THE SNEEZE THAT SHOOK THE WORLD

IT killed up to 100 million and devastated the world economy. But how did Spanish flu – which features in the climax to TV drama Downton Abbey this weekend – spread so fast?

TOWARDS the end of 1918, a new nursery rhyme started to be heard in playgrounds across Britain, sung by skipping schoolchildren: "I had a bird, its name was Enza. I opened the door and in-flu-enza." Like many such rhymes its chirpy cadence hid a far more macabre reality.

Its subject was the Spanish flu outbreak of the same year, a disease so virulent that it was responsible for the deaths of between 50 million and 100 million people worldwide, killing more men and women than any other single outbreak of disease to hit mankind – more even than the Black Death.

Tearing through a world still reeling from the horrors of the First World War, it hit households already grieving the loss of loved ones on the b­attlefields and in the trenches. Over two winters it claimed the lives of around five times as many people as the conflict – one of the deadliest wars in history. A third of the world's population became infected, piling tragedy upon tragedy.

Now viewers of the ITV drama Downton Abbey will be reminded of the disease in this Sunday’s series finale. Last week’s episode already gave a taster, showing a glimpse of Cora, Countess of Grantham, played by Elizabeth McGovern, laid low with the symptoms while her family gathered around her sick bed. In the 90-minute programme, the flu is expected to sweep through Downton, affecting both upstairs and downstairs.

Whether we will discover who survives by the end of the episode remains to be seen but while some of this series’ plot lines have been criticised for galloping along at an amazing rate, in this particular case rapidity would be entirely factual.

In 1918, the virus struck with fearsome speed, often killing its victims within hours of the first signs of infection. Eyewitness accounts of the time describe how a commuter began to cough and never made it home and how four women sat down to play bridge one evening and three were dead by the morning.

Jakarta Residents should be wary consume chicken. Therefore, 80 percent of shelters where poultry infected with avian influenza virus show.

Until now undertaken efforts to address Jakarta Governor Fauzi Bowo related to this issue is still very minimal.

Head of Operational Office Indonesia-Dutch Partnership on Highly Pathogenic Avian Influenza (HPAI-IDP), Ivo Claassen, said, based on surveillance in some poultry shelter facilities in Jakarta and the results of research conducted in 2007 and repeated again in 2009, showed 80 percent of the houses shelter these birds infected with avian influenza virus.

"The results of this study we have given to the government of DKI Jakarta. This became the basis for restructuring. But for some reason, the improvement was not so done. So, the situation has not changed," said Ivo told the press at the close of the IDP-HPAI project on Wednesday ( 11/02/2011).

According to him, in fact the source of the virus exists outside of Jakarta. However, the virus was brought to Jakarta for the distribution system that is not true that birds spread the Jakarta area.

"It's a matter of marketing chains that should receive immediate treatment," he explained.
Chairman of the Control Unit and the Control of Avian Influenza Ministry of Agriculture, M Azhar said the results of research that the government of Jakarta has been given a recommendation.

One was to make regulations regarding the prohibition of live birds enter into Jakarta. In the field realization is to make integrated slaughterhouse.
"Capital regulation restrukurisasi make poultry market chain, although not yet optimal path. The strategy places relocated poultry pieces making it easier to control and reduce risk, is currently being pursued," he said.

http://www.tribunnews.com/2011/11/02/80-penampungan-unggas-di-jakarta-terinfeksi-flu-burung

Recombinomics Commentary 12:45
November 1, 2011
 The CDC has released sequences (at GISAID) for new trH3N2 cases in Indiana, A/Indiana/11/2011, and Maine, A/Maine/07/2011.  Full sequences from the Indiana case (59M collected September 22) indicate all 8 gene segments are closely related to the five prior 2011 trH3N2 cases.  Partial sequences (HA, NP, MP) from the Maine case (8M collected September 24) indicate it is also closely related to the prior human isolates from 2011.  The CDC is again commended for the rapid release of these important sequences.

These sequences leave little doubt that the novel trH3N2 human contagion is transmitting in humans.  More detail on swine contacts would be useful.  However, it is clear that trH3N2 in humans is far more common than indicated by the seven trH3N2 cases. 

A recent CDC paper describes fatal unsubtyables in the 2009/2010 season, which may represent additional trH3N2 cases which have not yet been confirmed.

Three October trH3N2 Maine and Indiana Cases Match
Recombinomics Commentary 16:45
November 1, 2011

The CDC has released two more sets of trH3N2 sequences from recent cases and once again the CDC is commended for the rapid release of sequences from these October cases.  The two cases (A/Indiana/11/2011 and A/Maine/07/2011) were collected two days apart (October 22 and October 24), but are closely related to each other, as well as the Maine case, A/Maine/06/2011, also collected in October (October 10, 2011).  The close relationship between all three October cases strongly supports human transmission, which is further supported by the close relationship between all seven of the 2011 cases, which are distinct from all swine isolates.

Thus, the human cases form two branches, those collected in July and August (A/Indiana/08/2011, A/Pennsylvania/09/2011, A/Pennsylvania/10/2011, A/Pennsylvania/11/2011) forming one branch, and those collected in October (A/Maine/06/2011, A/Indiana/11/2011, A/Maine/07/2011) forming another. 

The close relationship between isolates from different states also supports human transmission.

Similarly, the first Maine case was from Cumberland County and he had attended an agricultural fair prior to disease onset on October 7.  This fair was likely the Cumberland County fair, which ended October 2 and therefore was an unlikely source for the more recent Maine case, whose trH3N2 came from a sample collected two weeks after the first Maine case.  Moreover, the Indiana case is not likely to have been linked to the two cases in Maine.

The bizarre reporting of early unsubtypables suggested additional cases without swine “exposure” would be reported. 

Detail on swine exposure for the two latest cases would be useful.

Recombinomics Commentary 12:25
October 31, 2011
CDC has confirmed the fifth case of human infection with a swine–origin influenza A (H3N2) virus that carries the M gene from the 2009 H1N1 virus. This virus was first detected in a child in Indiana in July.  Subsequently three additional cases of human infection with swine–origin influenza A (H3N2) viruses carrying the same genetic change were detected in Pennsylvania. Though rare, human infections with swine–origin influenza viruses can occur, usually after close contact with infected swine.

The acquisition of the M gene likely occurred as a result of swine being co–infected with the swine influenza A (H3N2) virus and the human 2009 H1N1 virus. While we know the M gene plays a role in influenza virus infection, assembly and replication, the significance of this change in these swine–origin influenza A (H3N2) viruses is unknown at this time. CDC continues to investigate the implications of this genetic change.

The above comments from the latest CDC “Have You Heard?” acknowledges the fifth trH3N2 human isolate with the M gene from H1N1pdm09 (pandemic H1N1), as well as an interest in this acquisition, but still maintains the CDC narrative that these infections are rare and linked to close contact in swine, which is not supported by the sequences.  The Maine case provided compelling evidence for an emerging trH3N2 human contagion based on sequence data supporting evolution in humans.

This sub-clade has been reported in all five 2010 human isolates A/Indiana/08/2011, A/Pennsylvania/09/2011, A/Pennsylvania/10/2011, A/Pennsylvania/11/2011, A/Maine/06/2011), in contrast to the human trH3N2 sequences in late 2010, where most of isolates shared most of the gene segments.  In 2011 all human isolates share all gene segments which create a novel sub-clade which has never been reported in swine, in spite of increased surveillance for SOIV (swine origin influenza virus) in swine.

Recent reports have highlighted the importance of the M gene.  One report looked at gene segments in H1N1pdm09 to determine how the virus jumped from swine to humans, and concluded that the M gene segment was critical.  Another report noted the increased reassortment in swine from the US and noted that the M gene from H1N1pdm09 was central to the reassortants, which had various H and N swine triple reassortant combinations surrounding  internal genes from H1N1 pnd09, including the M gene segments.

Sequences from the increased swine surveillance describe two July isolates (July 16), A/Texas/A01104003/2011 and A/Texas/A01104004/2011, which have all eight gene segments from H1N1pdm09, which contain S188T, which represents the dominant H1N1 circulating in humans in 2011.  The recent collection date signals an active surveillance campaign, which has identified additional constellations with an M gene from H1N1pdm09.

Another July isolate (July 8), A/swine/Illinois/A00907647/2011, has an H1N1pdm09 M gene, as well as an NA gene that is closely related to the human trH3N2 isolates.  However, this swine isolate has an H1 and is likely to be similar to other H1N2 isolates collected in 2010 (A/swine/Minnesota/A01047604/2010 and A/swine/South Dakota/4/2010)) and 2011 (A/swine/Minnesota/A01049956/2011, A/swine/Iowa/A01049723/2011, A/swine/Iowa/A01049728/2011, A/swine/Indiana/A01049964/2011, A/swine/Illinois/A01049871/2011, A/swine/Illinois/A01049872/2011, A/swine/Iowa/A01049887/2011, A/swine/Iowa/A01049722/2011), which have multiple internal genes from H1N1pdm09.

In addition to H1N2 isolates with an H1N1pdm09 M gene, enhanced surveillance has also found H3N2 swine isolates (A/swine/Texas/A01049555/2011, A/swine/Texas/A01049556/2011, A/swine/Indiana/A01049750/2011, A/swine/Texas/A01049914/2011, A/swine/Texas/A01049915/2011) which likely have a similar set of internal genes (only the M gene sequence has been released in addition to the H3 and N2 sequences).  However, this swine H3 gene is easily distinguished from the H3 sequence found in all human 2011 trH3N2 isolates, which is closely related to the dominant sequence found in the human 2010 trH3N2.

This sequence has also been found in 2010 and 2011 swine isolates (A/swine/Indiana/A0109091/2010, A/swine/Indiana/A01049744/2011, A/swine/Indiana/A01049745/2011, A/swine/North Carolina/A01049436/2011, A/swine/Indiana/A01049653/2011),  but these swine isolates have a swine M gene. 

Thus, none of the swine isolates, including those from July, 2011,, match the human 2011 isolates, which match each other in all 8 gene segments.

This human sub-clade has evolved from the 2010 human trH3N2 isolates, which match in 5 of the 8 gene segments (PB2, PA, HA, NP, NS).  The PB1 represents the same lineage, but is more closely related to the sequences from 2007 H1N1 isolates, A/Ohio/01/2007 and A/Ohio/02/2007, which did not have E618D, which emerged in human trH3N2 (and is present in virtually all H1N1 pdm09 isolates).  The NA is in the above swine H1N2 isolates, but is also in the second 2010 human trH3n2 isolate, A/.Pennsylvania/14/2010, from Pennsylvania.  Thus, all eight gene segments in all five human 2011 isolates have been found in prior human isolates, once again signaling human adaptation.

Thus, the presence of these eight gene segments in all five human isolates, and the absence in all reported swine isolates, strongly supports human transmission, and the absence of human isolates without swine contact raises concerns that such isolates have been withheld because the absence of a swine epidemiological link is still under investigation.

Details on such cases should be released immediately.

By reason of the image of tourism, the provincial government of Bali has chosen not to announce the status of Extraordinary Events (KLB) bird flu in humans in Bali.Though based on a ministerial decree kesehatah (Health Minister) in 1371 In 2009, the status of bird flu in Bali has been entered in the status of an outbreak, after the death of two sisters from Bangli District Sanglah Hospital in Denpasar. 
Nyoman Sutedja Simakrama when met after the ceremony the Governor of Bali in Renon (29/10) image reveals a reason other than tourism, the status of bird flu outbreaks have also not announced because of bird flu in general has been endemic in Bali since 2007. Status of bird flu outbreaks have also not announced to avoid unrest in the community. 
"Not for political reasons, because otherwise disturbing the public does not want to eat chicken's multiple effects, which the farm could go bankrupt, the public be not eating, nutrition into malnutrition," said dr. Nyoman Sutedja. Nyoman Sutedja. 
Sutedja confirmed although not announced the status of the bird flu outbreak, but the standard of care and prevention of bird flu in Bali in accordance with the standards and protocols outbreaks. (mlt) (MLT)

Mother and Child''Suspect''Bird Flu Denpasar (Bali Post) -

Suspected of having bird flu, mother and child from Banjar Pande, Abiansemal, Badung, each Ni Nyoman S. (42) and Ni Kadek S. (10), Saturday (29/10) yesterday, was treated at Sanglah Hospital. Both were treated intensively in the living bird flu Sanglah Hospital. Both patients were referred from the Hospital Ship, Friday (28/10) and then, at 15:32 pm by ambulance.

According to the Head of Public Relations Sanglah Hospital, dr. Kadek Nariyantha, patients present with complaints of fever, fever, and cough. Although referred to the status of suspect bird flu, but the history of contact with poultry remains unclear. Meanwhile, the lab results for the two patients are still not yet out, so to treatment while the patient is treated in accordance with SOPs handling of bird flu.

It is said, while the second condition of the patient is still stable. That is, the patient had no heat or cough again.

With the receipt of two patients suspect bird flu origin Abiansemal, Badung, at Sanglah Hospital, then throughout the year 2011 the total number of suspect bird flu patients who received approximately 20 people, two of whom tested positive for bird flu and eventually died.

Recombinomics Commentary 12:40
October 28, 2011

*** CDC discontinued reporting of individual confirmed and probable cases of 2009 pandemic influenza A (H1N1) virus infections on July 24, 2009. During 2009, four cases of human infection with novel influenza A viruses, different from the 2009 pandemic influenza A (H1N1) strain, were reported to CDC. The four cases of novel influenza A virus infection reported to CDC during 2010, and the seven cases reported during 2011, were identified as swine influenza A (H3N2) virus and are unrelated to the 2009 pandemic influenza A (H1N1) virus. Total case counts are provided by the Influenza Division, National Center for Immunization and Respiratory Diseases (NCIRD).

The above comments from the week 42 MMWR confirm that the novel influenza listed in the provisional table was trH3N2, and is almost certainly the last reported case (8M) from Maine, A/Maine/06/2011.  The seven cases confirmed in 2011 strongly support human to human (H2H) and contradict the CDC narrative citing a very loose “swine exposure” as a source of the infections.

The first case confirmed in 2011 is from a 2010 infection in a case, A/Pennsylvania/40/2010. who was symptomatic on Sept 6, 2010, a week prior to the Wisconsin case, A/Wisconsin/12/2010, and 7 weeks prior to Pennsylvania case, A/Pennsylvania/14/2010, which were the subject of the WHO pager alert.  That alert noted the Wisconsin and Pennsylvania cases and assurance were then issued by the CDC that the two cases had sequence differences indicating that the infectiones were not from a common source. 

However, the sequence from the first Pennsylvania case was virtually identical to the Wisconsin case, but the reporting of the first Pennsylvania case delayed 5 months due to technical issues linked to the growth and isolation of the virus.  However, the CDC has a PCR tested for swine H3, which can quickly identify trH3N2 in samples directly.  Similarly, the CDC can sequence from the clinical sample without virus isolation.  These abilities were clearly demonstrated in the Maine case.  The state agency notified the CDC of an influenza A positive, subtype inconclusive case, on October 14.  The CDC confirmed trH3N2 on October 16, and released full sequences for all eight gene segments on October 17, using the clinical sample collected in Maine on October 10.  Thus, cases that support the CDC can be analyzed and reported in a few days, not 5 months.

A long delay was also associated with the second trH3N2 reported in 2011.  This was another 2010 case who was the daughter of a case (31M) confirmed in 2010, A/Minnesota/11/2010.  She had no swine contact and her trH3N2 was confirmed serologically.  Other symptomatic family members were “inconclusive” for trH3N2, suggesting many family members were infected by A/Minnesota/11/2010, and the CDC has used this isolate to create an H3N2 pandemic vaccine.  This cluster represented the first acknowledged H2H transmission of trH3N2.

However, the five trH3N2 cases infected in 2011 provide compelling evidence that this new human contagion is widespread in humans.  In 2010 most of the human cases shared most of the flu trH3N2 genes, but in 2011 this clustering evolved into identities where all 5 2011 cases match each other in all five gene segments, including an M gene from H1N1pdm09, which was critical for the jump of H1N1 from swine to humans.

The first 2011 case, A/Indiana/08/2011, had no swine contact.  His caretaker had swine exposure, but the caretaker and swine were asymptomatic and no SOIV has been reported.  Moreover, enhanced surveillance of swine in the United States and swine worldwide has failed to identify the constellation present in all five human cases.

Moreover, the next three cases attended the Washington County Fair in Pennsylvania and two of the sequences, A/Pennsylvanai/10/2011 and A/Pennsylvania/11/2011, were virtually identical to the Indiana, infected a month earlier, while the third case in Pennsylvania, A/Pennsylvania/09/2011, was a drift variant, signaling a second source for the Pennsylvania, but the constellation of gene segments was the same.

The most recent case from Maine, A/Maine/06/2011, is also a drift variant.  It began to diverge from the 2010 sequences at an earlier date, adding support for a widespread distribution of this human contagion.

However, all five of the confirmed 2011 trH3N2 have a loose association with swine exposure raising concerns that case with no swine exposure have not been disclosed because they are still being investigated for a swine exposure, leading to bizarre reporting of unsubtypables, which resemble a shell game, with clear examples of “now you see it / now you don’t”.

Recombinomics Commentary 17:30
October 24, 2011

"The acquisition of the M gene likely occurred as a result of swine being co–infected with the swine influenza A (H3N2) virus and the human 2009 H1N1 virus".

The above comments are from the latest CDC “Have You Heard” which discusses the most recently reported trH3N2 cases (8M), A/Maine/06/2011.  This isolate increases the overwhelming evidence for the transmission of trH3N2 in humans, yet the CDC continues to cite swine involvement, which is not supported by data.

The sequence data provides compelling evidence for human transmission, and the evidence was initially made public in November, 2010 when the CDC released the sequence data on trH3N2 cases. The sequences were released just after the WHO issued a pager alter on two trH3N2 patients and the sequences (A/Wisconsin/12/2010 and A/Pennsylvania/14/2010) raised concerns. Many of the internal genes from cases were clustering phylogenetically, signaling adaptation to humans. However, the CDC put out its first “Have You Heard” on trH3N2, which suggested the two cases did not represent human transmission because of differences between the two sets of sequences.

Shortly after these assurances were given, another case was reported.  This case was in Minnesota and the sequences, A/Minnesota/11/2010, were closely related to the Wisconsin case, providing more evidence for human transmission.  This sequence data was strengthened by 2011 reports on additional 2010 cases.

The first data set came from the report of a second Pennsylvania case, A/Pennsylvania/40/2010, who developed symptoms less than a week prior to the Wisconsin case.  However, the sample was initially classified as seasonal H3N2, and additional analysis / reporting was delayed because of technical difficulties in growing the virus.  In week 4 of 2011 the case was reported as another trH3N2 case, and the sequence was closely related to the Wisconsin case, demonstrating clear clustering of sequences from human trH3N2.

The concern that this clustering signaled human transmission was confirmed in week 21, when the daughter of the Minnesota case was confirmed to have also been trH3N2 infected, even though she had no swine contract.  The CDC then acknowledged limited human transmission (additional family members were also symptomatic, but trH3N2 confirmations were reported as “inconclusive), and selected the isolate from the father as a pandemic H3N2 vaccine target.

However, the sequence data for human transmission was significantly strengthened, when sequences from the first 2011 trH3N2 case (2M), A/Indiana/08/2011, were released at GISAID without comment, other than a note mentioning the presence of an M gene segment from pandemic H1N1 (H1N1pdm09). The acquisition of the M gene was a concern because an independent reported cited the M gene as being critical for the jump of H1N1pdm09 from swine to humans.  Therefore, this acquisition could drive the jump of trH3N2 from swine to humans.  The sequences of the other genes also increased concerns.  5 gene segments (PB2, PA, HA, NP, NS) including H3 matched the most common 2010 human trH3N2 sequences, while the NA was closely related to the second Pennsylvania isolate (PA/14/2010) and the PB1 was related to two other human cases, A/Ohio/01/2007 and A/Ohio/02/2007, linked to the Huron County outbreak.  This, all seven of the trH3N2 gene segments matched prior human isolates, adding to the evidence of human adaptation.

The release of the Indiana sequence was followed by an early release MMWR which described the Indiana case (2M) as well as a 2011 case (2F), A/Pennsylvania/09/2011, who was from Schuylkill County in eastern Pennsylvania, but attended the Washington County agricultural fair in western Pennsylvania.  The Indiana case had no swine contact, but his caretaker contact with swine was cited as a potential trH3N2 source leading to limited human to human contact.  However, the caretaker and associated swine were asymptomatic, so no true link was established.  Similarly, the Schuylkill resident attended an agricultural fair, but no symptomatic swine was identified.  The MMWR also cited sequence differences between the Indiana and Pennsylvania cases, suggesting the infections did not come from a common source.  However, both sets of sequences had the same constellation of genes, including the M gene from H1N1pdm09, as well as matches for all 7 trH3N2 gene segments.

The early release MMWR was followed by another “Have You Heard” which described two addition cases (both 9F), A/Pennsylvania/10/2011 and A/Pennsylvania/11/2011, which had the identical set of gene segments.  These three cases from the same county fair represented the largest number of trH3N2 isolates from a single location.  However, the investigation, which the CDC characterized as “intensive”, failed to identify a source for any of the 2011 cases.

The release of the sequences from the 2011 trH3N2 cases in Pennsylvania strongly supported human transmission.  Although the sequences from PA/09/2011 signaled a different source, the sequences from the other two cases, PA/10/2011 and PA/11/2011, were virtually identical to each other as well as IN/08/2011, even though the Indiana case was a month earlier and at a location 100’s of miles away.  The sequence identity between these three cases, which were not epidemiologically linked, strongly supported sustained transmission, and the identical constellation of genes in the third Pennsylvania case strong supported human adaptation.

The support was increased with the report of the 5th trH3N2 case (8M), A/Maine/06/2011, which also had the M gene from H1N1pdm09.  The sequences confirmed that the identical constellation of genes was involved, although several gene segments began evolving away from the 2010 human trH3N2 sequences at an earlier data, strongly suggesting that this novel trH3N2 represented a new human contagion, and represented sustained transmission.

The CDC has denied sustained transmission based on epidemiological data, which was generated using the same approach that failed to identify a source for any of the 5 2011 trH3N2 cases.  The linkage to swine was based solely on the pseudo linkages, which led to trH3N2 testing, which is only done by the CDC and is limited to samples received, which are flagged due to pseudo linkage to swine, including the Indiana case which had no direct linkage, and the other four cases who had attended fairs where asymptomatic swine were exhibited.

However, no symptomatic swine have been identified at these fairs, and no swine have been identified with the constellation of genes found in all five human cases from three states (Indiana, Pennsylvania, and Maine).

Thus, in spite of this lack of any real data linking human trH3N2 to trH3N2 infected swine, the CDC continues to statements such as the one quoted above, which are based on hopes and dreams, and lack any real data.

Virus Involved in Cuban Dissident’s Death Is Spreading

HAVANA – Cuban health authorities warned Saturday that two flu viruses are spreading on the island that particularly affect the elderly and babies, one of which struck Laura Pollan, leader of the Ladies in White, who died a week ago.

"At the moment the flu viruses that are spreading are the H3N2 that chiefly affects the adult population, and respiratory syncytial virus that affects children of less that a year old, causing bronchial complaints in some babies," the official daily Granma said Saturday in an article about seasonal flu.

"That does not exclude either of these pathogenic agents from afflicting people of any age," the report adds, without ever mentioning the case of Pollan.

Last Oct. 14 the leader of the Ladies in White dissident group, Laura Pollan, 63, died after suffering respiratory failure and diabetic decompensation combined with respiratory syncytial virus, a type of dengue and her chronic diabetes, members of her family said at the time.

An official government "blog" mentioned Pollan's death, citing the head of the intensive care unit where the dissident was hospitalized for a week, saying that the diagnosis was "pneumonia from respiratory syncytial virus, a bacterial respiratory infection and acute respiratory failure."

This past week, dissidents have expressed their doubts and suspicions about Laura Pollan's death, among them her companion and Ladies in White spokeswoman Berta Soler.

Several days ago, Soler told foreign media that during Pollan's hospitalization there was some confusion about whether or not she had dengue, and said that the test results took longer than expected.

In the article published Saturday, the public is advised to take preventive and hygienic measures to ward off flu, to see a doctor when the first symptoms appear and to remember that children and those older than 65, as well as people with chronic ailments, are the groups most at risk of possible complications, above all those derived from pneumonia.

Granma, the official organ of the Communist Party of Cuba, said that an anti-flu vaccine will soon be administered to the groups that are most vulnerable.

http://www.laht.com/article.asp?ArticleId=435385&CategoryId=14510

108CSR.com - The bird flu virus has claimed three victims in Bali, Wayan brothers Ari Aldiawan and Nengah Rica, along with their mother, Ni Wayan Purnami. All three are citizens of the Village Jehem, Bangli regency, Bali.


But the Governor of Bali, Made Mangku Pastika, not too worried about the bird flu virus will develop into a plague. According to him, Bali has been experienced to handle the bird flu virus. "We are very experienced. All appropriate SOPs already set standards. Living community participation needs to be improved to prevent the spread of the deadly virus," said Pastika in Bali Parliament House on Friday (21/10).

Pastika said the Provincial Government of Bali has been attempts to localize the birds and make the vaccine. "I appealed to the district government is also doing the same thing," he said. During this time, continued Pastika, has never been any protest from the central government and relevant international world of bird flu in Bali, because of all SOPs handling of bird flu has been conducted properly.

Meanwhile, the rapid test (rapid test) has shown, that the 62 villages in Bali have been infected. Rapid test were retested several times in a number of laboratories, and the result is the same, namely 62 birds in the area of bird flu positive.

http://www.108csr.com/home/news.php?id=2651

Recombinomics Commentary 23:15
October 21, 2011

CDC has confirmed the fifth case of human infection with a swine–origin influenza A (H3N2) virus that carries the M gene from the 2009 H1N1 virus. This virus was first detected in a child in Indiana in July. Subsequently three additional cases of human infection with swine–origin influenza A (H3N2) viruses carrying the same genetic change were detected in Pennsylvania. Though rare, human infections with swine–origin influenza viruses can occur, usually after close contact with infected swine.

While we know the M gene plays a role in influenza virus infection, assembly and replication, the significance of this change in these swine–origin influenza A (H3N2) viruses is unknown at this time. CDC continues to investigate the implications of this genetic change.

The above comments are from the latest “have you heard” put out by the CDC.  The statements represent an agency in the state of denial with regard to the human transmission of trH3N2.  They confuse reported trH3N2 with actual trH3N2 infections.  The association with swine is directly linked to the CDC trH3N2 testing which is largely limited cases with some kind of pseudo-link to swine.

The report acknowledges that the 5 trH3N2 in 2011 all involve the same trH3N2 virus which has an M gene from pandemic H1N1, but ignores the data indicating the M gene of pandemic H1N1 is critical for human transmission.

The CDC has yet to provide any direct evidence for human trH3N2 infections from swine in 2011.  The first case (from Indiana) has no known swine contact, and the CDC has acknowledged likely human to human transmission, which has also been acknowledged for the two most recent 2010 trH3N2 cases (father and daughter from Minnesota represent by A/Minnesota/11/2010 isolated from the father).

For the four most recent trH3N2 cases (in Pennsylvania and Maine) no link has been established between SOIV infected swine and the four cases.  The three Pennsylvania cases attended an agricultural fair (which is why they were tested for trH3N2), but no swine with symptoms or trH3N2 swine infections have been identified.  The same is true for the Maine fair in Cumberland County.  Moreover, no swine anywhere at any time have been identified with the human constellation, even though swine surveillance in 2010 and 2011 has been dramatically increased in the US.

Similarly, the CDC has failed to demonstrate that trH3N2 is rare in recent human H3N2 cases.  They have released sequences from 15 US H3N2 cases infected since July, and 5 of the 15 were trH3N2.

Thus, the CDC is relying solely on its heavily biased testing to claim the swine linkage.

Distribution of trH3N2 PCR kits to state labs is long overdue. 

Such state testing will determine the true extent and transmission of trH3N2 in humans in the US in the 2011/2012 season.

PORTLAND, Maine (AP) — An unusual strain of swine flu has infected five young children in Maine, Pennsylvania and Indiana, health officials said Friday.

A young boy of 7 or 8 from Cumberland County, Maine became the latest case when he came down with flu symptoms in early October, not long after being exposed to pigs at an agricultural fair, the Maine Center for Disease Control and Prevention said. He and the other four children have recovered, health officials said.

The H3N2 swine-origin strain was confirmed by the U.S. Centers for Disease Control as the same strain identified earlier in three cases in Pennsylvania and one case in Indiana, according to Maine's state epidemiologist Stephen Sears.

The three infected children in Pennsylvania had all attended an agricultural fair in August where pigs were exhibited, the CDC said. The Indiana child had not been exposed to pigs, but is thought to have been infected in late August by another person who had recently been exposed to pigs, but who did not have flu symptoms.

Unusual strains of influenza pop up virtually every year, health officials said, and there's nothing to suggest that this H3N2 strain is being widely transmitted from person to person. The infected boy in Maine was treated by a family doctor and is back up and playing, Sears said.

"We're taking a prudent public health approach to this," Sears said. "This is an unusual virus, but it doesn't appear to be spreading in people, so we don't think it's a major issue."

The first case of H3N2 was reported to the federal CDC in late August after a boy under 5 from Indiana experienced a fever, cough, shortness of breath, diarrhea and a sore throat. The boy was hospitalized for treatment and has since recovered.

Like humans, pigs can become infected with influenza viruses and suffer the same symptoms people do. Pigs can become infected not only with swine flu viruses, but with human and avian influenza viruses as well, the CDC says. On rare occasions, humans can become infected with swine flu viruses; the CDC says fewer than two dozen cases have been documented in the last five years.

The H3N2 virus contains a gene picked up from H1N1 swine flu virus that resulted in global pandemic in 2009, the first combination virus to turn up in people since the pandemic, according to the CDC. It is a hybrid of viruses that have infected pigs over the last decade.

Influenza viruses are constantly changing and picking up genes from other viruses, and the H3N2 strain represents a step in the evolutionary process of a virus taking on new genetic properties, said federal CDC spokesman Tom Skinner.

"Right now we don't see any widespread person-to-person transmission and that's the key when it comes to influenza cases," Skinner said.

Meanwhile, seasonal influenza activity remains low around the country with the arrival of seasonal flu season, the CDC says. The agency said earlier that this year's vaccine, the same as last year's, likely would not protect against the new swine strain.

http://www.southbendtribune.com/news/sbt-new-swine-flu-virus-sickens-5-children-in-3-states-20111021,0,3133475.story

Recombinomics Commentary 01:30
October 18, 2011
The latest trH3N2 set of sequences, A/Maine/06/2011, released by the CDC match the 2011 trH3N2 sequences from Indiana, A/Indiana/08/2011, and Washington County (A/Pennsylvania/09/2011, A/Pennsylvania/10/2011, A/Pennsylvania/11/2011), confirming human to human transmission.  The sample was collected October 10, 2011 from an 8M in Maine and the CDC is commended for the rapid release of this set of sequences. However, the detection of this case in Maine suggests a lack of swine contact.

The Indiana case had no swine contact, and the latest comment from the CDC, in week 40 FluView, only states that the three Pennsylvania cases attended a county fair that exhibited swine.  There was no statement claiming swine contact (and there have been no reports of symptomatic swine at the Washington County fair and no reports of any influenza infections in swine). 

In contrast, all five human cases in 2011 have the identical constellation of flu genes including a PB1 that lacks E618D, an NA that is similar to A/Pennsylvania/14/2010, and an MP that matches pandemic H1N1.

The CDC claim of no sustained transmission merely reflects the limitations in the CDC sample collections and testing, which failed to find a source for any of the cases, including the caretaker of the Indiana case. The pseudo-linkage to swine drives trH3N2 testing of cases infected prior to the start of the flu season.  Details on the present case have not been released, but in contrast to earlier locations for 2011 trH3N2 cases in states that have high levels of swine, the location of this case, Maine, is not noted for swine farms or fairs.

The circumstances associated with the detection of the current case in unclear, but the bizarre reporting on unsubtypables raises concerns that testing for influenza A and/or seasonal H3 is a less than ideal approach for detecting human trH3N2 cases.

The CDC should distribute swine H3 PCR kits to the state labs to determine the true level of human trH3N2 infections and transmission in the United States.

Maine trH3N2 Sequences Signal Human Transmission
Recombinomics Commentary 20:40
October 21, 2011

One case of human infection with a novel influenza A virus was reported by the Maine Center for Disease Control and Prevention. The patient was infected with a swine origin influenza A (H3N2) virus. Testing performed at Maine’s Health and Environmental Testing Laboratory on October 14, 2011 indicated a likely swine origin influenza A (H3N2) virus and this result was confirmed at CDC on October 16, 2011. The patient reported attendance at an event where pigs were present in the week preceding symptom onset on October 7, 2011, did not require hospitalization, and continues to recover. No illness has been identified in family members or close contacts, but the investigation is ongoing.

Swine-origin triple reassortant Influenza A (H3N2) viruses have been circulating among North American swine herds since the late 1990's. Human infections with these viruses are detected sporadically, and cases usually occur following direct or indirect contact with pigs.

The above comments are from today’s (week 41) CDC FluView, which highlights the rapid generation and release of sequences from this case (8M).  The confirmation was two days after Maine tests, and a full set of sequences were made public (at GISAID) the following day (and made available at Genbank 2 days later).

However, the CDC has not addressed the significance of the 2011 trH3N2 sequences, which provide compelling data for human to human transmission.  Instead the CDC recites its standard comment on triple reassortants, and ignores the fact that all five isolates from 2011 have the same constellation of genes, which goes beyond the more general composition of 7 gene segments from trH3N2 cases and an M gene segment from pandemic H1N1.

The human trH3N2 sequences, release on November, 2010 had obvious clustering, which increased as additional cases were identified.  WHO issued a page alert on two of these cases, A/Wisconsin/12/2010 and A/Pennsylvania/14/2010 and offer assurance of o transmission based largely on significant differences in the sequences from these two isolates.  However, when those assurances were presented, another Pennsylvania case, A/Pennsylvania/40/2010 (PA/40/10), was being analyzed.  That patient developed symptoms less than a week prior to the Wisconsin case, but the PA/40/10, was initially designated seasonal H3N2 and was reported to be trH3N2 in 2011, five months after infection, and the sequence was virtually identical to the Wisconsin case. 

Moreover, just after the pager alert another case was identified in Minnesota, A/Minnesota/11/2010, and most of the gene segments, including H3, were closely related to the Wisconsin and Pennsylvania cases.  In addition, the daughter of the Minnesota was subsequently trH3N2 confirmed (serologically), increasing the number of confirmed trH3N2 cases infected between September and November 2010 to five, and four of the five had gene segments, including H3 that were closely related, signaling human adaptation.

This adaptation was significantly increased in the 2010 isolates.  The early release MMWR report by the CDC described the first two cases, A/Indiana/08/2011 and A/Pennsylvania/09/2011, and noted that both had an M gene from pandemic H1N1.  Again assurances were offered based on sequences differences because although both isolates had the same constellation of genes, the Pennsylvania isolate was a drift variant and a few of the genes had evolved further from the 2010 sequence than the Indiana isolate.  However, two additional cases were identified in Pennsylvania (A/Pennsylvania/10/2011 and A/Pennsylvania/11/2011) which were virtually identical to each other as well as the Indiana case.  Thus, these three cases not only had the same constellation of genes, but the sequences of all 8 gene gene segments were virtually identical, even though infections in Indiana and Pennsylvania were a month apart and not link epidemiologically, supporting human to human (H2H) transmission.

The H2H transmission was further supported by the Maine sequence, A/Maine/06/2011, which had the same constellation of genes as seen in the four earlier 2011 cases, but evolution from the 010 sequences was slightly different.  The Maine genes branched off the 2010 sequences earlier, and consequently were more closely related to several of the 2010 gene than the IN/PA cases even though the ME case was infected more recently.

This earlier divergence indicates human trH3N2 infections have more heterogeneity than seen in the five sets of sequences released, and this earlier divergence highlights the significance of the lack of the detection of this constellation in swine isolates, which has not been reported in any swine, including a high number of 2011 isolates collect as recently as July, 2011.

This, the identity in the overall constellation of flu genes in all five 2011 human cases and its absence in all swine cases signals H2H transmission, as does the acquisition of the M gene segments from pandemic H1N1, and the close relationship to the 2010 human trH3N2 sequences.

In contrast to the public data supporting human to human transmission, the CDC focuses of linkage to direct or indirect swine exposure based largely on selective testing of patients with a swine linkage for trH3N2.  To date the CDC has released H3N2 sequences from 15 US cases collected since July 2011, and 5 of the 15 cases have been trH3N2.

This high frequency, coupled with the sequence identities in these five cases, indicates the number of trH3N2 cases in the US is orders or magnitude higher than the five cases reported to date, and PCR test kits for swine H3 should be distributed to all state labs as soon as possible.

Recombinomics Commentary 13:30
October 17, 2011

Four residents of Central Lombok, West Nusa Tenggara, were treated in isolation rooms General Hospital (RSU) province of West Nusa Tenggara (NTB) as so suspect the H5N1 virus (bird flu). The four residents of Central Lombok each of initialed ADT (11 months), SHN (56), STK (10) from Peringgarata village, Central Lombok, and DSH (5 months) from Semayan, Central Lombok.

The above translation described four hospitalized suspect H5N1 in Central Lombok, which is just east of Bali, where a fatal H5N1 cluster of three has been reported.  Two of the three fatal cases have been lab confirmed locally, but the Indonesian Ministry of Health and WHO have not acknowledged any of these cases.
 
However, H5N1 confirmations are typically delayed.  The most recent confirmed H5N1 case in Indonesia died in Jakarta on August 25 after developing symptoms on August 8.  This case was not reported by WHO until October 10, although IHR requires reporting within 48 of lab confirmation.

Recently, media reports cited the spread of H5N1 in poultry in Bali, raising concern that the H5N1 has evolved to avoid prior immunological responses.  H5N1 has been endemic in Indonesia for many years and Indonesia no longer reports H5N1 poultry cases to OIE.

Monitoring H5N1 in humans is difficult because the most recent public sequences (at GISAID) are from patients infected in 2008, although all human and poultry H5N1 from Indonesia are clade 2.1.

Timely reporting of human cases and release of current H5N1 cases is long overdue.

machinetranslation

"Increase Bird Flu death toll '

The [number of] victims died from bird flu in Bali, is increased.

Biological mother of two children who died from bird flu in Bali, died at her home. Before burial, the officers took a blood sample suspected suspect bird flu in the village Jehem Tembuku Bangli district of Bali.The victim is the biological mother of two children who a few days ago died in hospital Sanglah Bali positive result contracted bird flu. She experienced symptoms of fever and heat, although the results of her blood tests last week declared negative bird flu . She died two days after leaving the hospital treatment room Bangli.

Relatives and families of victims, including her husband, wept as the bodies were taken to be treated like a corpse ambulans.Jenazahnya suspect bird flu. The whole etugas wear sterile clothing and cover the bodies obliged to use a mask.

Anticipating the spread of the H5N1 virus, Department of Health and Husbandry Bangli, spraying disinfectant around the victim's home. The remaining birds were still alive immediately burned en masse.


http://news.mnctv.com/index.php?option=com_content&task=view&id=18616&Itemid=14

Recombinomics Commentary 12:20
October 17, 2011
Biological mother of two children who died from bird flu in Bali, died at his home. Before burial, the officers took a blood sample suspected suspect bird flu in the village Jehem Tembuku Bangli district of Bali. The victim is the mother of two children who a few days ago died in hospital Sanglah Bali positive result contracted bird flu. He experienced symptoms of fever and heat, although the results of his blood tests last week declared negative burung.Ia flu died two days after leaving the hospital treatment room Bangli.

The above translation indicates the mother of the two fatal cases in the Bagli district in Bali, Indonesia has also died.  Although the earlier test on the mother was negative, she had H5N1 symptoms, including a drop in platelet count.  Moreover, the delay in the date of death strongly suggests human to human transmisson.

Negative H5N1 results for Indonesian patients who recover are common, but confirmation of fatal is more frequent, leading to a case fatality rate of over 80%, which has been the situation in Indonesia since the first confirmed H5N1 cases in 2005.  The Ministry of Health and WHO have not reported H5N1 confirmation of any of the three fatal cases, which is also not unusual for Indonesia.  IHR requires notification with 48 hours of lab confirmation of novel influenza cases, including H5N1, but several years ago Indonesia announced reporting changes for H5N1 cases.  The timing of notication of WHO remains unclear, but WHO announcements of confirmed cases follows announcements by the Indonesian Ministry of Health.

In addition to the three fatal cases in Bali, four additional suspect H5N1 cases have been hospitalized in central Lombok.. which is east of Bali

Recombinomics Commentary 02:20
October 17, 2011
Wayan Aldiawan, 10, and his 5-year-old sister Nengah Rika Ani died Sunday after being treated for two days, Sanglah hospital official Elzarita Arbain said.

'Throat swabs and blood samples came back positive for H5N1,' he said, referring to the deadliest strain of bird flu.

The chief of the hospital's bird flu ward, Ken Wirasandi, said the children had contact with dead fowl in their neighbourhood in Bangli district.

The above comments describe a fatal H5N1 cluster in the Bangli district on the island of Bali in Indonesia. Although these fatalities have not yet been confirmed by the Indonesian Ministry of Health or WHO, confirmation of fatal cases is far more common than suspect cases that survive, including those confirmed locally.

This cluster is of concern because of reports indicating the mother of the above children has been hospitalized with symptoms, including a low platelet count, which is characteristic of H5N1 infections.  More detail on the mother and other symptomatic contacts would be useful.

Recombinomics Commentary 19:40
October 4, 2011
The latest series of trH3N2 and trH1N2 swine sequences from 2011 (released at Genbank by Iowa State University) provide additional insight into the evolution of the new human contagion, trH3N2. Although the new swine sequences have key components of the 2011 trH3N2 reported in Indiana (A/Indiana/08/2011), and the Washington County fair in western Pennsylvania (A/Pennsylvania/09/2011, A/Pennsylvania/10/2011, A/Pennsylvania/11/2011), the swine isolates fail to match the constellation of genes fund in all four human cases, providing additional evidence for the emergence of a new human contagion, trH3N2, and another influenza pandemic.
 
The 2011 trH3N2 human sequences extended the spread of the 2010 human trH3N2 sequences by retaining 5 of the 8 gene segments. The new contagion has swapped out the other three gene segments, PB1, NA, MP for genes found in earlier human triple reassortants (trH1N1, trH3N2, pandemic H1N1), to create a new human contagion, trH3N2, that can efficiently transmit in humans. As has been mentioned by the CDC and WHO, the 2011 human trH3N2 sequences have acquired a pandemic H1N1 M gene segment, which is critical for the efficient transmission of pandemic H1N1 between humans.

However, the human trH3N2 sequences have also acquired the N2 that was in one of the 2010 Pennsylvania cases, A/Pennsylvania/14/2010, as well as a PB1 more closely related to sequences from the Huron County fair (A/Ohio/01/2007 and A/Ohio/02/2007) and this new constellation of genes was in all four 2011 human trH3N2 cases reported to date, and not in any of the reported swine sequences, including the recently released sequences (trH3N2 and trH1N2) from 2010 and 2011.
 
The recently released 2011 swine sequences had information on HA, NA, and MP, but this limited sub-set failed to match the human trH3N2 constellation.  In 2010 there were H1N2 sequences (including A/swine/Minnesota/A01047604/2010 and A/swine/South Dakota/4/2010) with a pandemic H1N1 M gene and an N2 that matched the recent human trH3N2 sequences.  However, a more complete analysis of the Minnesota sequence showed that all six internal genes matched pandemic H1N1, and other such sequences (all six pandemic H1n1 internal genes wrapped in H and N from other triple reassortants) have been widely reported in swine, but not in humans.  Therefore, it is likely that the recent H1N2 swine sequences (including A/swine/Minnesota/A01049956/2011, A/swine/Iowa/A01049723/2011, A/swine/Iowa/A01049728/2011, A/swine/Indiana/A01049964/2011, A/swine/Illinois/A01049871/2011, A/swine/Illinois/A01049872/2011, A/swine/Iowa/A01049887/2011, A/swine/Iowa/A01049722/2011) have a similar constellation (as well as a different serotype). 
 
Other recent trH3N2 isolates (including A/swine/Texas/A01049555/2011, A/swine/Texas/A01049556/2011, A/swine/Indiana/A01049750/2011, A/swine/Texas/A01049914/2011, A/swine/Texas/A01049915/2011) have a pandemic M gene segment, but different H3 and N2.  Similarly, recent isolates have a matching H3 and N2 (including A/swine/Indiana/A01049744/2011, A/swine/Indiana/A01049745/2011, A/swine/North Carolina/A01049436/2011, A/swine/Indiana/A01049653/2011, A/swine/Indiana/A0109091/2010) but have an M gene related to the 2010 trH3N2 isolates.  
 
Thus, even though the surveillance of 2010 and 2011 swine has increased (including one sequence from July, 2011), none of the public sequences match the 2011 human trH3N2 constellation, strongly suggesting that this new pathogen is transmitting in humans.
 
The number of human cases has been limited, but all four 2011 isolates have the same constellation of genes including a pandemic H1N1 M gene, which is critical for human to human transmission. Moreover, three of the four sequences are virtually identical, but isolated from distinct locations, including the Indiana case with no swine contact.  Moreover, none of the four cases were epidemiologically linked, indicating each infection was independent. 
 
The matching of all four human cases, in the absence of any matches with swine isolates signals an adaptation and spread of this trH3N2 contagion with a novel constellation of flu genes.
The limited testing of H3N2 cases, and the focus on patients with links to swine, continues to raise pandemic concerns.

Remember the flu pandemic?

The one that swept the world just two years ago? You might be forgiven if this has slipped your mind – after all, it doesn’t seem like such a big deal now. That’s because we got lucky: despite many dire warnings about the danger of another 1918 “Spanish flu”, when the 2009 pandemic arrived, it was far milder than previous pandemics. Hundreds of millions of people got the flu in 2009, but for most of them, it wasn’t so bad. In fact, the new flu is less severe the old flu – the strain that was circulating before the new pandemic hit.

Now we have two flus circulating: the “old” H3N2, and the 2009 pandemic flu, called H1N1. (And the vaccine protects against both of them, so get your flu shot! Your friends, neighbors, and co-workers will all benefit.)

We really dodged a bullet in 2009. Despite our best efforts, it took 7 months (April to November) before a new vaccine was ready. Before we realized how mild it was, people were desperately snapping up stores of Tamiflu, an anti-viral medicine that only barely helps to treat the flu. If it had been like 1918, Tamiflu wouldn’t have helped much, and tens of millions would have died.

The 2009 pandemic originated in pig farms in Mexico. We don’t know precisely where it made the first leap into humans, but it appears that two different strains joined together in a pig somewhere to create the new H1N1. The flu has a nasty habit of jumping the species barrier, hopping to humans from both pigs and chickens.

So now that we know all this, next time will be different, right? The world’s influenza scientists are monitoring pigs and chickens closely now, keeping a close eye on any new flu strains. Right? RIGHT???

Er, no. Not exactly. For one thing, surveillance in pigs appears to be nonexistent. I checked to see how many flu sequences from pigs in Mexican have been desposited in the public archive at GenBank since 2009 (using this terrific database). The result? One, in 2009. Nothing from 2010 or 2011. Hello, is anyone awake at the CDC and the WHO?

This despite the fact that scientists have serious concerns that the deadly H5N1 avian flu (the “bird flu”) could combine its genes with H1N1 and create a really nasty new flu strain. And scientists have long had concerns that pigs could be the mixing vessels for new flu outbreaks – exactly what happened in 2009.

But wait… maybe they are monitoring the flu, but they’re just not telling us. That would feed into all the fringe government conspiracy groups that claimed the 2009 pandemic was an intentionally engineered government-funded enterprise (see this BMJ article for more). I don’t believe any of those conspiracy theories – most of them are just nuts – but read on.

Sharing data about flu viruses has been a touchy subject with the WHO and the CDC for years. As reported by the University of Minnesota’s CIDRAP:

“In late 2006, virus sharing became an international flash point when Indonesia broke a long tradition of free international sharing of flu virus specimens by withholding its H5N1 virus samples as a protest against the high cost of commercial vaccines derived from such samples. The controversy has drawn attention to the problem of equitably distributing vaccines in the event of a pandemic.”

A few months ago, the WHO finally agreed on a new set of principles on data sharing, which states that

“The WHO GISRS laboratories [which includes the CDC] will submit genetic sequences data to GISAID and Genbank or similar databases in a timely manner.”

Excellent!  So are they doing it?

As every biomedical scientist knows, GenBank is a free, public database of genetic sequence data that contains millions of sequences, from humans, bacteria, viruses, you name it. But GISAID is a Swiss database – one that I initially supported – just for flu data. The original mission of GISAID was that data deposited there would go to GenBank as well, with little or no delay. But in a classic bait-and-switch move, the GISAID board changed that policy after the database was up and running, and now they can sit on data as long as they want.

OK, it’s a private database, so they can do what they want. True enough. But here’s the surprising bit: the CDC deposits most of its flu sequences ONLY in GISAID, where they can milk them for scientific results for years without sharing them with others. As one of GISAID’s original supporters, I have an account there, and here’s what I found.

So far, the CDC has deposited sequences from 6,801 flu isolates in GISAID, of which only a tiny handful are in GenBank. 3201 of these originated in the U.S., so there can’t be any foreign government insisting that they be kept secret. These provide critical data that could help scientists predict what is coming in the next flu season. But you can’t get these sequences without a GISAID account. And even if you have a GISAID account, as I do, you have to agree not to release the data as a condition of getting a look.

So why does the CDC deposit sequences in GISAID? I think it’s precisely because of the restrictions. CDC’s scientists don’t want others to look at “their” data, because they’re afraid someone else might discover something important and publish it before them.

The CDC, of course, is part of the U.S. government, and all its work is funded by the public. But it seems that the CDC flu scientists have forgotten their public health mission – or at least, they appear to be more concerned about their own careers (and the papers they might publish) than about making sure the world is ready for the next pandemic.

And by the way, even these sequences don’t seem to include anything from pigs in Mexico. Hello, CDC? You are looking at swine flu now, aren’t you?

Perhaps I’m being a bit harsh. I love the CDC: they do a terrific job most of the time, providing vital services to protect the public from infectious diseases. But their internal scientists sometimes seem to operate within a cocoon, and I’m afraid that’s happening here. This culture of secrecy has got to stop, and I suspect that will only happen under pressure from the outside. The CDC Director, Thomas Frieden, needs to tell his flu people to start sharing what they know with the rest of the world. And they can start by putting their data in GenBank.

http://www.forbes.com/sites/stevensalzberg/2011/10/02/is-the-government-hiding-something-about-swine-flu/