bashi
18th December 2010, 17:52
You have to read this very carefully:
“These four cases share multiple polymorphisms in multiple genes which are not found in any recent swine sequences, even though swine surveillance has increased because of the 2009 pandemic.
Thus, the four human sequences are more closely related to each other than any public swine sequences.”
source: http://www.recombinomics.com/News/12171002/H3N2_swine_pandemic.html
Now what are they talking about?
Lets assume you have an original virus M with a gene sequence of
ABCDEFGHIJKLMNOP.
After this virus has spread, it can mutate into, say
ABCDEXGHIJKLMNOP
which I will call here (Mutant virus) M1.
This new mutant virus will have to spread and multiply in order to create a new basis for future mutations. During this spread will create a lot of sick people or sick swine and the mutation will be detected soon and recognized by implemented monitoring procedures of whatever health care authority.
After M1 has spread it can then mutate again into a gene sequence, say ABCDEXGHIJKLYNOP ,
which I call here M1A.
Now, after some time to multiply and spread, M1A can mutate into, say ABCDEXGHIJKLYNZP,
called M1A2.
During all these mutation steps, it is most likely that these mutations will be found out and catalogued, because it requires a lot of spreading in order to facilitate a mutation.
What are the chances that the virus M will skip the detection of a M1 mutation and jumps to M1A? Very little, near to zero; but still possible.
What are the chances of a mutation from M to M1A2 without detection of the mutation-steps inbetween? We are talking about three mutations, with two being undetected! The probability is ZERO ! So is a further mutation in a fourth sequence.
Specially because these mutations are not found in the swine population, they were supposed to be found in humans:
“the human trH3N2 sequences have polymorphism present in all four human isolates, but no recent swine sequences”
But no massive spread of any single mutation step in humans has been found.
But we can still imagine an impossible gene-pool which is so dynamic that it mutates faster than the sleeping scientists can detect. This would require a single fast evolving gene-pool at a single location, isn’t it? That has never been observed in Nature, but lets –for the sake of argument – assume this impossibility to happen just once.
Now look at the geographical spread:
“These four sequences include the first case (Kansas/13/2009 in August 2009) as well as the three most recent sequences (Minnesota/09/2010 in May 2010, Pennsylvania/14/2010 in October 2010, and Wisconsin/12/2010 in November 2010).
”
For this to happen naturally, you will have to have FOUR (impossible) single, fast evolving gene-pools at four different locations.
This is as impossible as you can walk on the sun’s surface in pyjamas…
Conclusion: This virus has been artificially altered and then released at different locations.
It is the same agenda as it was with the H1N1 in Mexico.
Let’s hope that Nature will mutate this “improved “ version into oblivion…
.
“These four cases share multiple polymorphisms in multiple genes which are not found in any recent swine sequences, even though swine surveillance has increased because of the 2009 pandemic.
Thus, the four human sequences are more closely related to each other than any public swine sequences.”
source: http://www.recombinomics.com/News/12171002/H3N2_swine_pandemic.html
Now what are they talking about?
Lets assume you have an original virus M with a gene sequence of
ABCDEFGHIJKLMNOP.
After this virus has spread, it can mutate into, say
ABCDEXGHIJKLMNOP
which I will call here (Mutant virus) M1.
This new mutant virus will have to spread and multiply in order to create a new basis for future mutations. During this spread will create a lot of sick people or sick swine and the mutation will be detected soon and recognized by implemented monitoring procedures of whatever health care authority.
After M1 has spread it can then mutate again into a gene sequence, say ABCDEXGHIJKLYNOP ,
which I call here M1A.
Now, after some time to multiply and spread, M1A can mutate into, say ABCDEXGHIJKLYNZP,
called M1A2.
During all these mutation steps, it is most likely that these mutations will be found out and catalogued, because it requires a lot of spreading in order to facilitate a mutation.
What are the chances that the virus M will skip the detection of a M1 mutation and jumps to M1A? Very little, near to zero; but still possible.
What are the chances of a mutation from M to M1A2 without detection of the mutation-steps inbetween? We are talking about three mutations, with two being undetected! The probability is ZERO ! So is a further mutation in a fourth sequence.
Specially because these mutations are not found in the swine population, they were supposed to be found in humans:
“the human trH3N2 sequences have polymorphism present in all four human isolates, but no recent swine sequences”
But no massive spread of any single mutation step in humans has been found.
But we can still imagine an impossible gene-pool which is so dynamic that it mutates faster than the sleeping scientists can detect. This would require a single fast evolving gene-pool at a single location, isn’t it? That has never been observed in Nature, but lets –for the sake of argument – assume this impossibility to happen just once.
Now look at the geographical spread:
“These four sequences include the first case (Kansas/13/2009 in August 2009) as well as the three most recent sequences (Minnesota/09/2010 in May 2010, Pennsylvania/14/2010 in October 2010, and Wisconsin/12/2010 in November 2010).
”
For this to happen naturally, you will have to have FOUR (impossible) single, fast evolving gene-pools at four different locations.
This is as impossible as you can walk on the sun’s surface in pyjamas…
Conclusion: This virus has been artificially altered and then released at different locations.
It is the same agenda as it was with the H1N1 in Mexico.
Let’s hope that Nature will mutate this “improved “ version into oblivion…
.