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Avian influenza infection was confirmed among chickens at a poultry farm in Chiba city, marking the first such case in the Kanto region centering on Tokyo, the Chiba prefectural government said. Local authorities began culling about 35,000 birds at the farm yesterday and restricted the movements of another 869,000 birds being raised within a 10-kilometer radius of the farm in question. ''This is a very severe situation as damage from the huge earthquake is also serious,'' Chiba Gov Kensaku Morita said at a press conference, referring to the powerful quake that struck northeastern and eastern Japan on Friday. A total of four birds were found dead at the Chiba farm on Friday and Saturday, and a genetic test confirmed that four out of seven birds checked were infected by a highly pathogenic strain of bird flu virus, local government officials said. Chiba is Japan's second-largest chicken egg producing prefecture.
The evolution of the highly pathogenic H5N1 virus produces genetic variations which can lead to changes in antiviral susceptibility and in receptor-binding specificity. In countries where highly pathogenic H5N1 virus is endemic or causes regular epidemics, surveillance of these changes is important for assessing the pandemic risk. In Cambodia between 2004 and 2010, there have been 26 outbreaks of highly pathogenic H5N1 influenza in poultry and 10 reported human cases, of which 8 were fatal. We have observed naturally occurring mutations on the HA and NA of Cambodian H5N1 viruses which were predicted to alter sensitivity to neuraminidase inhibitors and/or receptor-binding specificity. We tested H5N1 viruses isolated from poultry and humans between 2004 and 2010 for sensitivity to the neuraminidase inhibitors (NAIs) oseltamivir (Tamiflu®) and zanamivir (Relenza®). All viruses were sensitive to both inhibitors, however, we identified a virus with a mildly decreased sensitivity to zanamivir, and have predicted that a V149A mutation is responsible. We also identified a virus with a hemagglutinin A134V mutation, present in a subpopulation amplified directly from a fatal human patient's sample. Using reverse genetics, we verified that this mutation is adaptative for human 2,6-linked sialidase receptors. The importance of ongoing surveillance of H5N1 antigenic variance and genetic drift which may alter receptor binding and sensitivities of H5N1 viruses towards NAIs, cannot be underestimated whilst avian influenza remains a pandemic threat.
Suspect Fujian H5N1 Case In Israel Recombinomics Commentary 22:10 March 8, 2011 Concern that a poultry farmer from Kibbutz Rosh Tzurim in Gush Etzion contracted bird flu. The man was hospitalized a few days at Shaare Zedek Hospital in Jerusalem. The deadly virus was discovered yesterday in one of his kibbutz runs. Blood tests of laboratory testing verbalist transferred, and results are expected tonight.
The above translation describes a suspect H5N1 case associated with an outbreak on a turkey farm, which led to the culling of 40,000 birds. This outbreak follows reports of H5N1 in poultry in Palestine. Although H5N1 has been reported previously in Israel and Palestine, the latest outbreak likely involves the Fujian strain (clade 2.3.2), which has been associated with recent wild bird and poultry outbreaks in South Korea and Japan, as well as earlier wild bird outbreaks. The recent outbreaks in Japan included the receptor binding domain change, S227R (in addition to M230I). Tthe first reported human case west of China involved the Qinghai train with the receptor binding domain change S227N, which was predicted.
These earlier reports strongly suggested that the Fujian strain would subsequently be reported in wild birds, poultry, and humans in Europe, the Middle East, and Africa.
If confirmed, this would be the first reported case in Israel, and if clade 2.3.2 is confirmed, this would be the first reported human case west of China. All prior human cases (in Turkey, Iraq, Azerbaijan, and Egypt) have been the Qinghai strain (clade 2.2).
Originally posted by quackers
reply to post by apacheman
Er do you know the difference between an epidemic and a pandemic? Call me pedantic but theres a fine line between telling the news and blowing it totally out of proportion.
Originally posted by quackers
reply to post by apacheman
Er do you know the difference between an epidemic and a pandemic? Call me pedantic but theres a fine line between telling the news and blowing it totally out of proportion.
The persistence of H5N1 avian influenza viruses in many Asian countries and their ability to cause fatal infections in humans have raised serious concerns about a global flu pandemic1. Here we report the isolation of an H5N1 virus from a Vietnamese girl that is resistant to the drug oseltamivir2, which is an inhibitor of the viral enzyme neuraminidase and is currently used for protection against and treatment of influenza. Further investigation is necessary to determine the prevalence of oseltamivir-resistant H5N1 viruses among patients treated with this drug. An H5N1 influenza virus, A/Hanoi/30408/ 2005, was isolated on 27 February 2005 from a 14-year-old Vietnamese girl (patient 1) who had received a prophylactic dose (75mg once a day) of oseltamivir from 24 to 27 February and was given a therapeutic dose (75mg twice daily) for 7 days starting on 28 February. No virus was isolated from specimens after the administration of increased doses of oseltamivir. The patient recovered and was discharged from hospital on 14 March 2005...Patient 1 had not had any known directcontact with poultry, but had cared for her 21-year-old brother (patient 2) while he had a documented H5N1 virus infection (for details of the disease course and treatment in these patients, see supplementary information). We found that the neuraminidase gene of the brother’s virus was identical to clone 7 of the girl’s virus (see supplementary information). Also, the haemagglutinin gene of the brother’s virus was identical to clones 2 and 9 of the girl’s virus, apart from a nucleotide change at position 271. The timing of infection in these two patients, together with the lack of known interaction of the girl with poultry, raises the possibility that the virus could have been transmitted from brother to sister
Preparedness for a possible influenza pandemic caused by highly pathogenic avian influenza A subtype H5N1 has become a global priority. The spread of the virus to Europe and continued human infection in Southeast Asia have heightened pandemic concern. It remains unknown from where the pandemic strain may emerge; current attention is directed at Vietnam, Thailand, and, more recently, Indonesia and China. Here, we report that genetically and antigenically distinct sublineages of H5N1 virus have become established in poultry in different geographical regions of Southeast Asia, indicating the long-term endemicity of the virus, and the isolation of H5N1 virus from apparently healthy migratory birds in southern China. Our data show that H5N1 influenza virus, has continued to spread from its established source in southern China to other regions through transport of poultry and bird migration. The identification of regionally distinct sublineages contributes to the understanding of the mechanism for the perpetuation and spread of H5N1, providing information that is directly relevant to control of the source of infection in poultry. It points to the necessity of surveillance that is geographically broader than previously supposed and that includes H5N1 viruses of greater genetic and antigenic diversity.
J Mol Neurosci. 2008 Jul;35(3):339-43. Epub 2008 Feb 28.
The H5N1 influenza variant Fujian-like hemagglutinin selected following vaccination exhibits a compromised furin cleavage : neurological Consequences of highly pathogenic Fujian H5N1 strains.
Pasquato A, Seidah NG.
Laboratory of Biochemical Neuroendocrinology, Clinical Research Institute of Montreal, Montreal, Quebec, Canada.
Abstract
The outbreak of H5N1 avian influenza strains infectious to human has dire neurological and pathological consequences. This led to the massive vaccination of host poultry, resulting in a Fujian-like variant (vFJ) resistant to immunization with two mutations at the furin-processing site of hemagglutinin: loss of the P2 Lys and P9 substitution of Gln to Leu within the cleavage site. We synthesized 14mer peptides mimicking the processing site of Fujian-like strains. We found that the peptide with the vFJ sequence is less cleaved as compared to the parent FJ-derived peptide by furin at either neutral or acidic pH values. We hypothesize that the double hemagglutinin mutations in vFJ may result in viruses with less processed hemagglutinin, thereby providing a mechanism for evading immune neutralization.
NEWS SCAN: Egyptian H5N1 cases, more H5N1 outbreaks, vaccine-narcolepsy probe, anthrax testing
Mar 7, 2011
Egypt reports two more H5N1 infections Egypt's health ministry has announced two more H5N1 avian influenza cases, in a 32-year-old woman and a 2-year-old boy, the World Health Organization (WHO) reported today. The woman, from northern Egypt's Sharkia governorate, got sick Feb 10 and was hospitalized 4 days later; she is in critical condition. The boy is from Kafr el Sheikh governorate, located in northern Egypt along the western branch of the Nile River. He became ill with flulike symptoms on Feb 18, was hospitalized on Feb 20, and is reportedly in good condition. Investigations into the source of their illnesses revealed both patients had been exposed to sick poultry. The illnesses are listed as Egypt's 126th and 127th H5N1 cases, of which 41 were fatal. They raise the WHO's global H5N1 total to 528, including 311 deaths.
Originally posted by apacheman
reply to post by ommadawn
I take it you don't follow links?
What do you think bird flu is? H5N1 is bird flu.
Avian Influenza Mutation, H5N1
H5N1 is a type of avian influenza virus (bird flu virus) that has mutated through antigenic drift into dozens of highly pathogenic varieties. The first of these appeared in China in 1996 in birds and in Hong Kong in 1997 in Humans.
This infection of humans coincided with an epizootic (an epidemic in nonhumans) of H5N1 influenza in Hong Kong's poultry population. This panzootic (a disease affecting animals of many species esp. over a wide area outbreak was stopped by the killing of the entire domestic poultry population within the territory. The name H5N1 refers to the subtypes of surface antigens present on the virus: hemagglutinin type 5 and neuraminidase type 1.
Recombinomics Commentary 18:10
March 16, 2011
Hokkaido University released the H5N1 sequence from a duck in Fukushima, A/duck/Fukushima/2/2011, which was collected in January, 2011. Like the sequence from the whooper swan in Hokkaido, A/whooper swan/Hokkaido/4/2011, it had S227R (in addition to V223I and M230I). A third sequence from Tochigi, A/peregrine falcon/Tochigi/15/2011, had the earlier changes (V223I and M230I), but did not have S227R.
The duck sequence was closely related to the whooper swan protein sequence (the duck also had E362D), raising concerns that the receptor binding domain changes (V223I, S227R, M230I) are widespread in H5N1 clade 2.3.2 in northern Japan, including the region most affected by the earthquake and tsunami.
March 17, 2011
Information received on 16/03/2011 from Dr Toshiro Kawashima, CVO, Animal Health Division, Ministry of Agriculture, Forestry and Fisheries, Tokyo , Japan
Summary
Report type Follow-up report No. 8
Start date 15/12/2010
Date of first confirmation of the event 19/12/2010
Report date 16/03/2011
Date submitted to OIE 16/03/2011
Reason for notification Reoccurrence of a listed disease
Date of previous occurrence 01/04/2009
Manifestation of disease Clinical disease
Causal agent Highly pathogenic avian influenza virus
Serotype H5N1
Nature of diagnosis Clinical, Laboratory (basic), Laboratory (advanced), Necropsy
This event pertains to the whole country
Related reports Immediate notification (20/12/2010)
Follow-up report No. 1 (22/12/2010)
Follow-up report No. 2 (19/01/2011)
Follow-up report No. 3 (23/01/2011)
Follow-up report No. 4 (04/02/2011)
Follow-up report No. 5 (14/02/2011)
Follow-up report No. 6 (24/02/2011)
Follow-up report No. 7 (03/03/2011)
Follow-up report No. 8 (16/03/2011)
The above comments summarize OIE reports on confirmed H5N1 in wild birds identified throughout Japan, including northern Japan. Sequences from three isolates from these outbreaks have been made public at Genbank. Two of the three (in Hokkaido and Fukushima) have S227R. All three sequences are the Fujian strain (clade 2.3.2) which have been circulating in wild birds for several years, including the large outbreaks in Japan, South Korea, and Russia in the spring of 2008. The clade 2.3.2 sequences have two additional receptor binding domain changes (V223I and M230I), which were present in the clade 2.2 sequences from the Gharbiya cluster in Egypt in late 2006. The Gharbiya cluster is the largest H5N1 cluster in Egypt reported to date. All three patients died and the RBD changes raised concerns of increase transmission in human.
The recent acquisition of S227R increased concerns because of the known changes in receptor binding specificity due to S227N, which was predicted and confirmed in 2 of the 4 sequences from Turkey in 2006. The recent reports of two confirmed cases in Kamalpur, a Bangladesh slum have increased concerns that clade 2.3.2 has migrated to Bangladesh and is involved in the two recent cases (as well as symptomatic contacts).
The worsening situation at the Daiichi nuclear power facility in Fukushima, Japan increases concerns that the H5N1 circulating in wild birds and poultry in the region will be impacted by the release of ionizing radiation. This radiation can lead to rapid evolution of clade 2.3.2 H5N1, which may lead to selection of changes that increase transmission in humans in the region. These changes could quickly spread through displaced persons living in crowded conditions that are far from ideal.
Close monitoring of these persons as well as H5N1 sequences from wild birds and poultry, a timely release of such sequences would be useful.
=================================
4) UPDATE: March 20, 2011
There is also a concern that organisms in the sea water being used to cool the reactors and fuel rods may mutate and return to the sea (which they presumably may if the ponds are allowed to overflow) with unforeseeable consequences...asks a concerned Smart Economy Blog reader.
A retired nuclear scientist in Europe responds:
"The H5N1 Flu pandemic is not over, despite media ignoring it. For instance, there has been a renewed wave of H5N1 Flu pandemic here in Switzerland that started BEFORE the Fukushima event, and it is clear to all and any epidemiologist this flu strain is continuously mutating and WILL keep MUTATING with or without the Fukushima event, the human body itself being the site where it mutates. Outside the human body, influenza viruses typically do not remain infectious for long, become inactive via sessication, decay, sterilizing by solar radiation etc. So there should be no worries of H5N1 Flu viruses that may have landed in seawater and then be sucked into the reactor.
Seawater contains naturally radioactive elements such as Uranium, the whole Uranium decay series, but also low concentrations of Fissogenic products (i.e. the same "waste products" you find in nucl. reactors, that includes of course radioactive Plutonium, Iodine, Cesium, Strontium etc.) but all that stuff naturally derived from cosmic-ray bombardment of Uranium in seawater. Furthermore, there is radioactive activated and spallation products from other, more stable elements, and pristine radioactive isotopes such as Potassium 40 (and many many more).
That means the natural marine environnment is per se radioactive and fertile/prone to continuosly trigger mutations of any lifeform swimming on it. This has always been the case, AB INITIO, and will stay so (with or without human activities), until to the dead of times.
My first guess is that viable mutations are arguably created at sea, more than in a nuclear reactor where I expect radiation is intense enough to kill off most life (but radiudurans type bacteria).
Avian influenza – situation in Indonesia - update 2
25 March 2011 - The Ministry of Health of Indonesia has announced a confirmed case of human infection with avian influenza A(H5N1) virus.
The case is a 2 year old female from Bekasi City, West Java Province. She developed symptoms on 2 March, was admitted to a health care facility on 3 March and referred to a hospital on 9 March. She has fully recovered from her illness.
The case’s mother (see update, 14 March) died of confirmed avian influenza A(H5N1) virus infection one day prior to onset of illness in the new case...
...Of the 175 cases confirmed to date in Indonesia, 144 have been fatal.
In a new study, a team of researchers at the Massachusetts Institute of Technology (MIT) have successfully identified a single mutation in the H1N1 genetic make-up. This mutation would allow the virus to be transmitted between people much more easily.
H1N1, first reported in March 2009 in Mexico, contains a mix of human, swine and avian flu genes, which prompted fears that it could prove deadlier than typical seasonal flu viruses. However, the death toll was much lower than initially feared, in large part because the virus turned out to be relatively inefficient at spreading from person to person...
...Some new H1N1 strains have already emerged, and the key question, Sasisekharan adds, is whether those strains will have greater ability to infect humans.
World Health Organization (WHO) labs around the world are collecting samples of human and avian flu strains, whose DNA is sequenced and analyzed for potential significant mutations...
In the new PLoS study, the MIT researchers focused on a segment of the HA protein that they have shown affects its ability to bind to respiratory cells. They created a virus with a single mutation in that region, which replaced the amino acid isoleucine with another amino acid, lysine. That switch greatly increased the HA protein’s binding strength. They also found that the new virus spread more rapidly in ferrets, which are commonly used to model human influenza infection.
If such a mutant virus evolved, it could generate a ‘second wave’ like the ones seen in 1918 and in 1957 (known as the ‘Asian flu’). “If you look at the history, it takes a very small change to these viruses to have a dramatic effect,” Mr Sasisekharan says.
The amino acid in question is located in a part of the viral genome prone to mutate frequently, because it is near the so-called antigenic site - the part of the HA protein that interacts with human antibodies. Antigenic sites tend to evolve rapidly to escape such antibodies, which is why flu vaccine makers have to use new formulas every year. This year’s vaccine included a strain of H1N1, which is still circulating around the world.
RNA is a less stable molecule than DNA, so it is subject to more mutations. Riboviruses like influenza use RNA exclusively, and as a result they mutate faster than any other kind of virus.
Virus mutation rates are measured as the mutations per genome per replication (μg) — that is, the average number of mutations that will occur each time a single virus particle (virion) copies its genome. DNA viruses — those that use only DNA at all stages of their replication cycle — have the lowest mutation rate, μg = 0.0034. Retroviruses, which use both DNA and RNA in their replication cycle, have a much higher rate of about 0.2. Influenza and other riboviruses have an incredible μg of about 0.67 to 0.76. Since each complete virus replication cycle requires two transcriptions, that means each daughter virus has an average of 1.34 to 1.52 mutations! The superfast mutation rate of influenza is what fuels its ability to evolve and adapt, overcoming the immune system's method of recognizing old pathogens.