the features calling for explanation.”3

Why is influenza seasonal? he still wondered. Why is influenza almost completely absent except during the few weeks or months of an epidemic? Why do flu epidemics end? Why don’t out-of-season epidemics spread? How do epidemics explode over whole countries at once, and disappear just as miraculously, as if suddenly prohibited? He could not figure out how a virus could possibly behave like this. Why does flu so often target young adults and spare infants and the elderly? How is it possible that flu epidemics traveled at the same blinding speed in past centuries as they do today? How does the virus accomplish its so-called “vanishing trick”? This refers to the fact that when a new strain of the virus appears, the old strain, between one season and the next, has vanished completely, all over the world at once. Hope-Simpson listed twenty-one separate facts about influenza that puzzled him and that seemed to defy explanation if one assumed that it was spread by direct contact.

He finally revived a theory that was first put forward by Richard Shope, the researcher who isolated the first flu virus in pigs in 1931, and who also did not believe that the explosive nature of many outbreaks could be explained by direct contagion. Shope, and later Hope-Simpson, proposed that the flu is not in fact spread from person to person, or pig to pig, in the normal way, but that it instead remains latent in human or swine carriers, who are scattered in large numbers throughout their communities until the virus is reactivated by an environmental trigger of some sort. Hope-Simpson further proposed that the trigger is connected to seasonal variations in solar radiation, and that it may be electromagnetic in nature, as a good many of his predecessors during the previous two centuries had suggested.
**

Firstenberg, Arthur; Firstenberg, Arthur. The Invisible Rainbow (pp. 80-83). Chelsea Green Publishing. Kindle Edition.

He has also said that he doesn't believe that the flu is contagious and provided evidence in his book that this is the case, so clearly his definition of this flu virus is a lot different than the mainstream here.

 

[Scott]

my dad purposefully swam in a polio pool, giving no fucks.

no polio.

polio is a mental disease caused by 5g.

5G wasn't around back when polio was raging, but DDT and other very harmful pesticides certainly were. As they reduced DDT exposure and decreased the whopping amount of pesticides spewed into the environment, polio decreased as well.

 

[Scott]

So you are going to argue that parasites exist but parasites can't exist?

No, I've never made such an argument.

Yes, you did.

Where?

You know I no longer believe that biological viruses exist, so I clearly don't agree with any of this.

I have never made such a claim. The claim I've made is that I don't believe they exist because of the lack of solid evidence that they exist.

It would appear you think logic no longer exists as well.

Enough platitudes -.-

If viruses exist then they clearly have many hosts that would allow them to reproduce.

Let's focus on whether they exist or not before going off on the alleged qualities of these hypothetical entities.

According to Wikipedia, rabies is usually transmitted via a bite:
**
The virus is usually present in the nerves and saliva of a symptomatic rabid animal.[47][48] The route of infection is usually, but not always, by a bite.
**

Source:
https://en.wikipedia.org/wiki/Rabies

Sounds contagious to me.

So if someone is contagious it means they might bite you?

No, it means that this alleged rabies virus is allegedly transmitted through saliva, which is the way one can allegedly catch it.

Sorry, but you don't get to redefine words.
Here this seems to about your level :
https://kidshealth.org/en/teens/contagious.html
Infectious diseases that spread from person to person are said to be contagious.
When you require biting to infect, then it is not contagious.

You notice that your definition doesn't actually say that getting something via a bite means it's not contagious?

 

[Poor Richard Saunders]

What I picked were sources that I feel provide solid evidence for my beliefs in regards to biological viruses and vaccines.



I included my source every single time. Had you truly been paying attention, you would have noted that my source was a book, Virus Mania, to be precise. You want to see the original source, you'll have to buy the book. I bought the kindle version, as is clear from my references.

It seems you aren't actually trying to find the truth. Instead you are selectively using 3-4 sources that confirm your bias and refusing to look at anything else.

I would have preferred to see a graph that included actual numbers of deaths instead of just the percentage of deaths from polio, but to say that the percentage of people who had polio who died from it is meaningless is false. The death or mortality rate of Covid 19 is certainly tracked extensively:
https://www.worldometers.info/coronavirus/coronavirus-death-rate/

So the fact that the death rate was going down long before polio vaccines is a very important point, suggesting that the vaccines had nothing to do with polio not having as severe an effect on people.



Not according to to the states that adopted compulsory polio vaccinations, as I pointed out in my last post. For those who missed it:

**
Listed below are public health statistics (U.S. Public Health Reports) from the four states which adopted compulsory vaccination, and the figures from Los Angeles, California (similar results in other states available from books listed at the back of this booklet):

[cherry picked data deleted.]

Source:
Vaccines: The Biggest Medical Fraud in History (History of Vaccination Book 26) | Amazon.com



That chart actually makes the point of Virus Mania, namely that polio deaths peaked back in the 1910s or so.



DDT exposure was around its highest at that time as well, as I pointed out in Diagram 3. Let's see if I can get it a bit bigger this time:

**

A look at statistics shows that the polio epidemic in the United States of America reached its peak in 1952, and from then on rapidly declined. We have seen that this cannot be explained by the Salk-inoculation, since this was first introduced in 1955. There is a most striking parallel between polio development and the utilization of [pesticides.] historian Pete Daniel goes a step further in saying that “[the officials in charge] knew better, but the bureaucratic imperative to protect pesticides led the division into territory alien to honesty.”392
**

[Cherry picked data deleted.]



Don't you find it just a -tad- surprising the the places that had outbreaks were from the 4 states which adopted compulsory vaccination?

Death rates don't show anything about how contagious a disease is.
DDT was used more but was less prevalent? ROFLMAO. That has to be one of the stupidest arguments ever.
Because polio deaths peaked in 1910 is meaningless. Medicine learned how to treat the disease to prevent deaths. The number of cases in the 1952 and 1953 were substantially more than in 1910.
Epidemics and pandemics are not a straight line, the number infected goes up and down from year to year. A statistical analysis of using regression shows an increase from 1900 - 1955 and a decrease from 1955 to today. Your idiocy is getting tiring at this point. Can you buy or borrow a brain?
What I don't find surprising is that you continue to rely solely on cherry picked data. Why don't you post the polio cases in 1952-1957 for those cities and states? But you do love your cherries so I'm sure you won't check out the complete facts.

 

[Scott]

Always snipping bits of sentences giving the wrong impression.

I wonder why you don't apply this to [Bailey] whom you keep quoting and yourself who you have also taking to quoting.

I imagine you're referring to the one incidence where Dr. Mark Bailey decided to not include an important first sentence while quoting an analysis in his 67 page document. No one's perfect. Furthermore, clipping the first sentence didn't actually help his argument. You, on the other hand, have clipped a lot of sentences that suggest very different things when not in their proper context. I think I understand why you would do it, as the way you clip these sentences seems to support your world view.

 

[Poor Richard Saunders]

Where?



Enough platitudes -.-



Let's focus on whether they exist or not before going off on the alleged qualities of these hypothetical entities.



No, it means that this alleged rabies virus is allegedly transmitted through saliva, which is the way one can allegedly catch it.





You notice that your definition doesn't actually say that getting something via a bite means it's not contagious?

LOL. So biting is now a form of contagion?
The definition is quite clear. It requires infection to occur through direct or indirect contact. Shaking hands is direct contact. Being in the same room is direct contact. Biting requires more than just direct contact.
From the CDC website -

Other types of contact, such as petting a rabid animal or contact with the blood, urine or feces of a rabid animal, are not associated with risk for infection and are not considered to be exposures of concern for rabies.

...

Bite and non-bite exposures from an infected person could theoretically transmit rabies, but no such cases have been documented. Casual contact, such as touching a person with rabies or contact with non-infectious fluid or tissue (urine, blood, feces), is not associated with risk for infection. Contact with someone who is receiving rabies vaccination does not constitute rabies exposure, does not pose a risk for infection, and does not require postexposure prophylaxis.

https://www.cdc.gov/rabies/transmission/index.html

Rabies is not contagious. You can't get it from someone that has rabies.

 

[Poor Richard Saunders]

Where?



Enough platitudes -.-



Let's focus on whether they exist or not before going off on the alleged qualities of these hypothetical entities.



No, it means that this alleged rabies virus is allegedly transmitted through saliva, which is the way one can allegedly catch it.





You notice that your definition doesn't actually say that getting something via a bite means it's not contagious?

Let me ask you,
If I have evidence of a virus being grown in a culture and then people becoming infected by being injected with the virus grown in that culture, would you accept the evidence or not?