dothedd
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Post by dothedd on Apr 3, 2012 13:49:52 GMT -5
4 3 12 TODAY POSTS CONTINUED FROM PREVIOUS PAGE
Maryland Death Cluster Due To H3N2 Drift Variant Recombinomics Commentary 22:50 March 27, 2012
The CDC has released five sets of H3N2 from recent collections in Maryland. All five sequences were generated directly from the clinical samples, strongly suggesting that all five were linked to the recent death cluster.
Three of the samples (A/Maryland/04/2012, A/Maryland/05/2012, A/Maryland/06/2012) were from March 5 collections, the date of death for two of the siblings. The other two, A/Maryland/08/2012 and A/Maryland/09/2012, were from collections on February 21 and February 20 respectively. Although the ages and gender of the index case and three children involved in the Maryland death cluster have been cited in media reports, the CDC withheld the age and gender for all five sequences.
Thus, the assignment of each of the five samples was not possible from the public data released by the CDC. However, all five H3 sequences were virtually identical and related to the drift variant, A/Brisbane/299/2011, which has S199A, as noted for prior sequences designated as low reactors by the CDC.
A reassortant of A/Brisbane/299/2011 (designated A/Brisbane/299/2011 X-215) has been generated as a potential H3N2 vaccine target because it is a variant that produces a low reaction when tested against the current vaccine, which is directed against A/Perth/16/2009.
Thus, the sequence data confirmed that the Maryland cluster were from a drift variant and were unlikely to react well with the current vaccine, in contrast to the CDC comments and internet rumor.
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dothedd
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Post by dothedd on Apr 3, 2012 13:51:52 GMT -5
CDC Maryland Death Cluster H3N2 Variant Denial Concerns Recombinomics Commentary 02:15 March 28, 2012
A/Brisbane/299/2011 X-215
IVR-164(A/Brisbane/299/2011)
Genetic sequencing has confirmed that this is a typical human seasonal H3N2 virus that is more than 99% similar to other H3N2 influenza viruses submitted by the state of Maryland this season. While full antigenic testing is pending, based on genetic sequencing of some of the samples, these viruses are close to the H3N2 component of the 2011-2012 seasonal vaccine such that vaccination should offer protection against these viruses.
The above constructs (in red) were created for the CDC from an August 13, 2011 Brisbane isolate for testing as an H3N2 vaccine target because the CDC was well aware of low reactors with S199A, which caused concerns in 2010. The recently released sequences from the Maryland death cluster also contained S199A and were drift variants and Brisbane/299-like.
However, prior to the release of the sequence data, the CDC claimed (see above quote in blue) that the vaccine targeting A/Perth/16/2009, would react with the Maryland sequences, even though the CDC had released Brisbane/299-like 2012 sequences, A/Colorado/05/2012 and A/California/07/2012, which had been designated as low reactors by the CDC.
In addition to the official CDC claim, an internet rumor was published citing anonymous sources at the CDC who claimed that the Maryland death cluster was not due to an H3N2 drift variant.
This misleading information increases concerns that the internally inconsistent antigen characterization data generated by the CDC is used for propaganda purposes, such as use of the data to claim vaccine matches for mismatches, and claim that the mismatched vaccine is efficacious for drift variants, like the sequences linked to the Maryland death cluster.
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dothedd
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Post by dothedd on Apr 3, 2012 13:58:49 GMT -5
Similarities in Nature Science and Virology H5N1 Studies Recombinomics Commentary 20:15 March 30, 2012
However, he said his group found a number of mutations in common when they sequenced the viruses that had made the jump to airborne spread. "Most of those were pretty interesting," he said, adding that some of the mutations are the same ones Kawaoka's group found, though that group took a different approach to the study. "That was a shock to me and to Yoshi," he said.
The above comments confirm similarities between the H5N1 transmission studies described in the delayed paper at Nature with the delayed paper at Science and the CDC paper published at the journal Virology. These similarities add to the evidence that the current position of the NSABB is little more than a publicity stunt.
The NSABB initially recommended that the papers at Nature and Science be redacted because they provided recipes for a transmitting H5N1 which could be used for nefarious groups. However, transmitting H5N1 has never been a good choice because it can’t be controlled once released and the NSABB recommendation was made after the CDC paper was published in Virology and could be accessed by anyone who could double click on a link.
The CDC paper was published in November, 2011 and described transmission of a clade 2.2 H5N1 (A/egret/Egypt/1162/2006) after three receptor binding domain changes were introduced. Two of the changes, Q226L and G228S, have been investigated for years since they were both present in 1957 and 1968 pandemics, although neither has been reported in natural H5N1. The CDC added Q196R because of increased affinity for mammalian gal 2,6 receptors whne added to the above two changes. This modified H5 was placed on a clade 1 background (A/Vietnam/1203/2004) from an isolate that grew well in ferrets, due in part to PB1 E627K, and the CDC also used an N2 from seasonal H3N2 (A/Brisbane/10/2007). This construct transmitted via aerosol in a ferret model, as reported in the published and non-redacted paper in Virology.
The delayed Science paper by Ron Fouchier uses a different H5 (clade 2.1 from Indonesia), but uses three of the four changes in the CDC study (H5 Q226L / G228S with PB2 E627K). That construct is then passaged in ferrets ten times to produce a transmitting H5N1 that has acquired two additional changes. Fouchier comments indicate one of the two is Q196R, since he noted that a published study had 4 of the 5 changes, strongly suggesting that he was referring the CDC’s paper in Virology. The above recent comments indicate similar changes were introduced into a clade 2.3 (from Vietnam) in the Yoshi Kawaoka paper delayed by Nature. That paper places the modified H5 on an H1N1pdm09 genetic background, removing the requirement for PB2 E627K. Thus, the Nature paper almost certainly reported the use of Q116L and G228S and either added or acquired Q196R.
Thus, although all three studies generated H5N1 transmission in ferrets using three different approaches, all used the same small number of receptor binding domain changes on H5 three different sub-clades (clade 2.1, 2.2, and 2.3) which are responsible for all human cases outside of southeast Asia (where clade 1 continues to cause human cases).
The delayed papers were distributed at the WHO meeting in Geneva, which was also attended by the acting chair of the NSABB, so all members should now realize that the recipe for all three studies are public, and the current NSABB meeting is little more than a publicity stunt that is hazardous to the world’s health.
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dothedd
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Post by dothedd on Apr 3, 2012 14:07:44 GMT -5
NSABB Withdraws H5N1 Publication Objections Recombinomics Commentary 22:15 March 30, 2012
A panel of U.S. biosecurity experts is withdrawing its objections to the publication of two controversial bird flu studies.
The National Science Advisory Board for Biosecurity says after reviewing revised versions of the studies it is recommending they can be published in full. The board voted unanimously to clear for publication a study by Yoshihiro Kawaoka of the University of Wisconsin-Madison.
The committee voted 12 to 6 on the second study, done by Dutch virologist Ron Fouchier. The above comments indicate the NSABB has withdrawn its objections to the studies withheld at Nature and Science. Although the initial objection came after a similar study by the CDC had already been published in Virology, and Ron Fouchier had presented his data at a scientific meeting, the NSABB raised concerns that the new publications represented a recipe for turning H5N1 into a potent (but uncontrollable) bioweapon.
However, as more detail was released via media reports, the recipes, and relationship to the published recipe became clear, and there was no scientific basis for objections, since all key details had already been made public.
The NSABB is congratulated on its decision.
However the scientific understanding of the six who voted for redactions in the Science paper is in need of careful review.
NOTE REPOST FROM JANUARY:
NSABB Comments on H5N1 Transmission Censorship Recombinomics Commentary 23:00 January 31, 2012
Recently, several scientific research teams have achieved some success in isolating influenza A/H5N1 viruses that are transmitted efficiently between mammals, in one instance with maintenance of high pathogenicity. This information is very important because, before these experiments were done, it was uncertain whether avian influenza A/H5N1 could ever acquire the capacity for mammal-to-mammal transmission.
Now that this information is known, society can take steps globally to prepare for when nature might generate such a virus spontaneously. At the same time, these scientific results also represent a grave concern for global biosecurity, biosafety, and public health. Could this knowledge, in the hands of malevolent individuals, organizations, or governments, allow construction of a genetically altered influenza virus capable of causing a pandemic with mortality exceeding that of the “Spanish flu” epidemic of 1918?
The above comments are from the US National Science Advisory Board for Biosecurity (NSABB) report, “Adaptations of Avian Flu Virus Are a Cause for Concern”, which was issued today. The report fails to note reasons why a transmitting H5N1 is a poor choice as a bioweapon (because it can’t be controlled), and instead elevates the transmitting H5N1 into a desirable goal by “malevolent individuals, organizations, or governments", which is to be controlled by censoring papes at Nature and Science which use very different approaches to create a transmitting H5N1 using well known receptor binding domain changes and techniques that have been known for decades.
The main finding of the two papers, efficient transmission of H5N1 in mammals, is now well known, and the achievement of this goal by two groups using very different approaches, indicates any serious program not only could easily replicate these results, but could easily increase transmission and lethality.
Prior to these two reports, “experts” had claimed that H5N1 couldn’t efficiently transmit in mammals because it had not been reported evenb though H5N1 has been infecting humans since 1997, or claimed that efficient transmission would markedly reduce lethality. Now that it is known that both of these claims have no real scientific basis and have been thoroughly refuted, the NSABB wants to take one fantasy, that a transmitting H5N1 is a desirable bioweapon, and add another fantasy, that censoring the publications at Nature and Science will somehow limit programs targeting an efficiently transmitting H5N1, when in reality, the censorship will only limit those who are not actively involved in transmission experiments.
A state sponsored program would have far more resources than the two labs which demonstrated transmission In the censored papers. One lab (in the Netherlands) started with H5N1 with three changes and passaged the H5N1 in ferrets 10 times to select two additional changes. These five changes in two gene segments created an H5N1 with transmission efficiencies in ferrets that were similar to seasonal influenza, but maintained lethality. The other lab (in the United States)created a reassortant with an H5 on a pandemic H1N1 (H1N1pdm09) genetic background. This reassortant transmitted efficiently, but with a low fatality rate.
However, both of these results can be easily improved using additional combinations, which are either passed in ferrets or placed on a genetic background composed of various H1N1pdm09 genes. These state sponsored programs would use scientists familiar with the scientific literature, which details transmission experiments, as well as a vast array of H5N1 receptor binding domain changes identified in clustered H5N1 cases and/or receptor binding experiments.
Thus, the NSABB has merely elevated the interest in a bad idea (a transmitting H5N1 as a bioweapon) and attempts to limit future activities in this area by censoring the combinations used in the papers at Nature and Science, while acknowledging “some success” which effectively destroyed any benefit from the recommendation for censorship.
The 25 members of the board who voted for this recommendation should seriously consider other endeavors, because they fail to understand the true significance of the findings, which identify real bioterrorism due to the natural evolution of H5N1, which is very close to transmitting in mammals, no bioterrorists or NSABB board members required.
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dothedd
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Post by dothedd on Apr 9, 2012 20:42:07 GMT -5
H5N1 N158D Is Missing Link for Human Transmission Studies Recombinomics Commentary 20:15 April 4, 2012
The isolated viruses with two mutations in HA — N224K and Q226L — that could stick to receptors in human tracheal cells.
Kawaoka noticed that one of the ferrets he infected had especially high levels of virus in its nose. These viruses had picked up a third HA mutation — N158D — and could now spread between neighbouring ferrets. Kawaoka found that two of six healthy animals picked up infections from neighbours they had no contact with. Along the way, the virus acquired a fourth mutation — T318I.
The above comments describe the H5 changes in the clade 2.3.4 sequence from Hanoi (A/Vietnam/HN31604/2009) used in the Nature paper by Kawaoka. Media reports have noted the presence of N158D in recent human clade 2.2 cases in Egypt, but N158D was present in the initial wild bird sequences from Egypt, including the H5 sequence used by the CDC (A/egret/Egypt/1162/2006). Moreover, most clade 2.2 H5 sequences from Egypt do not have a T at position 160, so position 158 is not a glycosylation site, so the presence of N or D is not a glycosylation factor.
However, T is present at position 160 in the clade 2.1 sequence used by Fouchier (A/Indonesia/5/2005) so it is likely that this change was also found in the sequences from H5N1 collected after 10 passages in ferrets. Moreover, since N158D is also in the CDC clade 2.2, the four matches with Fouchier would be three HA changes (N158D, Q226L, and G228S), as well as PB2 E627K.
Thus, all three studies had N158D and Q226L as well as a PB2 that has been adapted to mammals. G228S was used in the CDC and Fouchier studies, and each study had one or two unique changes (CDC had Q196R, Kawaoka had N224K and T318L. while Fouchier had an undisclosed acquired change.
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dothedd
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Post by dothedd on Apr 9, 2012 20:46:39 GMT -5
Widespread H5N1 N158D Raises Pandemic Concerns Recombinomics Commentary 13:15 April 5, 2012
One of the mutations is already common in the wild, Kawaoka said, appearing in all 46 viruses isolated from people in Egypt between 2009 and 2011. "The risk is out there in nature," Kawaoka said.
The above comments on N158D are true, but suggest that the acquisition in human cases in Egypt is relatively recent. However, N158D is widespread in clade 2.2 sequences and was present in initial wild bird sequences in Egypt isolated in late 2005 (A/teal/Egypt/14051-NAMRU3/2005) and early 2006, including the egret sequence (A/egret/Egypt/1162/2006) used by the CDC in their published H5N1 transmission studies.
The presence of N158D in the early wild bird and poultry isolates in Egypt led to human cases in the spring of 2006, and these sequences had N158D. As noted in the above quote, this presence has persisted and is seen in the most recent human public sequences from Egypt.
However, this acquisition was not limited to human H5N1 cases in Egypt. Clade 2.2 clusters and cases were also reported in Turkey, Iraq, and Djibouti in early 2006 and Nigeria in 2007. These human clusters / cases also had N158D (see list here).
Moreover, a 2.2 sub-clade maintained N at position 158, but had and A at position 160 which also abolished the glycosylation site at position 158. These sequences were found in human clusters and cases from Azerbaijain in 2006 and subsequent cases in Bangladesh (see list here).
Thus, the absence of a glycosylation site at position 158 is common in clade 2.2 and has been found in human cases since the first clade 2.2 cases were confirmed in early 2006.
Virtually all H5N1 cases in Turkey, Azerbaijan, and Iraq were in clusters which contained PB2 E627K in addition to the absence of a glycosylation site at position 158. Moreover, almost all had additional receptor binding domain changes including S227N in Turkey, Q196R in Iraq. The Iraq cases also had N186S, while the Azerbaijan cases had N186K. Thus, it is likely that these changes contributed to the formation of clusters, since N158D, Q196R and PB2 E627K have been cited as key changes in recent H5N1 transmission studies by Kawaoka, Fouchier, and the CDC.
Moreover, N158D is also circulating in recent clade 2.3.2.1 wild bird infections, as well as the recent case from Shenzhen (A/Guangdong-Shenzhen/1/2011), which also had S227R and Q196K.
Thus, N158D is associated with a range of human H5N1 cases that extend well beyond recent cases in Egypt.
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dothedd
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Post by dothedd on May 2, 2012 8:55:47 GMT -5
Adaptation of Egypt H5N1 Towards Human Transmission (05/01/12 19:15)
Illinois Swine Match 2011 Human H3N2v (04/26/12 13:45)
Dynamic H3N2v Human Adaptation (04/25/12 23:15)
CDC H3N2v Detection Failures Raise Pandemic Concerns (04/21/12 13:45)
Accumulation of H5N1 Transmission Changes in Egypt (04/17/12 13:45)
Wild Birds Have Most Kawaoka H5N1 Transmission Changes (04/17/12 10:30)
2012 Match Failure Between Swine and Human (04/16/12 19:45)
Absence of Utah / West Virginia H3N2v Constellation in Swine (04/13/12 19:45)
Utah West Virginia H3N2v Match Signals Human Transmission (04/13/12 18:15)
2012 H3N2v Evolution Raises Pandemic Concerns (04/13/12 14:15)
2012 Media Myth On H3N2v Transmission (04/13/12 02:00)
H3N2v Utah Match Raises Concerns (04/12/12/ 22:15)
H3N2v in Utah Child (04/12/12 19:15) LINK TO ARTICLES:www.recombinomics.com/whats_new.html
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dothedd
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Post by dothedd on May 9, 2012 14:05:10 GMT -5
Media Myth On CDC H5N1 Transmission Recombinomics Commentary 19:15 May 3, 2012
While our paper was under review, one study14 reported that a virus with a mutant H5 HA and a neuraminidase (NA) of a human virus in the H5N1 virus background caused respiratory droplet transmission in one of two contact ferrets.
Several groups had previously reported that mutations to the binding site could make the virus switch its preference from bird to human cells. Indeed, on 5 November 2011, while NSABB was debating the wisdom of publishing the Kawaoka and Fouchier papers in full, a report appeared online in Virology that identified two such mutations. But the mutations alone still didn't make the virus transmissible between ferrets through respiratory droplets.
The above comments are from the Kawaoka Nature paper (in blue) and Science comments on the paper (in red). The Science comments are grossly misleading and suggest that the published study in Virology did not lead to transmission via droplets, which is false. The published Nature paper reveals significant similarities between the published (November 5, 2011) Virology paper and the recently released Nature paper (as well as the Ron Fouchier Science paper, which has still not been made public).
Media reports on the initial NSABB request to censor or the Nature and Science papers began in mid-November, after the CDC paper was published in Virology. The Virology paper gave a complete recipe for the creation of an H5 reassortant that transmitted in ferrets, which is the topic of the Nature paper. However, the Nature and Science papers extended the studies by selecting variants generated via passage in ferrets, which the CDC paper did not.
The CDC paper started with a 2006 egret isolate, A/egret/Egypt/1162/2006, (clade 2.2) from Egypt and added two receptor binding domain changes, Q226L and G228S which were present in H2 and H3 pandemics and have been widely cited as changes that would alter the H5 receptor binding specificity. The CDC used a receptor binding assay to identify Q196R, which in combination with the above two changes led to a shift the exclusive binding to 2.6 gal (mammalian upper respiratory tract) receptors. These three changes, on a clade 1 background (A/Vietnam/1203/2004), which also had a seasonal N2, produced droplet transmission in ferrets..
The Nature paper used an H5 from the same clade I isolate, A/Vietnam/1203/2004 (not a clade 2.3.4 isolate from Vietnam, as guessed based on recent publications by Kawaoka, which was placed on an H1N1pdm09 genetic background.
Like the Virology paper, various changes were screened in a receptor binding domain assay, and the H5 was modified with N224K and Q226L based on a shift to exclusive binding to 2,6 gal receptors. Passage in ferrets led to partial droplet transmission (similar to the Virology result) and the recovered H5 had acquired N158D, which was already present on the egret isolate. Further passage in ferrets led to the identification of the fourth H5 change, T318I, which increased transmission frequencies. Thus, the Virology paper was virtually identical to the Kawaoka result prior to further passage in ferrets.
Although the Fouchier paper in Science has not been published, media reports indicate the Fouchier study was remarkably similar to the two published studies described above. Fouchier used a clade 2.1 H5 from Indonesia (A/Indonesia/5/2005), which used the same two changes used in the Virology study (Q226L and G228S). PB2 E627K was also added, which was also done in the Virology study because the clade 1 background also has E627K. Like the Nature paper, efficient transmission was achieved through passage in ferrets, which led to the acquisition of two additional H5 changes. One of those changes is almost certainly a change like N158D which eliminates the glycosylation site, since the Indonesian isolate also has N at position 158 and T at position 160, and Fouchier has noted similarities in acquired changes due to ferret passage described in the Nature and Science studies.
Thus, the publication of the Nature papers confirms the lack of any scientific basis for the initial NSABB request, which was unanimously approved even though a transmission recipe had already been published in Virology, and the published recipe was very similar to the Nature and Science studies. Moreover, the NSABB subsequently unanimously voted to withdraw request with regard to the Nature paper, yet six members still voted to censor the Science paper, even though the recipe (three changes on a clade 2.1 background) were well known and influenza selection via ferret passage was initially described in the 1930’s and has been described and refined many times since, including the published Virology and Nature papers.
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dothedd
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Post by dothedd on Jun 25, 2012 15:07:37 GMT -5
Fouchier H5N1 Transmission Paper Published (06/22/12 12:45)
Avian Genes in Clade 2.3.2.1 H5N1 Guangdong China Isolate (06/06/12 22:15)
Clade 2.3.2.1 H5N1 Guangdong China Case (06/06/12 13:30)
Egypt H5N1 NA Sequences Acquire H1N1 Polymorphisms (05/30/12 02:15)
PAHO Silence on H1N1pdm09 Tamiflu Resistance in Mexico (05/25/12 20:30)
Widespread H1N1pdm09 Tamiflu Resistance in the United States (05/23/12 23:45)
Widespread H1N1pdm09 Tamiflu Resistance in Mexico (05/23/12 14:15)
Emergence of H1N1pdm09 Tamiflu Resistance in North America (05/19/12 19:30)
Tamiflu Resistant H1N1 Clusters Raise Concerns (05/19/12 14:15)
Transmitting D225G Tamiflu Resistant H1N1 In Texas / California (05/18/12 20:15)
H1N1 H274Y Tamiflu Resistance Spreads to California and Illinois (05/18/12 18:15)
Egypt A242T Raises H5N1 Transmission Concerns (05/17/12 16:15)
Curious Kawaoka Comments On A242T In H5N1 Ferret Transmission (05/17/12 06:30)
Media Myth On H5N1 Transmission Cookbook Recipe (05/16/12 17:30)
Clonal Expansion of 2012 H274Y in Texas and Mexico (05/15/12 15:30www.recombinomics.com/whats_new.html
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dothedd
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Post by dothedd on Jun 27, 2012 18:08:25 GMT -5
Clade 2.3.2.1 H5N1 Guangdong China Case Recombinomics Commentary 13:30 June 6, 2012
The infected child developed fever and runny nose 10 days ago in Guangdong province.
He came to Hong Kong last Saturday and sought medical attention from a private clinic in Mong Kok.
He subsequently developed a fever and convulsions and was taken to the Accident and Emergency Department of Caritas Medical Centre on Monday, where he was admitted with suspected encephalitis.
Tests later showed he has H5 Influenza A.
The above comments describe an H5N1 case (2M) from Guangdong Province who was diagnosed in Hong Kong. The diagnosis was delayed because of the unusual presentation. Subsequent sequence analysis indicated the case was clade 2.3.2.1, which is frequently identified in wild birds in southern China, as well as the most recent prior H5N1 case from Shenzhen.
Sequences from that fatal case were promptly released by the WHO regional center in Beijing. There were multiple receptor binding domain changes associated with H5N1 spread in humans.
Prompt release of the H5N1 sequences from this case would be useful.
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dothedd
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Post by dothedd on Jun 27, 2012 18:11:27 GMT -5
Fouchier H5N1 Transmission Paper Published Recombinomics Commentary 12:45 June 22, 2012
The only amino acid substitution detected upon repeated passage of both A/H5N1wildtype and A/H5N1HA Q222L,G224S PB2 E627K was T156A
T156A was detected in 89% of the A/H5N1HA Q222L,G224S PB2 E627K sequences after 10 passages, and the other 11% of sequences possessed the substitution N154K, which removes the same potential N-linked glycosylation site in HA.
The above comments from the Fouchier Science paper highlight the importance of the abolition of the glycosylation of position 158 (H3 numbering), which was identified during ferret passage of clade 2.3 (A/Indonesia/5/2005) above (in wild type of modified H5), which matches the Kawaoka result using clade 1 (A/Vietnam/1203/2004). Moreover, the abolition was also present in the clade 2.2 H5 (A/egret/Egypt/1162/2006) used in the Donis (CDC) study.
The publication of the Fouchier paper also confirmed media reports on the recipe for H5N1, which involved the two most widely discussed receptor binding domain changes (Q226L and G228S) as well as the most widely discussed PB2 change (E627K) on a clade 2.1 background which is passaged in ferrets 10X.
The publication of the Science and Nature papers raising serious competency issues with regard to the NSABB board, which should resign en mass to restore credibility to that agency.
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dothedd
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Post by dothedd on Jul 12, 2012 21:38:44 GMT -5
August Iowa Swine H3N2v Human Matches Recombinomics Commentary 12:45 June 29, 2012
The USDA and Iowa State University have released a large number of swine sequences this week (largely HA, NA, MP sequences from latter 2011 / 2012 collections). These sequences included 13 isolates which matched the initial human H3N2v cases from 2011.
The latest sequences contained the earliest (August 22. 2011) matches (A/swine/Iowa/A01202529/2011 and A/swine/Iowa/A01202530/2011) with the human H3N2v cases, which are after the first human case in July, but in the same time frame as the three Pennsylvania cases in August, 2011.
The H3 from the two isolates were identical with each other and a September 9, 2011 collection from Iowa, A/swine/Iowa/A01202878/2011, as well as previously described sequences from Illinois (A/swine/Illinois/A00857300/2011, A/swine/Illinois/A00857138a/2011, A/swine/Illinois/A00857138b/2011. Matches were also seen in the N2 and MP gene segments.
Full sequences from the previously described Illinois isolates, as well as sequences from New York (A/swine/NY/A01104005/2011) and Iowa (A/swine/Iowa/A01202640/2011) match the human H3N2v cases in all 8 gene segments, indicating this sub-clade spread rapidly in swine in the fall of 2011.
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dothedd
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Post by dothedd on Aug 10, 2012 22:41:15 GMT -5
200 H3N2v Cases In Gallia County Ohio (08/10/12 14:00)
New York Summer Camp Outbreak Raises H3N2v Concerns (08/10/12 12:30)
CDC Cedes H3N2v Confirmatory Testing To State Labs (08/10/12 11:30)
150 Tested for H3N2v Influenza A In Gallia County Ohio? (08/09/12 01:30)
Explosion of H3N2v Cases In Monroe County Indiana (08/08/12 23:15)
Explosion of H3N2v Cases In Gallia County Ohio (08/08/12 21:30)
113 H3N2v Cases In 18 Indiana Counties (08/08/12 20:30)
H3N2v Testing On Symptomatic Case Near Mason Co Fair - WV (08/08/12 18:30)
Human and Swine H3N2v Sub-clade Discordance (08/08/12 16:30)
H3N2v Case Confirmed In White County Indiana (08/08/12 01:30)
Suspect H3N2v Cases At Monroe County Fair - Indiana (08/08/12 00:45)
H3N2v Confirmed in Washington County Fair Swine (08/07/12 22:15)
Butler H3N2v Confirmed Cluster Grows To Fourteen (08/07/12 15:15)
Confirmed H3N2v Case At Ohio State Fair (08/07/12 14:15)
Confirmed H3N2v Cases At Monroe County Fair - Indiana (08/07/12 12:15)
Confirmed H3N2v Cases At Jackson County Fair - Indiana (08/06/12 02:30)
Indiana Confirmed H3N2v Cases Widespread (08/04/12 03:30)
Hawaii Match With Indiana and Ohio Signals H3N2v Pandemic (08/03/12 22:30)
Indiana Opens H3N2v Call Center As Cases Explode (08/03/12 14:30)
H3N2v Cases at Washington County Fair - Indiana (08/03/12 12:45)
H3N2v Confirmed In Swine At Ohio State Fair (08/03/12 05:15)
LaPorte and Butler County H3N2v Sequences Match (08/02/12 22:00)
Expected H3N2v Cluster Explosion in Jackson County Indiana (08/02/12 19:15)
Cited H3N2v Cases At Monroe County Fair (08/02/12 12:15)
Confirmed H3N2v Jackson County Indiana Case (08/02/12 03:00)
H3N2v Butler County Cluster Grows to 41 (08/01/12 20:00)
Ten Confirmed H3N2v Cases at Butler County Fair In Ohio (08/01/12 17:45)
H3N2v Spread In Indiana Raises Pandemic Concerns (08/01/12 13:45)
Suspect H3N2v Cluster at Monroe County Fair - Indiana (08/01/12 13:00)
Confirmed H3N2v Case in Maui Hawaii (08/01/12 12:00)
Seal H3N8 Recombination With Canine and Equine Sequences (07/31/12 22:00)
PB2 D701N In Fatal H3N8 Habor Seal Infections (07/31/12 20:30)
Evolution of a Novel Human H3N2v Sub-clade (07/31/12 12:45)
Cited H3N2v Laporte County Fair Cases Grow (07/29/12 02:45)
Emergence of a Novel Human H3N2v Sub-clade (07/28/12 23:55)
More Cited H3N2v LaPorte County Fair Cases (07/28/12 14:45)
Identical H3N2v Sequences In LaPorte County Fair Cases (07/28/12 02:30)
Repeated 2012 Media Myth On H3N2v Transmission (07/27/12 23:30)
LaPorte County Fair Cluster Matches WV/UT Cases (07/27/12 15:15)
H3N2v In Asymptomatic Swine At LaPorte County Fair (07/27/12 12:30)
Dozen Symptomatic H3N2v Cases At LaPorte County Fair (07/27/12 11:15)
Many Symptomatic H3N2v Cases At LaPorte County Fair (07/27/12 04:45)
Widespread Swine H3N2v Matches With US Cases (07/27/12 03:30)
H3N2v In Symptomatic Swine At LaPorte County Fair (07/27/12 00:45)
H3N2v Transmission At LaPorte County Fair (07/26/12 23:30)
H3N2v Cluster At Indiana County Fair (07/26/12 22:30)
Swine H3N2v Matches With Current Human Cases (07/25/12 23:55)You can read each article on the LINK: www.recombinomics.com/whats_new.html
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dothedd
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Post by dothedd on Aug 14, 2012 14:18:12 GMT -5
23 Confirmed H3N2v Cases In Washington County Indiana (08/14/12 18:00)
Sustained Efficient Human Community Spread of H3N2v (08/14/12 14:45)
CDC H3N2v Testing Bias Raises Pandemic Concerns (08/14/12 11:15)
H3N2v Ohio Cases Increase To 47 In 11 Counties (08/13/12 23:15)
CDC Ignores NA Lineage Change In All 2012 H3N2v Cases (08/13/12 21:15)
CDC Cites Recent H3N2v Human Transmission (08/13/12 14:00)
CDC False Statements on Swine H3N2v Matches Raise Concerns (08/13/12 05:30)
Patient Zero In The 2011 H3N2v Pandemic (08/12/12 11:00)
H3N2v Testing Halt In Champaign County Ohio (08/11/12 09:00)Read the reports: www.recombinomics.com/whats_new.html
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dothedd
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Post by dothedd on Aug 17, 2012 15:29:34 GMT -5
H3N2v Ohio Cases Increase to 79 in 21 Counties (08/17/12 20:00)
10 H3N2v Cases In Huntingdon County Pennsylvania (08/17/12 16:45)
10 More H3N2v IN and OH Cases Match Novel WV Sub-Clade (08/16/12 22:30)
H3N2v Ohio Cases Increase to 72 in 20 Counties (08/16/12 20:00)
Likely H3N2v In Ashland Kentucky Without Swine Exposure (08/16/12 15:45)
CDC Obfuscation of H3N2v Sub-clade In 2012 Human Cases (08/16/12 13:45)
H3N2v Jumps from Gallia Ohio To Mason County West Virginia (08/16/12 02:00)
H3N2v Confirmed in Washtenaw County Michigan (08/15/12 23:30)
Hospitalized Ohio H3N2v Cases Raise Concerns (08/15/12 20:00)
H3N2v Ohio Cases Increase to 66 in 17 Counties (08/15/12 18:45)
Release of Illinois H3N2v Sequences Overdue (08/15/12 14:30)
California H3N2v Health Alert - PCR Testing of All ILI Cases (08/15/12 02:30)
H3N2v Ohio Cases Increase to 54 in 12 Counties (08/14/12 20:15)You can read each article on the LINK: www.recombinomics.com/whats_new.html
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dothedd
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Post by dothedd on Aug 22, 2012 16:47:18 GMT -5
H3N2v Ohio Cases Increase to 95 in 23 Counties (08/22/12 20:30)
H3N2v Heterogeneity Concerns In Jackson County Indiana (08/22/12 17:00)
HPA Recommends H3N2v Screening of US Travelers to UK (08/22/12 13:30)
ECDC H3N2v Risk Assessment Still Fatally Flawed (08/22/12 12:30)
CDC Retraction of H3N2v / H3N2pM Pseudolinkage Overdue (08/22/12 10:45)
CIDRAP Media Myth On H3N2v Matches In Ohio Swine (08/22/12 03:00)
CDC Expands H3N2v Tests To ILI Cases Without Swine Exposure (08/21/12 22:45)
Swine To Human Transmisison Not Supported By USDA Data (08/21/12 21:15)
H3N2 NA N234D In Laporte and Butler County Clusters (08/21/12 11:15)
H3N2v Cluster Linked To Dakota County Minnesota (08/20/12 22:15)
H3N2v Ohio Cases Increase to 87 in 21 Counties (08/20/12 20:15)
More CDC Obfuscation On Human / Swine H3N2v Sub-Clades (08/20/12 15:45)
H3N2v Coles County Cases Increase In Illinois (08/18/12 02:45)
Six H3N2v Cases In Queen Anne's County Maryland (08/17/12 21:30)
H3N2v Ohio Cases Increase to 79 in 21 Counties (08/17/12 20:00)
10 H3N2v Cases In Huntingdon County Pennsylvania (08/17/12 16:45)
10 More H3N2v IN and OH Cases Match Novel WV Sub-Clade (08/16/12 22:30)
H3N2v Ohio Cases Increase to 72 in 20 Counties (08/16/12 20:00)
Likely H3N2v In Ashland Kentucky Without Swine Exposure (08/16/12 15:45)
CDC Obfuscation of H3N2v Sub-clade In 2012 Human Cases (08/16/12 13:45)
H3N2v Jumps from Gallia Ohio To Mason County West Virginia (08/16/12 02:00)
H3N2v Confirmed in Washtenaw County Michigan (08/15/12 23:30)
Hospitalized Ohio H3N2v Cases Raise Concerns (08/15/12 20:00)
H3N2v Ohio Cases Increase to 66 in 17 Counties (08/15/12 18:45)
Release of Illinois H3N2v Sequences Overdue (08/15/12 14:30)
California H3N2v Health Alert - PCR Testing of All ILI Cases (08/15/12 02:30)
H3N2v Ohio Cases Increase to 54 in 12 Counties (08/14/12 20:15)
23 Confirmed H3N2v Cases In Washington County Indiana (08/14/12 18:00)
Sustained Efficient Human Community Spread of H3N2v (08/14/12 14:45)
CDC H3N2v Testing Bias Raises Pandemic Concerns (08/14/12 11:15)
Commentary
ECDC H3N2v Risk Assessment Is Still Fatally Flawed Recombinomics Commentary 12:30 August 22, 2012
As transmission of the disease is mainly related to direct contact with infected pigs, travellers to the affected states in the USA who have contact with pigs in farms or visit agricultural exhibitions may be at risk of being infected. In case they develop influenza-like symptoms after swine exposure, clinicians should consider and sample for the influenza A(H3N2)v viruses.
The above comments from the August 20, 2012 ECDC risk assessment fails to address the heavy sample bias in the CDC data. The recent release of details of the USDA H3N2pM cases indicates that the data has already been made public at Genbank and the sequence data in H3N2pM reveals a dominance of the sub-clade found in the first 10 human cases in 2011. However, there have been no reported 2012 H3N2v cases involving this sub-clade in spite of widespread detection in swine in 2012.
All of the 2012 H3N2v represent a novel sub-clade first reported in West Virginia in late 2011, which is rarely detected in H3N2pM.
Thus, the above ECDC risk assessment is still fatality flawed because of the focus on swine to human transmission.
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dothedd
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Post by dothedd on Aug 22, 2012 17:06:04 GMT -5
Commentary
Fatally Flawed ECDC H3N2pdm11 Risk Assessment Recombinomics Commentary 22:00 November 29, 2011
The public health importance of swine influenza is twofold. Firstly there is the direct risk of infection for those coming into close contact with pigs or through limited human-to-human transmission. Triple reassortant swine influenza viruses with avian, human and swine genes have been circulating in pigs in the US, and have been transmitted to humans. This is now also the case for the triple reassortant viruses with the additional A(H1N1) M-gene [1]. However, none of these reassortant viruses has been able to maintain themselves in the human population and, in addition, there have been no large clusters of infection. The second risk is of reassortment to produce a novel virus (possibly a strain with pandemic potential), either in the pig or in the human host, by co-infection with a human and a swine strain. The pandemic A(H1N1)pdm09 influenza virus is so far the only swine-origin virus that has shown the capacity to spread readily and extensively between humans. However, it demonstrates that this is a possibility.
The above comments are from the European (ECDC) risk assessment for “Swine-origin triple reassortant influenza (H3N2) viruses in North America, which is largely focused on swine. It notes shortfalls in swine surveillance in North America and Europe and cites a need for more surveillance (European swine surveillance is beyond abysmal).
The report acknowledges the technical difficulties in the detection of H3N2pdm11 (trH3N2 with an H1N1 M gene), even with PCR detection kits that include H1N1pdm09 H1 and NP targets, and the need for sequence confirmation (which is conclusive even when partial sequences are generated).
However, the report is overly focused on the swine aspects of the pandemic and fails to note that the CDC has only published sequences for 12 patients under the age of 10 who tested as influenza A samples collected since July, 2011.
Although the report notes the importance of testing children, since 9 of the 10 cases in the US are under 10 years of age, it fails to note that 9 of the 12 cases (75%) are H3N2pdm11 positive, signaling a serious surveillance failure that has created the illusion that the virus is not transmitting in a sustained manner.
The group appears to be seriously phylogenetically challenged because the sequence data is not a puzzle and clearly demonstrates sustained transmission of H3N2pdm11.
Therefore, the ECDC risk assessment for H3N2pdm11 is fatally flawed.
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dothedd
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Post by dothedd on Aug 24, 2012 23:07:56 GMT -5
CDC Acknowledges H3N2v Human to Human Transmission (08/24/12 21:00)
CDC H3N2v Sub-Clade Secret Raises Pandemic Concerns Recombinomics Commentary 14:30 August 24, 2012
What is H3N2v?
H3N2v is a new flu virus that is currently infecting both pigs and humans in the United States, including Pennsylvania. Although rare, the virus can spread from pigs to people and from people to pigs. This new virus is different from previous H3N2 human infections because it also contains part of the 2009 H1N1 virus. It is the same virus we saw in three ill people who had all attended the Washington County Fair last year in Pennsylvania.
The above description is from the Pennsylvania Department of Health Q&A page on H3N2v. Pennsylvania is currently reporting 31 H3N2v cases (6 confirmed and 25 probable) in at least three counties. However, the description of H3N2v uses a broad definition of the H3N2v with the H1N1pdm09 M gene, which first appeared in an Indiana case in July 2011 (A/Indiana/08/2011). This version was identified in the first 10 human cases in 2011, including the three at the Washington County Fair (A/Pennsylvania/10/2011, A/Pennsylvania/11/2011, A/Pennsylvania/12/2011). This sub-clade has subsequently been found in swine in many states, including four June, 2012 isolates in Ohio.
However, there have been no reported human cases involving this sub-clade since the November 2011 cluster in Iowa, which involved three confirmed cases (all attended the same day care center), A/Iowa/07/2011, A/Iowa/08/2011, A/Iowa/09/2011) and two suspect cases (untested but symptomatic father and brother of the index case). This cluster had no swine contact or exposure and the transmission at the day care center (as well as within the family) clearly demonstrated the ability of this sub-clade to transmit human to human (which was confirmed by virtually identical sequences in all three cases). However, in spite of widespread detection of this sub-clade in swine in 2012, none of the 2012 sequences released to date (from Utah, Hawaii, Indiana, and Ohio), match this earlier sub-clade, which destroys the CDC position that H3N2v frequently spreads from swine to human.
All of the human 2012 H3N2v sequences released to date match the sub-clade first detected at a Mineral County day care center in West Virginia (A/West Virginia/06/2011 and A/West Virginia/07/2011) where there was also no swine exposure or contact. The disease onset dates between the two confirmed cases was two weeks apart and the index cases was initially confirmed while hospitalized. Thus, the index case did not infect the classmate. Instead, that infection was due to human to human transmission at the day care center as indicated by an epidemiological investigation which initially identified ILI (influenza-like illness) in 23 of the 70 contacts of the index case.
The sub-clade in West Virginia was easily distinguished from the earlier cases because the N2 had been acquired via reassortment and represented a different linage one that had been evolving in H3N2 swine, instead of evolution in H1N2 swine, which was the lineage of the first 10 human cases. These two lineages are easily distinguished and can be classified within seconds of blast the full or partial N2 sequences. That BLAST approach well generate at match with the first 10 human H3N2v cases in 2011, or the 20 human H3N2v cases since the Iowa cluster (the last two sequences in 2011 and all 18 sequences from 2012.
Thus, swine sequences can be easily classified into the two sub-clades using the HA, NA, and MP sequences, which are represented in all sequences released by the USDA. A summary of the USDA data was posted on the CDC website, which cited 138 H3N2 sequences since October 1, 2011 (FY2012), which included 57 with an H1N1pdm09 M gene (which these CDC is now calling H3N2pM). USDA sequences at Genbank collected in FY2012 total 67, with 45 designated as H3N2pM. The 12 case difference between the public sequences, which go through June, and the USDA cases which go through the end of July, are the likely the 12 swine isolates from the LaPorte County Fair, where there have been at least 5 confirmed H3N2v cases and more than a dozen who were symptomatic and therefore would be classified as probable using the new CDC guidelines. Thus, it is likely that the 12 recent swine cases were due to human to swine transmission.
However, the 45 public H3N2pM sequences provide clear data on the USDA surveillance of US swine. These sequences represent all of the USDA data on H3N2pM isolates from collections through June, 2012. 19 of these sequences have an H3 lineage that matches the 2011/2012 human H3N2v cases, but only two match the recent lineage identified in humans. Thus, the CDC claim that the H3N2v in the 2012 cases has been detected by the USDA in many states is false. The N2 match for H3N2pM is limited to a February isolate from North Carolina and a May isolate from Indiana. The CDC statement is only accurate if the N2 differences are ignored.
Thus, the CDC and USDA sequence data thoroughly refutes the CDC position. The 2011 sub-clade is widespread in swine in 2012, but has produced no 2012 human cases, while the 2012 sub-clade is rare in swine but has produced all of the 2012 human cases (as well as the 2011 West Virginia cluster).
Therefore, for the CDC to maintain its frequent swine to human position, the sub-clade differences are kept secret, leading to misstatements such as the quoted statement by the Pennsylvania Department of Health claiming a match between the 2012 cases in Huntingdon County and the 2011 cases in Washington County.
The CDC sub-clade secret remains hazardous to the world’s health and hides the serious pandemic potential of the 2012 sub-clade, which has acquired NA N234D, which is in all of the cases from the Laporte and Butler County Fairs.
CONTINUED: www.recombinomics.com/whats_new.html
CDC H3N2v Sub-Clade Secret Raises Pandemic Concerns (08/24/12 14:30)
H3N2v Pennsylvania Cases Increase to 31 in 3 Counties (08/24/12 12:00)
H3N2v Ohio Cases Increase to 98 in 23 Counties (08/23/12 21:00)
Curious H3N2 Cluster In Tri-State (KY/WV/OH) Area (08/23/12 20:30)
H3N2v Ohio Cases Increase to 95 in 23 Counties (08/22/12 20:30)
H3N2v Heterogeneity Concerns In Jackson County Indiana (08/22/12 17:00)
HPA Recommends H3N2v Screening of US Travelers to UK (08/22/12 13:30)
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dothedd
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Post by dothedd on Aug 25, 2012 9:10:02 GMT -5
Wisconsin and Pennsylvania H3N2v Match WV Sub-Clade Recombinomics Commentary 04:45 August 25, 2012
The CDC has released 8 more sets of H3N2v sequences (at GISAID). Six of the sequences are from Indiana samples collected in late July (A/Indiana/14/2012 and A/Indiana/16/2012) or early August (A/Indiana/43/23012, A/Indiana/46/23012, A/Indiana/49/23012, A/Indiana/52/23012). One sample is from Wisconsin (A/Wisconsin/22/2012 collected August 13) and one from Pennsylvania (A/Pennsylvania/13/2012 collected August 15). All are closely related to each other and match the sub-clade first reported in the West Virginia day care cluster, which had no swine exposure or contact and 23 of the contacts of the index case had ILI.
This sub-clade has only been reported in 2 swine isolates. In contrast, the H3N2v sub-clade identified in the first 10 cases in 2011 is widespread in 2012 swine isolates, but has caused no reported human cases since the Iowa cluster in November, 2011, casting serious doubt on swine to human transmission as a common mechanism for the reported human infections.
Instead, the finding that all 26 2012 isolates from 6 states (Utah, Hawaii, Indiana, Ohio, Wisconsin, Pennsylvania) match the 2011 West Virginia sub-clade, signals human to human transmission, which is detected by the CDC in their heavily biased testing of cases with swine exposure. Although this approach has identified a large number of human cases, it has failed to identify the true extent of spread in the US population, such as the “seasonal” H3 cases in Kentucky and West Virginia in counties adjacent to the large cluster in Gallia County.
The CDC’s refusal to answer direct questions about this cluster suggests they are well aware of H3N2v community transmission.
Disclosure of the sequences from these “seasonal” H3 cases is long overdue, as is a critical evaluation of the CDC RT-PCR kit’s rate of misdiagnosing H3N2v cases as seasonal H3N2.
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dothedd
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Post by dothedd on Aug 25, 2012 9:13:46 GMT -5
CDC Prepares to Pivot To H3N2v Community Transmission Recombinomics Commentary 07:15 August 25, 2012
“The guidance document is a heads up for schools to be aware of, and on the look-out for, illness with this virus,” Bresee explains. In 2011, there was at least one documented outbreak of H3N2v in a day care setting.
“It’s important to remember that this is an evolving situation that could change quickly,” Bresee notes. “We’re constantly looking at our data and re-evaluating.”
The above comments from the August 24 CDC H3N2v update, which acknowledges “limited” human to human transmission, mentions the West Virginia day care center cluster, as the CDC prepares to admit community transmission.
However, the CDC focus on pseudo-linkage to swine, and a failure to acknowledge the limited detection of the West Virginia sub-clade in swine, will delay a full understanding of the community spread, which has been largely ignored because of the focus on agricultural fairs.
Media continues to focus on swine to human spread, which has no real support, since the H3N2v sub-clade found in the first 10 cases in 2011 is widespread in swine, but has not caused any reported human cases in 2012.
The CDC should acknowledge community spread in Boyd County, Kentucky and Mason County, West Virginia, where H3 has been confirmed in children with no swine exposure. Ashland-Boyd County Health Department issued a press release and the Kentucky Department of Health issue a health alert on seasonal H3N2, yet neither will answer questions about CDC confirmation, which is also true for the CDC.
An outbreak of seasonal H3N2 in children in August in Kentucky near the Gallia Junior County Fair, were there were over 200 probable H3N2v cases (including 11 confirmed cases) is unlikely, and the refusal of the above agencies to answer questions on confirmation raise serious pandemic concerns, which have not been transparently addressed by the CDC.
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Aman A.K.A. Ahamburger
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Viva La Revolucion!
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Post by Aman A.K.A. Ahamburger on Aug 25, 2012 23:25:42 GMT -5
2013 is going to be one interesting year Dot.. Thanks for all the info!
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dothedd
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Post by dothedd on Aug 31, 2012 19:55:02 GMT -5
2013 is going to be one interesting year Dot.. Thanks for all the info! It is indeed Aham.
Pandemic Politics comes to mind.
dot
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dothedd
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Post by dothedd on Aug 31, 2012 20:10:37 GMT -5
H3N2v H2H Clonal Expansion Raises School Concerns (08/31/12 23:55)
Recent Seasonal H3N2 Cases Raise Pandemic Concerns (08/31/12 22:30)
First Confirmed H3N2v Death - Ohio (08/31/12 18:30)
Human Clonal Expansion of July/August H3N2v (08/31/12 14:30)
18 H3N2v Wisconsin Cases In 4 Counties (08/31/12 05:30)
Seven H3N2v Cases In Manitowoc County Wisconsin (08/31/12 00:15)
Wisconsin H3N2v Cases Increase To 18 (08/30/12 20:15)www.recombinomics.com/whats_new.html
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dothedd
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Post by dothedd on Sept 2, 2012 13:31:27 GMT -5
Ohio H3N2v Cases Increase to 102 in 25 Counties (09/02/12 09:45)
Kentucky H3N2v Case Raises Serious Pandemic Concerns (09/01/12 23:55)
Three H3N2v Case Cluster in Somerset County Pennsylvania (09/01/12 04:30)
Three H1N2v Case Cluster In Minnesota (09/01/12 02:30)CONTINUED: www.recombinomics.com/whats_new.html
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dothedd
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Post by dothedd on Sept 3, 2012 12:41:25 GMT -5
Kentucky H3N2v Matches Clark County Ohio Recombinomics Commentary 13:00 September 3, 2012
The recently released CDC H3N2v sequences included those from an August 5 isolate from Kentucky, A/Kentucky/11/2012. Although all of the July / August H3N2v (41 sets of sequences from Hawaii, Indiana, Ohio, Illinois, Kentucky, Maryland, Michigan, Minnesota, Pennsylvania, West Virginia, Wisconsin) are closely related to each and represent human to human clonal expansion of sequences first reported for the 2011 outbreak at the day care center in Mineral County, West Virginia (A/West Virginia/06/2011 and A/West Virginia/07/2011) and the first 2012 isolate, A/Utah/10/2012, the sequences cluster into sub-clades within the larger sub-clade. The 2011 West Virginia cluster included 23 ILI cases in the index case contacts, which also had no swine contact or exposure.
The H3 sequence from Kentucky clusters with the Ohio sequences from Clark County, A/Ohio/23/2012, as well as two early isolates from Indiana (A/Indiana/59/2012 and A/Indian/60/2012). This clustering provides further support for the human expansion.
Neither Kentucky nor the CDC has acknowledged H3N2v cases in Kentucky. Kentucky denies H3N2v ii its August 16 press release and health alert, which describe the detection of seasonal H3N2 in children in Ashland, Kentucky, which is in Boyd County. These cases were initially tested by local practitioners because of the massive outbreak at the Gallia Junior County fair in southeastern Ohio. In addition to the 200 cases in Ohio, the three H3N2v cases in Mason County, West Virginia were from cases who also attended Gallia fair, and sequences from one of these cases, A/West Virginia/15/2012, were also released by the CDC, and these sequences matched the first case from Jackson County, Indiana, A/Indiana/12/2012 or A/Indiana/13/2012 (as well as additional sequences from Indiana), which were distinct from the Kentucky sub-clade, suggesting the Kentucky case was not linked to Gallia fair.
The Kentucky sequence raises concerns that many of the 188 seasonal H3N2 cases in weeks 31-33 reported in the week 34 FluView represent multiple H3N2v isolates with no swine contact, representing widespread community transmission.
Kentucky and the CDC have failed to respond to repeated inquiries regarding the sequence confirmation of the “seasonal” H3N2 cases reported on August 16.
Answers to that question, as well as detail on the case linked to the Kentucky/11/2012 sequence, would be useful.
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dothedd
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Post by dothedd on Sept 3, 2012 12:54:34 GMT -5
Gallia Ohio H3N2v Matches Jackson County Indiana Recombinomics Commentary 19:30 September 3, 2012
The recently released CDC H3N2v sequences included those from an August 9 isolate from West Virginia, A/West Virginia/15/2012. Although all of the July / August H3N2v (41 sets of sequences from Hawaii, Indiana, Ohio, Illinois, Kentucky, Maryland, Michigan, Minnesota, Pennsylvania, West Virginia, Wisconsin) are closely related to each and represent human to human clonal expansion of sequences first reported for the 2011 outbreak at the day care center in Mineral County, West Virginia ((A/West Virginia/06/2011 and A/West Virginia/07/2011)) and the first 2012 isolate, A/Utah/10/2012, the sequences cluster into sub-clades within the larger sub-clade. The 2011 West Virginia cluster included 23 ILI cases in the index case contacts, which also had no swine contact or exposure.
West Virginia has reported three confirmed H3N2v cases and media reports indicate all three were from Mason County and attended the Gallia Junior County Fair in adjacent Gallia County in Ohio. There the 2012 West Virginia sequence represents the first public sequences from the outbreak, where hundreds of attendees had influenza-like illness. 200 of the cases were tested in Ohio with an influenza A rapid test, and 69 were positive. A subset of the positives were RT-PCR tested, and 12 confirmed cases from Gallia County have been reported by the Ohio Department of Health, which are in addition to the three cases reported by the West Virginia Department of Health and Human Resources.
The HA and NA sequences from A/West Virginia/15/2012 are identical to the first two sequences from Indiana (A/Indiana/12/2012 and A/Indiana/13/2012) following the four sequences from the Laporte outbreak (A/Indiana/06/2012, A/Indiana/07/2012, A/Indiana/08/2012, A/Indiana/09/2012). The positive samples fropm LaPorte led to increased surveillance in Indiana. However, prior to the LaPorte outbreak there was ILI in Jackson County, but these cases were not tested. The first 11 confirmed cases in Indiana included 5 from LaPorte and 4 from Jackson County. Thus, the West Virginia Gallia sequences match H3N2v in Jackson County, which was heterogeneous, signaling the prior human transmission.
In addition to the Gallia cases adjacent to Mason County, the Kentucky Ashland-Boyd reported ILI in children which were influenza A positive. These cases were reported as seasonal H3N2 and a press release and health alert were issued. However, the CDC released an H3N2v sequence, A/Kentucky/2012, which was collected August 5, consitent with the ILI cases, suggesting that the cases designated seasonal H3N2 based on the CDC RT-PCR test, were actually H3N2v cases, which is also likely true for many of the 188 seasonal H3N2 noted for weeks 31-33 in the week 34 FluView. The Kentucky sequence was distinct from the West Virginia sequence from Gallia.
Detail on the Kentucky cases and sequence testing of the 188 H3N2 ¡§seasonal¡¨ cases would be useful. The Kentucky sequence, and additional cases mis-characterized as seasonal H3N2 would represent conclusive evidence of sustained community transmission of H3N2v.
NOTE: Rockville, MD ¡V February 19, 2009 NOVAVAX (NASDAQ: NVAX) announced today favorable preclinical results for a new broadly immunogenic pandemic influenza virus-like particle (VLP) vaccine candidate that provided protection against several H5N1 virus strains. Results of a study conducted by a research group at The University of Hong Kong through a collaboration with Novavax, Inc. showed 100% survival of mice immunized with this broadly protective H5N1 VLP vaccine candidate. The H5N1 VLP contains three proteins, hemagglutinin (HA), neuraminidase (NA), and matrix 1 (M1), which are considered important for inducing protection against influenza infection and severe disease. This new influenza VLP, which was constructed and produced at Novavax, was uniquely designed to provide broad protection against several clades (or strains) of H5N1 avian influenza. In simple terms, the HA surface protein of this new VLP was modified to include the protein building blocks from several different H5N1 strains. This resulted in an immune response against several different H5N1 strains and may be a new approach to making broadly protective influenza vaccines.
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dothedd
Senior Member
Joined: Dec 27, 2010 20:43:28 GMT -5
Posts: 2,683
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Post by dothedd on Sept 17, 2012 11:54:17 GMT -5
Ohio H3N2v Cases Increase to 106 In 25 Counties (09/15/12 23:45)
H3N2v Community Transmission In Michigan? (09/15/12 11:00)
Missouri H1N1v Case Raises Concerns (09/14/12 17:15)
H3N2v Cases Linked to Minnesota State Fair (09/13/12 22:00)
CDC Human / Swine H3N2v Discordance Caught On Tape (09/12/12 19:30)
Wisconsin H3N2v Cases Increase to 20 (09/12/12 17:00)
More 2012 Swine H3N2pM Matches With 2011 Human Cases (09/12/12 16:00)
CDC Cites 10 Examples of Human H3N2v Transmission (09/11/12 22:30)
Wisconsin H3N2v Cases Increase to 19 (09/10/12 23:30)
PCR pdmInfA Negative = No H3N2v Community Transmission? (09/07/12 15:30)
Pennsylvania H3N2v Cases Increase to 41 in 5 Counties (09/06/12 22:45)
CDC In H3N2v Sequence Denial (09/06/12 21:30)
Pennsylvania H3N2v Cases Increase to 39 in 5 Counties (09/06/12 16:15)
H3N2v Sequences Refute CDC Swine Exposure Message (09/06/12 15:00)
LaPorte Human and Swine H3N2v Do Not Match (09/05/12 23:55)
LaPorte H3N2v Swine Match 2011 West Virginia Sub-Clade (09/05/12 12:00)
Pennsylvania H3N2v Cases Increase to 38 Cases In 5 Counties (09/04/12 21:15)
Minnesota H1N2v Has 2011 H3N2v Genes Including MP (09/04/12 01:15)
Hospitalized H3N2v Cases Identify Community Transmission (09/03/12 22:45)
Lake County Ohio H3N2v Without Swine Exposure (09/03/12 19:45
www.recombinomics.com/whats_new.html
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dothedd
Senior Member
Joined: Dec 27, 2010 20:43:28 GMT -5
Posts: 2,683
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Post by dothedd on Oct 24, 2012 19:42:11 GMT -5
Novel Michigan H3N2v Case With PB1 E618D (10/18/12 14:30)
H3N2v Transmission At 2011 Washington County Fair (10/11/12 20:00)
Increased Discordance Between Human and Swine H3N2v (10/09/12 01:15)
Michigan H3N2v Cases With PB1 E618D and H1N1pdm09 M Gene (10/04/12 20:45)
Ohio H3N2v Swine With PB1 E618D and H1N1pdm09 M Gene (10/01/12 19:45)
H1N1v Case In Ontario Canada Has H1N1pdm09 M Gene (10/01/12 11:45)
Human Betacornavirus 2c EMC/12 - Human SARS CoV Match (09/28/12 20:30)
CDC Describes 11 Hospitalized H3N2v Ohio Cases (09/27/12 19:15)
Wisconsin Mink H3N2v Matches Human 2011 Cases (09/26/12 23:45)
H3N2v Cases In Ohio Increase To 107 In 25 Counties (09/26/12 16:00)
Five Suspect London1 Coronavirus Cases In Denmark (09/26/12 13:00)
London1 Novel CoV 2012 nsp12 Coronavirus Sequence (09/26/12 01:00)
Acute Renal Failure In 2003 Probable SARS CoV Cases (09/25/12 22:15)
Acute Renal Impairment In 2003 SARS CoV Cases (09/25/12 20:30)
H1N1v Case In Ontario Canada (09/25/12 16:00)
Saudi Arabia SARS-CoV Case Fatality Rate Raises Concerns (09/25/12 13:00)
Saudi Arabia SARS-CoV Cluster Raises Concern (09/25/12 11:45)
Saudi Arabia SARS-CoV Closely Related to Bat Coronavirus (09/24/12 23:15)
Saudi Arabia SARS-CoV Causes Concerns (09/24/12 20:45)
Swine H3N2v Matches With LaPorte and Butler Cases (09/19/12 16:15)
Korea H1N2v Ferret Transmission (09/18/12 23:00)www.recombinomics.com/whats_new.html
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Colleenz
Senior Member
Joined: Dec 20, 2010 8:56:39 GMT -5
Posts: 3,983
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Post by Colleenz on Oct 24, 2012 19:58:34 GMT -5
Hi Dot
Can I help?
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dothedd
Senior Member
Joined: Dec 27, 2010 20:43:28 GMT -5
Posts: 2,683
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Post by dothedd on Oct 25, 2012 19:07:13 GMT -5
Thank you for asking, Colleenz, but life has its challenges that we all have to get through.
GOD BLESS AMERICA!
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