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WHO H5N1 Investigation In Sumatra Indonesia Raises ConcernsAugust 10, 2008 http://www.recombinomics.com/News/08100801...umatra_WHO.htmlThe United States consulate general (the USA) in Medan also asked about the situation and the last condition for the Damuli Hut community, the IV Village, the Air Batu Village of 39,Kecamatan Air Batu, this Regency Experts from the World Health Organisation (WHO) had arrived in the affected village in North Sumatra to help investigate the possible outbreak and the sudden death of three residents last week, a provincial health official said. The above comments on the outbreak in Medan reflect the level of concern of non-Indonesian agencies with the situation in Medan. As noted, three patients died with bird flu symptoms, and additional patients were hospitalized. Although these patients are said to have tested negative, poultry in the region is H5N1 positive. The presence of a WHO team, in the absence of confirmed H5N1 cases, is unusual, and raises concerns that there has been unreported lab evidence of H5N1 in patients in the region. This region has had a history of confirmed or suspect clusters. The largest confirmed cluster was in Karo over two years ago, The cluster was linked to clear human to human to human transmission which led to increased surveillance of poultry in the region. That cluster was followed by a cluster of similar size, but those patients tested negative. However, negative testing in Indonesia remains highly suspect. False negatives can be generated by widespread and aggressive Tamiflu use and the suspect sensitivity of the testing in Indonesia. In addition to the largest number of confirmed H5N1 cases and the largest number of confirmed H5N1 deaths, Indonesia also has the highest case fatality rate, over 80%, raising concerns that milder cases are either not tested or test negative. Indonesia’s failure to test H5N1 infected patients in clusters is also cause for concern. Recent confirmed cases have been associated with relatives who die with bird flu symptoms, but these fatalities are said to be lung inflammation, typhus, or dengue fever. These clusters, representing limited human to human transmissions have been followed by a new policy of delaying reports of cases. International Health Regulations require notification of WHO 24-48 hours after confirmed cases. Although WHO has stated that they have a good relationship with Indonesia, the WHO updates have been delayed and the two confirmed cases in Tangerang in July have not yet been reported in WHO updates, indicating Indonesia is not reporting these cases in violation of IHR requirements, or WHO is withholding reports of these confirmed cases in their situation updates, which report cases within a day or two of confirmation. The WHO team on the ground, coupled with reporting failures by Indonesia and WHO, continue to raise concerns about the true situation in the Medan region of North Sumatra.
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| QUOTE | Dengue Fever Diagnosis In Sumatra Raises Concerns
August 11, 2008
http://www.recombinomics.com/News/08110802...tra_Dengue.html
The concerned atmosphere was mixed with panic covered casualties's family from the Asahan Regency, they expected his two children terjangkit bird flu because by chance their area was found by casualties suspect bird flu. “Melihat our child's fever did not descend-descended we concerned was mixed with panic, we suspected our child of being affected by bird flu because in our area was found by bird flu casualties but after being brought by us to this hospital and results were stated positive DBD not flu burung” clear Zuhaina the mother Fitra and Aiman to the reporter.
the Team of the doctor suspected the patient of being suspected of by bird flu having the initials F (7) was attacked by dengue fever dengue fever or DBD. the Content trombosit in the F body was below normal.
We were not sure the dengue fever attack happened from here (Medan), said public relations of RSUP Adam Malik Medan Sinar Ginting, on Sunday (10/8).
The volunteer furthermore was assigned to monitor 5 to 10 families that suffered the sign of bird flu.
The above translation describes the hospitalization of more patients with bird flu symptoms. These comments suggest multiple members from the same family are being hospitalized, and some reports have piu the number of patients seeking treatment above 70. The above translation indicates some patients being hospitalized in Medan are being diagnosed with dengue fever.
Fatal dengue fever cases are being reported in other cities in the area, which raises additional concerns. In the past, H5N1 patients have been misdiagnosed as dengue fever because symptoms are similar, especially for the more serious dengue hemorrhagic fever. However, the dengue fever diagnosis for a family member of a confirmed H5N1 case raised serious questions about an increased reliance of a dengue fever diagnosis to reduce the number of confirmed H5N1 cases. This diagnosis was of particular concern because it was repeated by the Director General at the Ministry of Health, Nyoman Kandun, who has also indicated the the dramatic increase in hospitalized patients is due to villager concern over the H5N1 poultry. However, H5N1 positive poultry is common in Indonesia, where it has been declared endemic.
Recently, WHO has dispatched a team to North Sumatra in the absence of any confirmed H5N1 cases, raising concerns that the public denials of cases is inconsistent with the situation on the ground. Similarly, Japan agreed to supply an additional 500,000 courses of Tamiflu to southeast Asian countries, raising additional concerns regarding the situation in Indonesia. The earlier shipment of 500,000 courses of Tamiflu was stored in Singapore, which is adjacent to North Sumatra.
More information on the patients with bird flu symptoms and those being diagnosed with dengue fever would be useful |
| QUOTE | Indonesian Denials of H5N1 Cases In Sumatra Raise Concerns
August 11, 2008
http://www.recombinomics.com/News/08110801...tra_Denial.html
A senior health official says 13 villagers hospitalized with bird flu-like symptoms in western Indonesia have tested negative for the disease.
Nyoman Kandun said the test results came back negative on Saturday and the patients' conditions are improving.
He says dozens of chickens started dying last week from the H5N1 bird flu virus in Air Batu, a village on Sumatra Island, sending panicked residents rushing to a nearby hospital.
The above comments provide an update on the situation in northern Sumatra, but it is not convincing. H5N1 is endemic in poultry in Indonesia, and the fully extent is unclear because Indonesia has not filed an OIE report since 2006. Although their reporting requirement is every six months, since they declared H5N1 endemic, they have not met the six month requirement.
Similarly, they have not released any sequence data on human H5N1 isolates since early 2007, and have only sent samples from a handful of patients who have died in the past 18 months. Their recent announcement that they will limit reports on human cases, and the absence of WHO confirmation of the patients who were confirmed in July, continues to raise concerns due to lack of transparency.
These changes happened while clusters were obvious, even though Indonesia denied their existence. One of the clusters was specifically denied by Kandun, who stated that the brother of an H5N1 fatal case died of dengue fever.
This is of concern, because now media reports are stating that the patients who are being hospitalized with bird flu symptoms are being diagnosed with dengue fever. The association of H5N1 positive poultry, patients with bird flu symptoms, including fatal cases, and a diagnosis of dengue fever, are cause for concern.
Clarification of the situation by the WHO team on the ground in northern Sumatra would be useful. |
| QUOTE | ProMED Halts Reports Of Suspect H5N1 Cases in Indonesia
August 11, 2008
http://www.recombinomics.com/News/08110803...tra_ProMED.html
Until further notice, ProMED-mail will not report suspected human cases of avian influenza in Indonesia until they have been confirmed by the Indonesian Ministry of Health.
The above statement by ProMED is unfortunate. It is in response to Indonesia's failure to confirm H5N1 in the 13 hospitalized patients in North Sumatra. Indonesia's track record on confirming H5N1 patients has been poor. In addition to having the largest number of confirmed H5N1 cases and confirmed H5N1 deaths, it also has the highest case fatality rate, raising questions about its ability to detect non-fatal cases of H5N1.
'
Although Indonesia has failed to recently confirm H5N1 in patients in North Sumatra, H5N1 has been confirmed in poultry and three patients recently died with H5N1 symptoms. However, these patients were not tested for H5N1, which is still not uncommon in Indonesia.
The number of hospitalized patients continues to rise, and some are being diagnosed with dengue fever. However, Indonesia's record on diagnosing H5N1 patients as dengue fever cases has also raised concerns, especially when the dengue fever diagnosis is confirmed by the Minister of Health even when the sister of the dengue fever patient tested positive for H5N1.
The presence of a WHO team investigating the three fatal cases is unusual, especially since no H5N1 cases in humans has been reported.
ProMED's reliance on confirmation by the Indonesian Ministry of Health is unfortunate. The Ministry of Health has yet to issue a report the lab confirmed cases from July, and they have stated that they will report cases on a delayed basis.
ProMED's aiding and abetting of this diminished transparency in Indonesia, the country with the highest number of confirmed H5N1 cases in the world, should not stand. |
| QUOTE | Contact With Birds Not Required to Contract Bird Flu Infection
Saturday, August 09, 2008 by: David Gutierrez
http://www.naturalnews.com/023815.html
The World Health Organization (WHO) has warned that it may be possible to contract the avian flu without coming into direct contact with infected poultry.
In a report published in the New England Journal of Medicine, WHO researchers examined all 350 known cases of infection with the H5N1 strain of influenza, known popularly as "bird flu." Approximately three-quarters of these cases could be attributed to close contact with infected birds, often by poultry workers. A very few cases of human-to-human transmission are suspected, always between family members who came into close contact with each other. But the rest of the cases were more ambiguous.
"In one quarter or more of patients with influenza A (H5N1) virus infection, the source of exposure is unclear, and environment-to-human transmission remains possible," the researchers wrote. Some of the unclear cases occurred in people whose only contact with birds was walking through live poultry markets.
The authors speculated that the virus may remain active in fertilizer made from bird feces, or in certain fluids that stick to surfaces eventually touched by humans. The question has also been raised as to whether the virus needs to enter the nose or can infect humans by merely being eaten.
"It is unknown whether influenza A (H5N1) virus infection can begin in the human gastrointestinal tract," the researchers wrote. "In several patients, diarrheal disease preceded respiratory symptoms, and virus has been detected in feces."
The report confirmed government reassurances that well-cooked food is not a source of the disease, but cautioned that non-potable water might be: "Drinking potable water and eating properly cooked foods are not considered to be risk factors, but ingestion of virus-contaminated products or swimming or bathing in virus-contaminated water might pose a risk."
Bird flu is a highly lethal strain of the influenza virus, killing 61 percent of the people that it has infected. Scientists fear that it might mutate into a variety that passes easily to and between humans, with catastrophic public health consequences.
http://www.naturalnews.com/023815.html |
| QUOTE | H5N1 Clade 2.2.3 Migrates Into Nigeria
August 11, 2008
http://www.recombinomics.com/News/08110804...igeria_223.html
A strain of Highly Pathogenic Avian Influenza previously not recorded in sub-Saharan Africa has been detected in Nigeria for the first time, FAO said today.
The new strain has never been reported before in Africa; it is more similar to strains previously identified in Europe (Italy), Asia (Afghanistan) and the Middle East (Iran) in 2007.
The above comments describe the migration of clade 2.2.3 into Africa. This is not unexpected. Almost exactly one year ago, clade 2.2.3 was detected in the heart of Europe (Czech Republic, Germany, and France). The vast majority of the outbreaks were in wild birds, even though migration in Europe in the middle of the summer is minimal. The widespread outbreaks indicated H5N1 had become endemic in wild birds and the reservoir in resident birds lead to the outbreaks in domestic poultry.
Clade 2.2.3 then expanded in the fall and winter. All reported isolates in Europe were clade 2.2.3 and the vast majority, including those detected over the summer, were the Uvs Lake strain.
Therefore it is likely that the clade 2.2.3 in Nigeria is also the Uvs Lake strain, although that is not clear from the description above. However, the isolates cited were from the Capua lab, who did the sequencing of the 2008 isolates in Nigeria, and the failure to mention Uvs Lake isolates is likely more linked to what the Capua lab has sequenced previously, rather than the closest match with public sequences, which were from northern Europe, the Middle East, Uvs Lake, and South Korea / Japan.
Although clade 2.2.3 has not been reported previously in Egypt, the most recent isolates were acquiring clade 2.2.3 polymorphisms via homologous recombination. |
| QUOTE | Jakarta Post Issues H5N1 Alert for North Sumatra
August 11, 2008
http://www.recombinomics.com/News/08110806...atra_Alert.html
Indonesia has been the worst hit by the bird flu epidemic, with more than 110 people dead. The virus has struck again, with at least 11 people hospitalized in North Sumatra. What's wrong with the government program handling the problem? Send your thoughts by SMS to +62 811 187 2772. Please include your name and city. –Editor
The above bird flu alert was published in the Jakarta Post today. The lack of transparency on the status of H5N1 in Indonesia has created concern within the country, as well as the international community. The United States consulate general in Medan, as well as a team from WHO, are seeking information and clarification.
Although no confirmed H5N1 cases have been reported in North Sumatra, poultry is H5N1 positive and patients have died or have been hospitalized with bird flu symptoms. The initial three fatal cases were buried without testing, and subsequent hospitalized patients are said to be negative for H5N1, although some have now been said to be suffering from dengue fever. However, dengue fever is not usually fatal, but fatalities have been reported in adjacent areas,
Indonesia has announce that they will delay reports on H5N1 confirmed cases, even though IHR requires notification of WHO within 24-48 hours after confirmation. There were two laboratory confirmed H5N1 fatalities in July, but neither Indonesia nor WHO has issued an update acknowledging the fatalities. The Ministry of health refused to confirm or deny the first case and acknowledged the second, but WHO has not recorded either as a confirmed case, even though the first case died a month ago on July 10.
The concerns over the delayed reporting have been amplified by the denial of clear H5N1 clusters in recent cases. Although H5N1 had been confirmed, relatives who died with bird flu symptoms were said to have died of lung inflammation, typhus, and dengue fever. These earlier examples of misdiagnosis increase concerns over the large number of hospitalized patients, including those said to be suffering from dengue fever.
Thus, the media in Jakarta has appealed to citizens fro clarification on the confusing situation in North Sumatra. |
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| QUOTE | More than 80 pct of Indonesia bird flu cases die
Wed Aug 13, 2008 6:30pm EDT Email | Print | Share| Reprints | Single Page| http://www.reuters.com/article/americasCrisis/idUSN13258075
WASHINGTON, Aug 13 (Reuters) - Late diagnosis and treatment means that more than 80 percent of people infected with H5N1 avian influenza in Indonesia have died, researchers reported on Wednesday.
An analysis of outbreaks in Indonesia, the country hardest hit by bird flu, affirms that quick treatment with antiviral drugs can save lives. But local health care workers are not properly trained in diagnosing bird flu and often do not have the needed drugs to treat it.
Indonesia has had one-third of the world's known cases of human infection with H5N1 avian influenza. It rarely infects people but globally has killed 243 out of 385 sickened since 2003. In Indonesia, 135 people have been infected and 110 have died, according to the World Health Organization.
Dr. Toni Wandra of the Ministry of Health in Jakarta and colleagues analyzed the known cases as of February and found it took on average six days for patients to be admitted to a hospital.
By the time they were admitted, 99 percent had a fever, 88 percent were coughing and 84 percent had breathing problems, they reported in the Lancet medical journal.
But for the first two days they were ill, most patients had hard-to-identify symptoms -- only 31 had both fever and cough, and nine had fever and breathing problems.
On average it took seven days to get oseltamivir -- Roche AG (ROG.VX: Quote, Profile, Research, Stock Buzz) and Gilead Sciences Inc's (GILD.O: Quote, Profile, Research, Stock Buzz) Tamiflu.
More than a third of patients who got Tamiflu within six days survived, compared to 19 percent treated at seven days or later survived.
This confirms other research that shows treatment with flu drugs such as Tamiflu needs to start right away to be effective, they said.
"There is a clear need to identify definite causes for high-case fatality," Wandra's team wrote.
"Poultry surveillance is being stepped up, and active human case finding by local health centers and village officials is being instituted in areas of poultry deaths."
Workers need to be trained in getting information about whether patients with flu-like symptoms were around sick poultry, they added.
"Finally, all health-care workers should be trained in case management of early H5N1 influenza, and should be equipped with oseltamivir to enable timely administration."
H5N1 currently infects mostly birds and has killed or forced the destruction of 300 million in Asia, Europe, the Middle East and Africa.
It rarely infects humans and almost all cases have been infected by sick birds. Doctors fear it could change into a form that easily infects people, in which case it could sweep the world, killing millions of people in months.
Tamiflu and GlaxoSmithKline's (GSK.L: Quote, Profile, Research, Stock Buzz) and Biota's (BTA.AX: Quote, Profile, Research, Stock Buzz) Relenza can treat the infection, but are in short supply, and a vaccine would take months or years to manufacture and deliver. (Reporting by Maggie Fox, editing by Will Dunham) |
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| QUOTE | Tamiflu Resistance in Recombined H1N1 in South Africa
August 12, 2008
http://www.recombinomics.com/News/08120801...ecombinant.html
Recent reports from South Africa indicated that Tamiflu (oseltamivir) resistance was running at 100% in H1N1 isolates. Twenty-three of the first 100 H1N1 isolates had been sequenced, and all 23 had H274Y. Yesterday, HA and NA sequences were released from 13 H1N1 infected patients collected this season in May and June. All eight of the NA sequences had H274Y. The eight HA sequences mapped with Tamfiflu resistant sequences from other countries. Three of the HA sequences mapped to a branch with sequences from French isolates which had H274Y, while the other five mapped with isolates from the United States which had H274Y. Moreover, the NA sequence from at least one South African isolate from each group was released (see red highlighted isolates in list below). Thus, it is likely that all 13 patients from South Africa were infected with H1N1 carrying H274Y.
However, the five isolates which mapped with the US sequences had five polymorphisms clustered together over a stretch of 18 nucleotides. The clustering of 5 changes over such a small region is a signal of homologous recombination, and the changes at the 3’ side of the cluster matched human H1N1 sequences from the 1940’s (see list below). The appending of this group of changes onto a Brisbane/59 genetic background that maps with isolates that have H274Y is cause for concern. The five nucleotide changes lead to three non-synonymous changes (N200S, G202N, A207T - H1 numbering), signaling rapid evolution away from the Brisbane/59 target.
The current vaccine in use in South Africa, like the vaccine for the 2007/2008 season in the northern hemisphere, uses Solomon Island/3 as the H1N1 target, reducing the effectiveness of the vaccine. Although Brisbane/59 will be the target for the upcoming season, the emergence of the rapidly evolving strain in South Africa raises concerns that the newer Tamiflu resistant H1N1 isolates will also escape from the seasonal flu vaccine, which is chasing the H1N1 evolution.
The high frequency of H274Y on N1 in H1N1 and the potential for further evolution away from the soon to be implemented new H1N1 vaccine, raises additional concerns about the utility of using Tamiflu to blunt an H5N1 pandemic. H274Y also produces significant resistance on an H5N1 background, and recombination in N1 involving H1N1 and H5N1 can easily transfer H274Y from one genetic background to the other.
Thus, the emergence of widespread Tamiflu resistance in seasonal flu continues to be cause for concern with regard to the utility of oseltamivir stockpiled worldwide to blunt an H5N1 pandemic.
NA Sequences with H274Y
A/Johannesburg/45/2008
A/Johannesburg/36/2008
A/Johannesburg/35/2008
A/Johannesburg/33/2008
A/Johannesburg/21/2008
A/Johannesburg/14/2008
A/Johannesburg/12/2008
A/CapeTown/26/2008
HA Sequences Mapping with H274Y Positive French Isolates
A/Johannesburg/28/2008
A/Johannesburg/21/2008
A/CapeTown/26/2008
HA Sequences Mapping with H274Y Positive US Isolates
A/Johannesburg/46/2008
A/Johannesburg/35/2008
A/Johannesburg/34/2008
A/Johannesburg/25/2008
A/Johannesburg/10/2008
Sequence donors
A/Fort Monmouth/1/1947
A/Rhodes/47
A/Cam/46
A/Hickox/1940 |
| QUOTE | New bird flu strain found in Nigeria, UN's FAO says
Mon Aug 11, 2008
http://www.reuters.com/article/africaCrisis/idUSN11394577
WASHINGTON, Aug 11 (Reuters) - A new strain of H5N1 bird flu has shown up among birds in Africa in a worrying development, the United Nations Food and Agriculture Organization reported on Monday.
The new strain of H5N1 avian influenza is genetically different from the strains that circulated in Nigeria during earlier outbreaks in 2006 and 2007 and is new to Africa, the FAO said.
"It is more similar to strains previously identified in Europe (Italy), Asia (Afghanistan) and the Middle East (Iran) in 2007," the FAO said in a statement.
"The detection of a new avian influenza virus strain in Africa raises serious concerns as it remains unknown how this strain has been introduced to the continent," said Scott Newman, International Wildlife Coordinator of FAO's Animal Health Service.
"It seems to be unlikely that wild birds have carried the strain to Africa, since the last migration of wild birds from Europe and Central Asia to Africa occurred in September 2007 and this year's southerly migration into Africa has not really started yet," Newman added.
"It could well be that there are other channels for virus introduction: international trade, for example, or illegal and unreported movement of poultry. This increases the risk of avian influenza spread to other countries in Western Africa."
Avian influenza is common, but the H5N1 strain is particularly worrying both to poultry producers and doctors. The highly pathogenic H5N1 strain has swept through flocks in many parts of Asia, Europe and Africa.
It rarely infects people but has killed 243 out of 385 known to have been infected since 2003, according to the World Health Organization. It has killed or forced the slaughter of 300 million birds.
The fear is it could mutate into a form that people can easily catch and transmit; this could cause a pandemic that could kill hundreds of millions of people.
And H5N1 has become entrenched in a way that no other form of bird flu has, WHO says.
"Uncertainty about virus spread and transmission is a major challenge for control campaigns. Increased surveillance is key to monitor the situation and keep track of virus spread," said FAO chief veterinary officer Joseph Domenech.
Just last month Nigeria reported its first outbreak of H5N1 in nearly 10 months, among chickens and ducks in the northern cities of Kano and Katsina. (Reporting by Maggie Fox, editing by Will Dunham and Todd Eastham) |
| QUOTE | Uvs Lake H5N1 Migration Into Nigeria
August 14, 2008
http://www.recombinomics.com/News/08140801...igeria_Uvs.html
Tests conducted at the laboratory confirmed that the virus from Gombe closely resembles the virus isolated from wild birds in Central Europe (Romania and the Czech Republic ) in 2007.
The above comments clarify the clade 2.2.3 H5N1 recently reported for Nigeria. The FAO press release compared the recent isolates to the sequences from 2006/2007 clade 2.2.3 isolates from Italy, Afghanistan, and Iran. Since these earlier isolates were all clade 2.2.3 it seemed likely that the isolates would be the Uvs Lake strain which flew into Kuwait in early 2007 and spread throughout central Europe (Czech Republic, Germany, and France) in the summer of 2007, followed by more locations in Europe and the Middle East in late 2007 / early 2008. The above mentioned isolates in the Czech Republic represent Uvs Lake isolates in the summer, while Romania represents Uvs Lake in the fall.
Thus, the spread of Uvs Lake to eastern Africa was not unexpected, and the comparison top 2006 sequences is curious. The FAO press release once again tried to link the outbreak to trade and ignore the fact that the sequences were commonly found in wild birds. The sequences were first identified in a massive wild bird outbreak in the summer of 2006 and involved wild birds at Uvs Lake, the largest lake in Mongolia, as well as wild birds in Tyve, Siberia, which is just north of the lake.
The press release was yet another example of FAO’s denial of the role of wild birds in the transport and transmission of H5N1 clade 2.2 into more than 50 countries west of China, include those in south Asia, Europe, the Middle East, and Africa. All isolates reported to date are clade 2.2 including the 2.2.3 sub-clade in Nigeria. The Uvs Lake strain is within the 2.2.3 sub-clade, and is readily distinguished by the isolates in the FAO press release. The curious use of these earlier isolates in the FAO press release is yet another example of the FAO’s state of denial, since the clade 2.2,3 identified in Nigeria is firmly linked to outbreaks tied to wild birds in Asia and Europe.
In the FAO press release, the lack of association with the upcoming migration is the same argument that was used when there was an outbreak in Europe in the summer of 2007, when there was little long range migration. However, the H5N1 in wild birds in the Czech Republic, Germany, and France indicated the surveillance had missed the earlier arrival of clade 2.2.3, which was repeated in Africa this year.
The clade 2.2.3 in Nigeria was recently detected, but the earlier arrival was missed because of poor surveillance, which is far less robust in Nigeria than western Europe, which also failed to detected the Uvs Lake strain prior to the outbreak in wild birds a year ago. |
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Coincident Tamiflu and Relenza Resistance Sequences in NJAugust 15, 2008 http://www.recombinomics.com/News/08150801...R_H274Y_NJ.htmlThe recently released H1N1 sequences from South Africa confirm earlier reports indicating Tamiflu (oseltamivir) resistance had increased to 100% (23 of the first 23 isolates had H274Y). The released 8 NA sequences all had H274Y while the 8 HA sequences mapped with other HA sequences from isolates with H274Y. Five of the HA sequences had a cluster of 5 polymorphisms, indicating they were rapidly evolving away from the oseltamivir resistant Brisbane/59 HA sequence via homologous recombination. Phylogenetic analysis of other HA sequences on the same branch indicated published NA sequences had H274Y. Most of these sequences were from New Jersey (see list below). However, one of the isolates, A/New Jesey/08/2008, did not have H274Y (Tamiflu resistance), but did have a mixed signal for Q136R, which likely caused zinamivir (Relenza) resistance. Isolates with Q136K have been reported to be Relenza resistance, so changing the acidic Q at position 136 to either basic amino acids (K or R) will likely cause Relenza resistance. The Relenza and Tamiflu resistance coincident with similar HA sequences raises concern that these polymorphisms create a selective advantage for H1N1 in the absence of either neuraminidase inhibitor. If true, the increasing level of the HA sequence associated with Tamiflu resistance may lead to an increase in Relenza resistance, regardless of Tamiflu or Relenza usage. The New Jersey sequences fro HA and NA are mixtures, so resequencing of plaque purified clones would be useful. Similarly, full sequencing of all eight gene segments may help taget changes that lead to selection of additional changes which confir resistance to the nuraminidase inhibitors, oseltamivir (Tamiflu) and zinamivir (Relenza). HA Sequences Mapping With New Jersey/08/2008 Hawaii/02/2008 Johannesburg/10/2008 Johannesburg/25/2008 Johannesburg/34/2008 Johannesburg/35/2008 Johannesburg/46/2008 Maryland/04/2007 Memphis/03/2008 New Jersey/15/2007 New Jersey/16/2007 New Jersey/20/2007 New Jersey/05/2008 New Jersey/06/2008 New Jersey/10/2008 North Carolina/02/2008 Pennsylvania/02/2008 South Carolina/01/2008 Washington/01/2008 Wisconsin/01/2008
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| QUOTE | H5N1 Clade 7 Spread to Vietnam
August 28, 2008
http://www.recombinomics.com/News/08280801..._Vietnam_7.html
Anh told VNA that the H5N1 strain was named "seven." The story did not mention a clade number. Typically, the story said, "strain one" of the H5N1 virus has infected birds in the Mekong delta, while strains two, three, and four have been found to infect birds in the country's Red River Basin.
Nguyen Van Cam, director of Vietnam's Central Animal Diagnosis Centre, told VNA the lab was doing more tests to better characterize the strain and that he expected results soon.
The above comments from a CIDRAP update describe a new H5N1 clade in Vietnam, which is likely clade 7. The first confirmed H5N1 in mainland China was A/Beijing/01/2003, which is a clade 7 isolate from a fatal case in Beijing in 2003, as seen in the WHO pandemic vaccine target phylogram. A more recent clade 7 isolate is from A/chicken/Shanxi/2/2006 which was involved a significant poultry outbreak in Shanxi in 2006. This outbreak was described in multiple OIE reports, which detailed the use of three different anti-sera in efforts to bring the outbreak under control. The public sequences include multiple non-synonymous changes clustered around receptor binding domain position 190 (H3 numbering), as well as additional acquisitions, which subsequently appeared in the clade 2.2 vaccine resistant strain in Egypt and Israel.
These shared polymorphisms which were reported on genetically distinct H5N1 backgrounds illustrate the movement of polymorphisms via homologous recombination. This type of rapid change can defeat efforts using mismatched vaccines.
It is of note that the poultry vaccine effort in Egypt, like the effort in Vietnam, includes use of an H5N2 vaccine directed against a low path H5 target, which has also been used in Hong Kong. The extended use of these poorly matched vaccines has been associated with the repeated re-emergence of H5N1 in vaccinated regions, which may also be associated with an accelerated evolution to escape from the mismatched vaccine.
This type of evolution associated with mismatched vaccines is not limited to H5N1. Last season the trivalent seasonal flu vaccine was mismatched in all three targets. The mismatch in H1N1 was less obvious because the Bribane/59 isolates were being characterized as Solomon Island/3-like, even though Solomon Island/3 was no longer in widespread circulation in 2007/2008. This season the H1N1 target is switching to Brisbane/59, but early HA sequences from South Africa already has a cluster of changes near the receptor binding domain position 190 including adjacent polymorphisms matching H1N1 sequences from the 1940’s.
These rapidly evolving sequences were on the common H1N1 sequences which included Tamiflu resistance marker, H274Y, which is now at 100% of H1N1 isolates in South Africa and Australia.
The season and pandemic vaccine mismatches, and associated influenza evolution, remain causes of concern. |
| QUOTE | High Path H5N2 Recombinants in Wild Birds in Nigeria
August 28, 2008
http://www.recombinomics.com/News/08280802...geria_HPAI.html
The presence of coexisting but genetically distinguishable avian influenza viruses with an HP viral genotype in two cohabiting species of wild waterfowl, with evidence of non-lethal infection at least in one species and without evidence of prior extensive circulation of the virus in domestic poultry, suggest that some strains with a potential high pathogenicity for poultry could be maintained in a community of wild waterfowl.
The above comments are from the recently published PLOS paper “Evidence of Infection by H5N2 Highly Pathogenic Avian Influenza Viruses in Healthy Wild Waterfowl” and as noted above, acknowledge possible maintenance in wild waterfowl. However, the paper fails to acknowledge that the HA cleavage site matches H5N1 in waterfowl in Thailand, supporting acquisition by homologous recombination, as well as long range transport and transmission in waterfowl, since the above isolates are from Nigeria (see list below).
The H5 is phylogenetically related to low path H5 in Europe, Africa, and Asia, but contains multiple polymorphisms that are shared with high path H5N1, including clade 2.2 isolates in Egypt. These relationships provide additional evidence for the evolution of both high and low path H5 via recombination.
The N2 is related to a number of serotypes containing N2, providing evidence for reassortment. The N2 does not have the deletion found in the N1 in H5N1 but the HA cleavage site suggests the virus would be lethal in poultry and could cause problems in commercial poultry, which could lead to further evolution of the H5.
The presence of the cleavage site from H5N1 in Thailand raises concerns of long range movement of high path H5N2, and demonstrates the genetic diversity and plasticity of H5 and the associated highly pathogenic cleavage site
A/spur-winged goose/Nigeria/5388-2/2007(H5N2)
A/spur-winged goose/Nigeria/5388-5/2007(H5N2)
A/spur-winged goose/Nigeria/5388-8/2007(H5N2)
A/white-faced whistling duck/Nigeria/3927-1/2007(H5N2) |
| QUOTE | Because it's utter shite and a poisonous drug which has had almost zero worth from day one. Garlic would destroy it completely! -Craig
Dramatic Spread of H1N1 Tamiflu Resistance Puzzles Experts
August 26, 2008
http://www.recombinomics.com/News/08260801/H274Y_Puzzle.html
In a summary of H1N1 resistance to oseltamivir in the the 2007-08 flu season, the WHO said in June that no link between "oseltamivir exposure and resistance at the individual patient level was noted."
The increasing oseltamivir resistance in H1N1 viruses has puzzled experts. In an editorial published by Eurosurveillance in January, authorities said resistant viruses with the H274Y mutation had been seen in previous flu seasons but were rare and did not spread easily. But the more recent H1N1 isolates with the mutation were "fitter" and were spreading in the community, they wrote.
A recent update by the European Centre for Disease Prevention and Control (ECDC) observed, "At this stage the significance of these [resistance] findings remains uncertain. The emergence of drug resistance in the context of limited drug use is unexpected, and the extent of future circulation is difficult to predict."
The above summaries at the end of the most recent CIDRAP report on the spreading Tamiflu resistance, highlight the confusion linked to the reliance of influenza “experts” on a dying paradigm which uses selection of random mutations to explain antigenic drift in influenza. Consequently there is little understanding of how the resistance became widespread, and why it is unlikely that the trend will significantly reverse in the upcoming season.
The history of the emergence clearly demonstrates that the increasing dominance violates the old paradigm, leading to the conclusion that the recent isolates with H274Y are fit. However, the lack of the expected selection by Tamiflu use is the most striking aspect of they spread, as is the failure to look at the origins of the outbreak.
The earlier cases are largely ignored, even though the earlier cases were also in patients who had not taken recent Tamiflu. This condition applies to the wild birds infected with H5N1 in 2005, the clade 2C infected patients in China in the 2005/2006 season, the clade 1 infected patients in the United States in 2006/2007, or the early clade 2B patients in Hawaii in 2007/2008, which includes the region of identity downstream from the H274Y acquisition in all of the above human isolates.
The dramatic spread was not on the radar screen when the earlier cases were infected. Widespread discussion began after the rate in Norway exceeded 50%, as reported at the beginning of this year. All cases were H1N1, had the identical genetic change leading to H274Y, and were in patients not taking Tamiflu.
However, the failure to recognize the role of recombination in moving single nucleotide polymorphisms from one genetic background to another created more confusion. The concept of H274Y moving from a clade 2C background in China, to a clade 1 background in the US to a clade 2B background in the US, followed by movement to the dominant clade 2B background violated the random mutation aspect of the paradigm, and therefore was discounted.
Similarly, the reliance of poor reference anti-sera and target led to a misclassification of the H1N1 clades. In the past season the H1N1 vaccine target switched from New Caledonia (clade 1) to Solomon Island (clade 2A), but both targets had dead ended and were no longer in circulation. Instead they had been replaced by Brisbane/59 (clade 2B) and Hong Kong 2652 (clade 2C). However, Brisbane/59 was being called Solomon Island-like and Hong Kong 2652 was called New Caledonia-like, creating an illusion that the H1N1 was a match, when in fact it was a mismatch. Later in the season, classification of new Brisbane/59-like isolates were corrected, creating a second illusion, that Solomon Island was being replace by Brisbane during the season, when in fact Solomon Island was not in circulation anywhere in 2007/2008 and most countries were misreporting Brisbane as Solomon Island-like. Brisbane/59 grown on mammalian MDCK cells demonstrated the striking differences between immune recognition of Brisbane/59 and the target of the vaccine, Solomon Island/3. Mammalian Brisbane/59 generated a titer of 320 against the Brisbane anti-sera, which dropped to 40 for Hong Kong 2652, and was below the detection limits for Solomon Ilsand/3 (and New Caledonia/20). Thus, the use of a New Caledonia target in 2006/2007 and Solomon Island/3 in 2007/2008 helped establish Brisbane/29-like as the dominant H1N1 strain in circulation, including the subset with H274Y.
The most recent sequences from South Africa had a cluster of additional changes near the receptor binding domain (position 190 in H3 numbering), raising concerns that the role out of the new trivalent vaccine, which includes Brisbane/59 as the new H1N1 target, will have limited utility, pushing the evolution of H1N1 carrying H274Y.
This evolution was supported by the Tamiflu resistance level of 100% in South Africa and Australia this season. |
| QUOTE | H5 Spread to Benin
August 27, 2008
Live chickens purchased at the market in Lokossa as part of the routine surveillance and of the training of managers and other laboratory officials on biomolecular techniques at the Veterinary Laboratory of Parakou.
Causal agent Highly pathogenic avian influenza virus Serotype H5
The above comments from the Benin OIE report describe two chickens that are H5 PCR positive. It is likely that the birds were infected with H5N1 clade 2.2.3 Uvs Lake strain recently reported at multiple locations in northern Nigeria (see satellite map). These outbreaks have a striking parallel with outbreaks in Europe a year earlier.
In June of 2007, a presentation at the Options VI meeting on influenza declared wild birds in Europe to be H5N1 free, based on live bird surveys by various bird conservation groups. These assays, especially when screening fecal samples or cloacal swabs have a notoriously poor record, beginning with testing of wild birds at Erhel Lake in Mongolia in 2005 by these same groups. In the summer of 2005 dead wild birds at the lake were positive for H5N1 clade 2.2, but the testing of live birds at the lake failed to find any H5N1 positives. H5N1 subsequently migrated to the south and west, spreading clade 2.2 into over 50 countries west of China.
Included in this spread were multiple countries throughout Europe, which were H5N1 positive in early 2006. However, the frequency of positives markedly decline in late 2006 and early 2007, which led to the announcement at the talk. However, within minutes of the conclusion of the talk, the Czech Republic reported H5N1 at a poultry farm, which was quickly followed by reports of H5N1 in dead wild birds at multiple locations in Germany, as well as neighboring countries of the Czech Republic and France. The H5N1 was the Uvs Lake strain of clade 2.2.3, which had not been previously reported in Europe. The strain was initially found at Uvs Lake in Mongolia and adjacent locations in Tyva, Russia in the summer of 2006. In the fall of 2006, the strain was found in South Korea and Japan, followed by outbreaks in early 2007 in Kuwait. After the reports of Uvs Lake clade 2.2.3 in the summer of 2007 in Europe, it then became the dominant strain throughout Europe in late 2007 and early 2008.
Last month the Uvs Lake was reported for the first time in Africa, when H5N1 was detected at multiple locations in northern Nigeria. It is likely that the H5 positive poultry in southern Benin is also the Uvs Lake strain of clade 2.2.3. |
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| QUOTE | H1N1 Tamiflu Resistance At 100% in Honduras and Guatemala?
August 31, 2008
http://www.recombinomics.com/News/08310801..._Guatemala.html
With respect to neumonía, Sanchez needed that 260 people died in which goes of the year, among them 127 smaller children of five years and 96 greater adults of 50, the most vulnerable groups to the respiratory affections. Between the diseases that have begun to appear in the last months it appears influenza type AH1 N1, that causes high fevers, cough, muscular pains and in some cases diarrea pictures, it explained.
The above translation describes recent deaths Nicaragua, that were linked to H1N1 infections. The comments expressed concerns that influenza from Honduras was spreading into Nicaragua.
HA sequences from H1N1 isolates from Honduras and Guatamala were recently released at GenBank as part of a US military (Air Force) surveillance program. These sequences were in addition to a large series released a few months. The H1N1 sequences were collected in 2007/2008 season, and the five recent isolates from Honduras and Guatemala listed below are Brisbane/59 and closely related to each other.
Phylogenetic analysis places these isolates on a branch with H1N1 isolates that have H274Y. Recently sequences from South Africa were released, where the frequency of H274Y in H1N1 cases were at 100%, suggesting the sequences provided a selection advantage. The HA sequences from South Africa fell into two major groups. One had a cluster on newly acquired polymorphisms onto a genetic background that was common among H274Y isolates in the United States. The second group was related bur fell onto a branch with H274Y isolates from France.
The isolates from Honduras and Nicaragua form a new branch from the second branch described above. This new branch also has an isolate from France, which has H274Y, strongly suggesting that there recent isolates from Guatemala (collected in early June) and Honduras (collected in early and late July) also have H274Y, raising concern that the frequency of H274Y in recent isolates in Guatemala and Honduras are also near 100% Tamiflu resistant, which may now also be true for Nicaragua.
The NA sequence from these patients as well as additional isolates would be useful. All recent isolates also have K99N, which was also present in sequences from a Siberian Lake, which were closely related to human H1N1 from the 1930’s.
These data raise concerns that high frequencies of Tamiflu resistance have also come to North America. In South Africa, the first 107 H1N1 sequences this season had H274Y, as did the first 10 sequences from Australia.
A/Guatemala/AF1969/2008 01-Jun-2008
A/Guatemala/AF1995/2008 08-Jun-2008
A/Honduras/AF1968/2008 07-Jul-2008
A/Honduras/AF1994/2008 21-Jul-2008
A/Honduras/AF1993/2008 22-Jul-2008 |
| QUOTE | 29-Aug-2008
http://www.eurekalert.org/pub_releases/200...t-seb082908.php
Contact: Craig Brierley
c.brierley@wellcome.ac.uk
44-207-611-7329
Wellcome Trust
Scientists examine bird flu infections to monitor for 'pandemic' mutations
Scientists funded by the Wellcome Trust are to examine what is preventing the H5N1 avian influenza virus from causing a human pandemic and what mutations are required to realise its deadly potential. The research could hold the key to early identification of a potential influenza pandemic, and to developing drugs and a vaccine.
Since its reappearance in 1997, the H5N1 influenza virus has caused disease and death in millions of birds around the globe. The number of infections in humans is still relatively small, however: from 2003 to the end of June 2008 there had been 385 known cases in humans, 243 of them fatal(1). So far, there appear to have been very few cases of human-to-human transmission.
Professor Ten Feizi at Imperial College London believes one reason why H5N1 has not yet evolved into an effective pathogen capable of widespread transmission between humans lies in how the virus attaches itself to the respiratory tract. She is leading an international research project which has received over £720,000 from the Wellcome Trust to identify the receptor molecules in the human respiratory tract to which viruses attach and to look at how changes in the binding protein on the surface of the virus might increase its ability to attach to the tract and cause infection.
Professor Feizi will work with Professors Menno de Jong and Jeremy Farrar from the Wellcome Trust's South East Asia Programme in Vietnam, Dr Alan Hay and Dr Steve Gamblin at the Medical Research Council National Institute for Medical Research, London, and Dr Mikhail Matrosovich at the Philipps University of Marburg, Germany.
"Over the last few years particularly in Asia we have seen just how deadly the H5N1 virus can be," says Professor Farrar from the Oxford University Clinical Research Unit in Ho Chi Minh City, Vietnam, where a number of people have been treated for infection by the virus. "So far, we have been relatively fortunate and there has been only limited evidence of the virus transmitting from human to human. The more we understand about the virus, how it interacts with the body, the better we will be prepared for any serious mutations that may arise."
In humans, influenza infection occurs via the respiratory tract, or airway. In order to cause disease, the virus must enter the body's cells where it can replicate and spread, but it must first find a site to which it can attach, known as a receptor. The virus can only attach to and enter the cells if the receptor fits into the binding proteins, or haemagglutinins (the "H" in H5N1), on the surface of the virus.
Previous research has shown that the haemagglutinin on H5N1 favours a particular form of receptor known as a "2,3 receptor". These are abundant on cells of birds, but in humans are found mostly on cells of the lower respiratory tract (the lungs). Professor Feizi and colleagues have shown that mucus in the upper airway in humans also contains 2,3 receptors, but here the mucus acts as a defence mechanism to which the virus binds, blocking its progress and enabling the body to "sweep out" the virus. Both factors suggest that huge doses of the virus are required in order to infect humans, a theory supported by evidence that those who have become infected have spent large amounts of time in close proximity to infected fowl.
As with all viruses, H5N1 is continually mutating, and it is changes that allow the virus to attach to "2,6 receptors" in the human upper airway which may enable the virus to become more infectious to humans.
"If the bird flu virus evolves to favour the receptors in our nose and throat like normal flu, the results could be devastating," says Professor Feizi from the Division of Medicine at Imperial College London. "We could have a virus which is not only highly infectious but is easily transmissible by coughing and sneezing."
Dr Hay and Dr Gamblin will isolate haemagglutinin from samples of the virus taken from the patients in Vietnam, and Dr Matrosovich will grow cultures of human airway cells and isolate cell-membrane receptors and secreted mucus. Then, using a technique known as neoglycolipid (NGL) microarray analysis developed by Professor Feizi and her colleagues, the team at Imperial College will identify which of the various receptor structures the haemagglutinins bind most strongly to. Dr Gamblin's team will then use X-ray crystallography to probe, at the molecular level, how mutations might cause the bird virus to change into a human virus.
"If we can find out which mutations of haemagglutinin prefer which receptors, we may be able to identify quickly or even predict which mutations give the virus pandemic potential," says Professor Feizi.
Current antiviral treatments for influenza, such as Tamiflu, target neuraminidase (the "N" in H5N1), which is responsible for allowing the virus to jump off receptors on one cell and bind to those on another cell, and to replicate and spread once inside the body.
"Targeting the virus's ability to bind to the receptors – which until now has proved far more difficult – may provide an alternative, more effective way of preventing infection," says Professor Feizi. "We hope that our work will make this process simpler and faster."
###
1. Cumulative Number of Confirmed Human Cases of Avian Influenza A/(H5N1) Reported to WHO, 19 June 2008. http://www.who.int/csr/disease/avian_influ...9/en/index.html |
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| QUOTE | Fatal H1N1 Tamiflu Resistance
September 5, 2008
http://www.recombinomics.com/News/09050801/H274Y_Fatal.html
Oseltamivir was administered for the influenza virus infection, beginning on the sixth hospital day, but it was discontinued on day 13 because sequence analysis revealed the H274Y mutation, and no decrease in the viral load was observed. In retrospect, the H274Y mutation was present in the specimen obtained before oseltamivir therapy was initiated. The patient's hospital record and his family indicated that he had had no contact with patients who had received oseltamivir. On day 15, amantadine was added to the patient's treatment regimen. Four days later, the neutrophil count increased, indicating bone marrow recovery. Mechanical ventilation was discontinued on day 20, and zanamivir by inhalation was initiated. However, respiratory failure occurred on day 22, mechanical ventilation was reinstituted, and therapy with zanamivir was discontinued. On day 26, the influenza virus was no longer detectable. Because sequence analyses showed an amantadine-resistance mutation in the viral M2 protein (L26F) and zanamivir therapy had been limited to three doses, clearance of the virus was probably due to recovery of the immune system. A second CT scan, obtained on day 28, revealed progression of the pulmonary infiltrates. Because of the poor prognosis, mechanical ventilation was discontinued on day 34. The patient died 3 days later.
The above comments are from a correspondence to the New England Journal of Medicine on a patient who was sequentially treated with three antivirals, oseltamivir (Tamiflu), amantadine, and zanamivir (Relenza). The death of the patient was directly linked to his underlying cancer, but the monitoring of viral load and sequencing of sequential isolates provided additional insight into antiviral resistance.
The oseltamivir treatment did not decrease viral load, but when H274Y was identified in an isolate, treatment shifted from oseltamivir to amantadine, which cause a brief decline in viral load, but the emergence of L26F in the M2 target. This led to a shift to zanamivir, and an associated re-emergence of a wild type M2, indicting the L26F variant was not evolutionarily fit. Zanamivir treatment was only for three days, and the viral load subsequently declined, but the H274Y was present in all isolates, including an isolate from a sample collected prior to treatment.
The above case demonstrates the evolutionarily fitness of H1N1 with H274Y, and the failure of oseltamivir treatment to reduce the viral load. Thus, in countries with high levels of H274Y in H1N1, initial treatment with zanamivir is preferred in the absence of sequence data demonstrating a wild type N1.
H274Y was reported widespread in northern Europe, but recent reports suggest resistance may now be at 100% in South Africa, Australia, Guatemala, and Honduras. The vaccine targets for 2007/2008 in the northern hemisphere, and 2008 in the southern hemisphere have Solomon Island/3 as the H1N1 target. The new vaccine for 2008/2009 has replaced Solomon Island/3 (clade 2A) with Brisbane/59 (clade 2B). The isolates described above are clade 2B, but the dominant sub-clade in South Africa has already acquire a cluster of polymorphisms, which may limit the utility of the new vaccine.
Thus, H274Y levels in H1N1 may increase in the upcoming season, which would lead to increased zanamivir usage. However, zanamivir resistance, Q136K or Q136R, has been reported on a clade 2B background in 2008 isolates in Thailand and the United States as well as 2007 isolates in South Africa and Australia, raising concerns of an increase in evolutionarily fit H1N1 with Q136K. |
| QUOTE | Spreading H1N1 Tamiflu Resistance in Australia?
September 5, 2008
http://www.recombinomics.com/News/09050802...lia_Spread.html
AN unexpected influenza strain has swept through Geelong and blown out waiting times at the hospital emergency department, Barwon Health says.
Barwon Health said reports of 20-hour waits in the hospital's ED were due to a "strain of influenza not covered by this year's vaccine".
"Consequently, the Geelong Hospital is experiencing a period of high demand and high acuity," the Barwon Health statement said.
Barwon Health could not confirm the strain's identity late yesterday, but said it caused respiratory problems, particularly among older people.
The above comments describe a flu outbreak in Australia. Since the influenza is said to not be covered by the current vaccine, it is likely an outbreak of H1N1. The vaccine for 2007/2008 northern hemisphere flu season mismatched all three targets. However, poor reference anti-sera failed to detect significant differences between Solomon Island/3, the H1N1 vaccine target, and Brisbane/59, the dominant H1N1 sub-clade outside of Asia. Consequently, the 2008 vaccine for the southern hemisphere had new targets for H3N2 and Influenza B, but the mismatched Solomon Island/3 target was used, extending the mismatch to another season.
As was easily seen by phylogenetic analysis, Solomon Island/3 (clade 2A) was not circulating in 2007/2008, and had been replaced by Brisbane/59 (clade 2B), which also had H274Y. The first 10 sequenced H1N1 isolates in Australia had H274Y, suggesting the Tamiflu resistance was widespread and likely to be present in the patients experiencing respiratory problems.
Similar respiratory problems were reported in Honduras recently, and H1N1 HA sequences recently released suggests that those isolates, as well as isolates from Guatemala, which were virtually identical, had H274Y in the NA sequence.
As was seen in the recent fatal case from the Netherlands, treatment of H274Y positive H1N1 with Tamiflu fails to reduce the viral load, which could create problems for immuno-compromised patients, leading to death.
More information on the recent outbreak in Australia would be useful. |
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| QUOTE | Dutch patient dies from Tamiflu-resistant H1N1 virus
Lisa Schnirring and Robert Roos Staff Writers
http://www.cidrap.umn.edu/cidrap/content/i...resistance.html
Sep 5, 2008 (CIDRAP News) – Amid concern about rising resistance to oseltamivir (Tamiflu) in influenza A/H1N1 viruses, a Dutch team this week reported the death of a leukemia patient who was infected with an H1N1 virus that was resistant to the antiviral drug.
In a letter in this week's New England Journal of Medicine (NEJM), the Dutch authors said the case suggests that oseltamivir-resistant H1N1 viruses can cause disease, despite evidence from animal studies that the resistance mutation makes the viruses much less dangerous. The letter said the man's virus was also resistant to amantadine, an older antiviral drug.
On Aug 20, the World Health Organization (WHO) reported that 31% of influenza A/H1N1 isolates from 16 countries that conducted recent tests carried the H274Y mutation, which confers resistance to oseltamivir. Resistance levels ranged from 100% (10 of 10 isolates) in Australia to 13% (4 of 32 isolates) in Chile.
Emergence of the oseltamivir-resistant H1N1 virus was first noted in Norway in January, and since then researchers have found the virus in 35 countries, including the United States and Canada.
The spread of the oseltamivir-resistant H1N1 virus has puzzled experts because it has not been clearly linked to treatment with the drug.
In the case report, authors from Erasmus University Medical Center in Rotterdam wrote that a 67-year-old man who was on chemotherapy in a 3-year battle with chronic lymphocytic leukemia was hospitalized with shortness of breath, a dry cough, and fever. On his second hospital day, he experienced acute respiratory failure, and his physicians placed him on a ventilator and started empirical antibiotic treatment.
Computed tomography (CT) revealed that the patient had patchy lung infiltrates, and tests on samples from his respiratory tract showed he had influenza A/H1N1.
On the sixth hospital day the man received oseltamivir, but by day 13 physicians discontinued the drug because sequence analysis of the virus revealed the H274Y mutation and there was no decrease in the viral load.
The authors reported that the mutation was found in samples obtained before the patient began oseltamivir therapy. The man's family and the hospital record revealed that he had had no contact with patients who were taking oseltamivir.
On the 15th hospital day the man's doctors prescribed amantadine, and after a few days his neutrophil count increased, a sign of bone marrow recovery, the group reported.
On day 20 doctors took the patient off the ventilator and instituted zanamivir treatment. However, 2 days later the man had respiratory failure again, and his medical team put him back on the ventilator and discontinued zanamivir therapy. (Like osteltamivir, zanamivir is a neuramnidase inhibitor, but no increase in zanamivir resistance has been reported recently.)
By day 26 physicians detected no influenza virus, but did note that sequence analysis showed an amantadine-resistance mutation in the viral M2 protein (L26F). They wrote that recovery of the immune system was probably responsible for clearing the virus, because the patient had received only three doses of zanamivir.
A repeat CT scan taken on day 28 showed that pulmonary infiltrates had progressed. Because of the man's poor prognosis, the ventilator was removed on day 34, and he died 3 days later.
The authors cited animal studies indicating that oseltamivir resistance leaves H1N1 viruses "severely compromised." Despite these reports, they wrote, "the case we describe suggests that this oseltamivir-resistant virus can be pathogenic, at least in an immunocompromised patient."
In an editorial published by Eurosurveillance in January, authorities said resistant viruses with the H274Y mutation had been seen in previous flu seasons but were rare and did not spread easily. But the more recent H1N1 isolates with the mutation were "fitter" and were spreading in the community, they wrote.
Van der Vries E, Van den Berg B, Schutten M. Fatal oseltamivir-resistant influenza virus infection. N Engl J Med 2008 Sep 4;359(10):1074-76 [Full text] |
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| QUOTE | CDC chief states flu pandemic is coming
Published on 08-09-2008 Email To Friend Print Version
http://www.blacklistednews.com/news-1411-0-6-6--.html
Ready or not, a flu pandemic is coming, says Dr. Julie Gerberding, director of the federal Centers for Disease Control and Prevention.
Gerberding talked about preparing for the pandemic threat at a national conference Thursday at Logistics Health in La Crosse. No one knows when the pandemic is coming or what strain of flu virus will cause it, but it is overdue, she said.
Director of the Center for Disease Control, Dr. Julie Gerberding, speaks Thursday during a flu pandemic preparedness conference at Logistics Health's Riverside Center South. PETER THOMSON photo
She said she has only two meetings a week at the CDC and one focuses on flu pandemic preparations. “We take it very seriously,” Gerberding said, adding that the national strategy is to “save lives and sustain a civil society” during a pandemic.
She said politicians are not talking about a flu pandemic or the bird flu virus, which may or may not be the virus that causes the next pandemic.
“No one is talking about it, and it’s not on their radar screen,” Gerberding said.
She said CDC officials are closely monitoring the bird flu virus, which has a death rate of 63 percent among the 385 cases reported worldwide since 2003.
“It is a moving target, and we have to stay on top of it,” Gerberding said.
She said CDC scientists have created a potential vaccine in case the virus develops into a pandemic strain and are conducting more research to develop a vaccine. They have recreated the virus that caused the 1918 flu pandemic to better understand it.
Gerberding said organizations and corporations need to come up with preparedness plans and confront the impact of a flu pandemic. Some people believe a pandemic won’t happen, while others feel too overwhelmed to do anything, she said.
“Complacency is the enemy of health protection,” she said.
Gerberding said CDC officials are working to decrease the time to detect a virus and strain by improving diagnostic tests and to protect people with stockpiled antiviral medication and speedy containment of the virus.
The CDC is building 18 global disease detection and response centers around the world, Gerberding said.
Despite all the planning so far, epidemiologist Michael Osterholm, who helped lead the CDC before Gerberding was appointed director, said everyone needs to be more prepared due to our global economy.
Osterholm, director of the infectious disease center at the University of Minnesota, said the death rate from the next pandemic could exceed 300 million.
Critical products and services including food, water and basic drugs won’t get to people due to transportation and energy problems in a pandemic, he said. Global supply chains may be severely challenged, he said.
“No one has addressed the food system yet,” Osterholm said.
Logistics Health, the Coulee Region Public Health Consortium and the La Crosse Medical Health Science Consortium sponsored the conference. More than 150 business and organization personnel attended in person, and another 1,200 people watched the Webcast. A majority of the Fortune 500 corporations were represented.
Tommy Thompson, the former Wisconsin governor who is now president of Logistics Health, hired Gerberding and Osterholm when he was secretary of U.S. Health and Human Services.
“Planning is important for survival,” Thompson said. |
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