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PostPosted: Thu Nov 24, 2011 1:16 pm 
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Commentary

http://www.recombinomics.com/News/11241 ... A_WHO.html

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PostPosted: Thu Nov 24, 2011 2:26 pm 
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http://www.recombinomics.com/News/11241 ... mples.html

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PostPosted: Thu Nov 24, 2011 3:09 pm 
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So your position, Dr. Niman, is that in 2010 or earlier a triple-reassortant H3N2 virus jumped from pigs to at least one human, and that virus then reassorted in a human with the 2009 H1N1 virus to pick up its "M" gene and create the trH3N2 virus that is now transmitting human-to-human at least somewhat efficiently?


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PostPosted: Thu Nov 24, 2011 3:17 pm 
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Jon Schultz wrote:
So your position, Dr. Niman, is that in 2010 or earlier a triple-reassortant H3N2 virus jumped from pigs to at least one human, and that virus then reassorted in a human with the 2009 H1N1 virus to pick up its "M" gene and create the trH3N2 virus that is now transmitting human-to-human at least somewhat efficiently?

There was limited tranmission prior to the acquisition of the M gene, as lab confirmed in the cluster in Minnesota and strongly suggested by the match between A/Pennsylvania/40/2010 and A/Wisconsin/12/2010. There were any more cases than the 6 that were lab confirmed for 2010.

The virus evolved further in 2011, by acquiring the M gene from H1N1pdm09, and reassorting to acquire the N2 gene from A/Pennsylvania/14/2010. The virus was concentrated in humans, but also in swine, so the acquisitions could have happened in either species, but right now the novel 2011 version is widespread in humans (and starting to jump to swine, as seen in NY).

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PostPosted: Thu Nov 24, 2011 3:28 pm 
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niman wrote:

Coverage expanding

http://www.episouthnetwork.org/sites/de ... %20_11.pdf

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PostPosted: Thu Nov 24, 2011 7:02 pm 
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niman wrote:
The virus evolved further in 2011, by acquiring the M gene from H1N1pdm09, and reassorting to acquire the N2 gene from A/Pennsylvania/14/2010. The virus was concentrated in humans, but also in swine, so the acquisitions could have happened in either species, but right now the novel 2011 version is widespread in humans (and starting to jump to swine, as seen in NY).


If the acquisitions could have happened in either species, how do you know the swine in NY were infected by a human and not other swine?

Happy Thanksgiving!


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PostPosted: Fri Nov 25, 2011 1:57 am 
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CDC confirms cases of new swine flu virus

The Centers for Disease Control and Prevention has confirmed three cases of a new flu virus, which originated in pigs but apparently spread from person to person, in three Iowa children.

However, there's no reason to fear the beginning of a new pandemic, says Arnold Monto, a flu expert and professor at the University of Michigan School of Public Health.

"I don't think this is anything to worry about for the moment," Monto says. "We have known that swine viruses get into humans occasionally, transmit for a generation or two and then stop. The issue is whether there will be sustained transmission (from person to person)- and that nearly never happens."

The CDC has counted a total of 18 cases of this new virus, an influenza A strain known as S-OtrH3N2, in two years. That suggests that it's not spreading quickly or easily, says William Schaffner, a professor at the Vanderbilt University School of Medicine and spokesman for the Infectious Diseases Society of America.

Schaffner notes that flu viruses mutate and swap genes all the time. Infectious disease experts may only be noticing these new viruses because of better technology, he says. The USA's beefed-up state medical labs, which have lots more firepower than before 2001, are much better at spotting novel viruses, which in the past might have gone unnoticed.

Thanks to the sophistication of these labs, scientists are getting a window into the inner workings of the flu that they haven't had in the past, Schaffner says. But that doesn't mean that these novel viruses are necessarily any more dangerous.

The H1N1 swine flu pandemic began in 2009 after flu viruses mutated to create a new strain that humans had never encountered before, leaving everyone vulnerable to infection. Although the H1N1 pandemic proved to be relatively mild, doctors fear new flu strains because of their lethal history. In 1918, a new flu strain killed more than 20 million people.

All three of the Iowa children had mild illness, the CDC reports. The virus also seems treatable with standard anti-viral drugs, Schaffner notes. The 10 cases of H3N2 in 2011 also have been spread throughout the USA -- in Pennsylvania, Maine, Indiana and Iowa -- which doesn't indicate a disease "cluster" or outbreak, Schaffner says.

In a report released late Wednesday night, the CDC noted that, as part of "routine preparedness," it has already produced a "candidate vaccine virus" that could be used against this new strain, and has given it to vaccine makers.

http://yourlife.usatoday.com/health/sto ... 51384636/1

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PostPosted: Fri Nov 25, 2011 2:13 am 
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Jon Schultz wrote:
niman wrote:
The virus evolved further in 2011, by acquiring the M gene from H1N1pdm09, and reassorting to acquire the N2 gene from A/Pennsylvania/14/2010. The virus was concentrated in humans, but also in swine, so the acquisitions could have happened in either species, but right now the novel 2011 version is widespread in humans (and starting to jump to swine, as seen in NY).


If the acquisitions could have happened in either species, how do you know the swine in NY were infected by a human and not other swine?

Happy Thanksgiving!

The sequence story is very clear, although the media quotes "experts" who are sequence challenged, so media the comments detract from the sequence story.

When the CDC released sequences (just after the Nov, 2010 pager alert) of prior human triple reassortants, and swine surveillance expanded, it was easy to see the clustering of most of the human cases from 2010, as seen in Nancy Cox's presentation in February. The HA tree had most of the 2010 human sequences clustered on one branch, even though the isolates were from Minnesota, Wisconsin, and Pennsylvania. These isolates represented the trH3N2 adapting to humans and these sequences were widespread, which is why they matched even though they were widespread and the number identified by the CDC was small. In contrast, the matching sequences were relatively rare in swine, especially when the full set of gene segments were analyzed. Thus, in 2010, most of the genes in most of the human isolates matched, and this was the human trH3N2 sub-clade.

This sub-clade adapted further and then represented all of the human isolates, which matched in all 8 gene segments. Now there are 10 isolates, even though the CDC is not targeting humans with trH3N2. In contrast, the swine surveillance does target all swine SOIVs, but failed to find this novel trH3N2 in any isolates prior to the cases in Indiana and Pennsylvania. This failure indicated the novel trH3N2 was circulating in humans, and the match of the July and August isolates in Indiana and Pennsylvania in human isolates indicated it was widespread.

Thus, the ONE isolate in New York in September indicated this common trH3N2 in humans jumped to swine to yield the ONE example.

Thus, the trH3N2 with the H1N1 M gene is a HUMAN pathogen, and the 10 isolates were identified by the CDC by accident, indicating it is VERY common in humans and very rare in swine.

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PostPosted: Fri Nov 25, 2011 2:22 am 
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niman wrote:
CDC confirms cases of new swine flu virus

"I don't think this is anything to worry about for the moment," Monto says. "We have known that swine viruses get into humans occasionally, transmit for a generation or two and then stop. The issue is whether there will be sustained transmission (from person to person)- and that nearly never happens."

http://yourlife.usatoday.com/health/sto ... 51384636/1

This is utter nonsense. The Iowa cluster represnts the largest number of isolates ffrom a cluster that is epidemiologically linked, and the cluster was clear FIVE. This has not happened since H1N1pdm09 jumped from swine to humans. Moreover, all three sequences match the seven earlier sequences from 2011, indicating it is a human pathogen which is WIDESPREAD, and this type of match wasn't seen prior to the 2009 pandemic, or after.

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PostPosted: Fri Nov 25, 2011 2:40 am 
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niman wrote:
Jon Schultz wrote:
niman wrote:
The virus evolved further in 2011, by acquiring the M gene from H1N1pdm09, and reassorting to acquire the N2 gene from A/Pennsylvania/14/2010. The virus was concentrated in humans, but also in swine, so the acquisitions could have happened in either species, but right now the novel 2011 version is widespread in humans (and starting to jump to swine, as seen in NY).


If the acquisitions could have happened in either species, how do you know the swine in NY were infected by a human and not other swine?

Happy Thanksgiving!

The sequence story is very clear, although the media quotes "experts" who are sequence challenged, so media the comments detract from the sequence story.

When the CDC released sequences (just after the Nov, 2010 pager alert) of prior human triple reassortants, and swine surveillance expanded, it was easy to see the clustering of most of the human cases from 2010, as seen in Nancy Cox's presentation in February. The HA tree had most of the 2010 human sequences clustered on one branch, even though the isolates were from Minnesota, Wisconsin, and Pennsylvania. These isolates represented the trH3N2 adapting to humans and these sequences were widespread, which is why they matched even though they were widespread and the number identified by the CDC was small. In contrast, the matching sequences were relatively rare in swine, especially when the full set of gene segments were analyzed. Thus, in 2010, most of the genes in most of the human isolates matched, and this was the human trH3N2 sub-clade.

This sub-clade adapted further and then represented all of the human isolates, which matched in all 8 gene segments. Now there are 10 isolates, even though the CDC is not targeting humans with trH3N2. In contrast, the swine surveillance does target all swine SOIVs, but failed to find this novel trH3N2 in any isolates prior to the cases in Indiana and Pennsylvania. This failure indicated the novel trH3N2 was circulating in humans, and the match of the July and August isolates in Indiana and Pennsylvania in human isolates indicated it was widespread.

Thus, the ONE isolate in New York in September indicated this common trH3N2 in humans jumped to swine to yield the ONE example.

Thus, the trH3N2 with the H1N1 M gene is a HUMAN pathogen, and the 10 isolates were identified by the CDC by accident, indicating it is VERY common in humans and very rare in swine.

See slide 7 for HA tree with 2010 human isolates in red

http://www.google.com/url?sa=t&rct=j&q= ... Q8C92QA5KQ

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