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| Tracking the next pandemic: Avian Flu Talk |
Altered Receptor Binding in H5N1 Bird Flu in Indo |
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 Topic: Altered Receptor Binding in H5N1 Bird Flu in IndoPosted: June 08 2006 at 6:20pm |
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Commentary
Altered Receptor Binding in H5N1 Bird Flu in Indonesia? Recombinomics Commentary June 8, 2006 This difficulty was caused by two matters that is receptor relations and spesifisitas the receptor and the difference of the temperature between the person and the poultry also were different. Therefore, I carried out the research in the month February-March 2006. This research was helped by Tokyo University. The aim of the research to know whether the circulating virus in the field, only had the shape of the virus from the poultry that is had spesifisitas the receptor alfa 2,3 or that had spesifisitas the receptor alfa 2,6 that is the virus that could infect direct to the mammal (the pig and humankind, etc..) . The sample that I the test came from the poultry, the pig, and humankind. From 100 samples, there is 20 that succeeded in being turned on and evidently 11 among them had spesifisitas the receptor 2,6. Meaning that, these viruses had the capacity immediately could infect humankind without must from the poultry before. Moreover, some of the samples had the amino acid lisin in the number 627 proteins PB2, that meaning that the virus could be stable in the temperature of the human body. The above translation of an interview with CA Nidom from the Airlangga University Vetereinary School in Surabaya is cause for concern. The comments indicate that 20% of the samples tested had virus (presumably H5N1) and 55% of the positives had a 2,6 receptor specificity, indicating they had an increased affinity for human receptors in the upper respiratory tract. In addition, many had PB2 E627K, which allows the H5N1 to grow at lower temperatures. Earlier reports described E627K in one of the initial samples from Jakarta, A/Indonesia/6/2005(H5N1). There was additional speculation that the high levels of H5N1 bird flu in the nose and throat of victims in Medan were also due to E627K. The above comments indicates thee are differences in receptor specificities in the H5N1 isolates from Jakarta. The comments above to not break down the number of H5N1's with 2.6 specificities, but H5N1 can readily recombine and exchange such information, so finding that specificity in H5N1 in any of the tested species is cause for concern. Media Source Link Phylogenetic Tree |
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Posted: June 08 2006 at 6:26pm |
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What can one say at a time like this?
I believe that I will say it one more time. May God have mercy on us. |
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Posted: June 08 2006 at 6:29pm |
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Im not the smartest person here. But this don't sound good. Could someone please explain what it means. In layman terms?
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Posted: June 08 2006 at 6:30pm |
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Does this mean the virus has mutated so it is now easy for a pandemic to occur?
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Zondar
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Posted: June 08 2006 at 6:33pm |
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I'm not an expert either, birdlady, but I believe it means there are signs the virus may be mutating in such a way that it can live higher up in the respiratory tract than before. This may make it more communicable.
It would also mean we've met the recently revised definition for pandemic alert level 4...
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Posted: June 08 2006 at 6:38pm |
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Thankyou for the reply.. Looks like we better speed things up and get all our preps in order. Sounds like just a matter of time.
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Posted: June 08 2006 at 6:50pm |
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Zondar, You're correct, once the virus gains this PB2 E627K (gene?) then it has the ability to bind with the receptors in cells found higher up in the respiratory tract. Since the nasal passages are of a lower temperature than the deep lungs and this (gene?) allows for lower temperature receptors. That's what makes it able to spread airborne. Virus in infections deep in the lung are not expellecd during coughing and sneezing or at least not in great amounts, therefore deep lung infections would not be very contagous. |
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Jhetta
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Posted: June 08 2006 at 7:05pm |
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I was worried that this was the case based on the entire family becoming infected and then dying.
This means MODS
Human Influenza A/H5N1 Clinical Features & Spectrum
Covers the following regarding H5N1
Helpful Terms:
Multiple Organ Dysfunction Syndrome (MODS)
Acute Respiratory Distress Syndrome (ARDS)
Cytokine storm is a common designation for the technical term hypercytokinemia (sometimes spelled hypercytokinaemia).
Gastrointestinal Symptoms ~ Avian influenza should be included in the differential diagnosis for patients with predominantly gastrointestinal symptoms
Page 7 Cases that developed GIT symptoms
Uncomplicated H5N1 cases Number = 5 2 showed GIT symptoms
Severe H5N1 cases Number = 7 5 showed GIT symptoms
Page 16 Patient positive for H5N1 Presenting with Fever, SOB, Vomiting, Diarrhea
Page 17 Productive cough, SOB, Diarrhea
Page 20 "We report the first case of avian influenza in a patient with fever and diarrhea but no respiratory symptoms. Avian influenza should be included in the differential diagnosis for patients with predominantly gastrointestinal symptoms" H5N1 Positive 30 yr old female 1 wk diarrhea, nausea, & vomiting, no initial respiratory symptoms. Day 13 died of ARDS & MODS
Page 21 More examples of diarrhea in H5N1 positive patient
Page 25 Detailed Presentation Info regarding H5N1 and Fever, Headache, Mylalgia, Diarrhea, Abdominal Pain, Vomiting, etc.
Page 27, 28 Summary: Features human flu A/ H5N1 ~ Clinical: Fever, Cough, Dyspnoea; GIT (diarrhea, vomiting, abdo pain); URT: myalgia Complications: Cytokine storms, ARDS, renal failure, MODS, encephalitis
More info from a previous post: Multiple Organ Dysfunction Syndrome (MODS) and eningoencephalitis have been detected in H5N1 infections.
Meningoencephalitis
http://www.diseasesdatabase.com/umlsdef.asp?glngUserChoice=22543 "An inflammatory process involving the brain (ENCEPHALITIS) and meninges (MENINGITIS), most often produced by pathogenic organisms which invade the central nervous system, and occasionally by toxins, autoimmune disorders, and other conditions." Pathology of Human Influenza A (H5N1) Virus Infection in Cynomolgus Macaques http://www.vetpathology.org/cgi/content/full/40/3/304 "...necrotizing broncho-interstitial pneumonia (4/4) similar to those found in primary influenza virus pneumonia in humans, with desquamation of respiratory epithelium (4/4), intra-alveolar hemorrhage (4/4), hyaline membrane formation (2/4), and infiltration with neutrophils and macrophages (4/4). Lesions in other organs consisted of a suppurative tonsillitis (2/4) and necrosis in lymphoid organs (1/4), kidney (1/4), and liver (1/4)..... The pathogenesis of MODS has not yet been elucidated. The primary defects are thought to involve the microcirculation and mitochondrial metabolism, and mechanisms may include the release of cytokines into the circulation. This is supported by the data of To et al., who found elevated levels of interferon-, soluble interleukin-2 receptor, and interleukin-6 in sera of two humans with fatal H5N1 virus infection.
We are currently investigating the role of different cytokines in the pathogenesis of H5N1 virus infection in our macaque model. " Proinflammatory cytokine responses induced by influenza A (H5N1) viruses in primary human alveolar and bronchial epithelial cells http://respiratory-research.com/content/6/1/135 "Conclusion: The H5N1/97 and H5N1/04 subtype influenza A viruses are more potent inducers of proinflammatory cytokines and chemokines in primary human respiratory epithelial cells than subtype H1N1 virus. We suggest that this hyper-induction of cytokines may be relevant to the pathogenesis of human H5N1 disease.... While dissemination outside the respiratory tract was not demonstrated in human H5N1 disease in 1997 and 2003 [4,7], there is some evidence that more recent H5N1 viruses may occasionally disseminate to multiple organs contributing to unusual disease manifestations such as meningo-encephalitis [8]. However, most patients with H5N1 disease had a primary viral pneumonia complicated by the syndromes of acute respiratory distress and multiple organ dysfunction [4-7,9] with lymphopenia and haemophagocytosis being notable findings. The syndromes of acute respiratory distress and multiple organ dysfunction as well as haemophagocytosis have previously been associated with cytokine dysregulation "
Cytotoxic therapy for severe avian influenza A (H5N1) infection. Here is another article
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Posted: June 08 2006 at 7:08pm |
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What do you mean this means MODS?
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Posted: June 08 2006 at 7:11pm |
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I have a question: The article states that of 100 samples, 20 were "turned on" (I guess that means reacted to show virus) and of those, 11 had 2,6 receptor specificity. If that is the case, why does Dr. Niman say that " the comments above do not break down the number of H5N1's with 2,6 specificities?" Assuming these were all positive H5N1 (the article never mentions H5N1, by the way), I'm missing something in Dr. Niman's comments. |
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Jhetta
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Posted: June 08 2006 at 7:11pm |
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More here... I will post some of it in this thread
A Nature report, by Declan Butler, says the virus samples from both Turkish patients have a mutation in the polymerase protein, which serves to replicate the virus's genetic material. The change is a substitution of lycine for glutamic acid at position 627. The same mutation has been seen before, including in Eurasian poultry recently and in the one person who died in the 2003 outbreak of H7N7 avian flu in the Netherlands.
"The polymerase mutation is one of the ten genetic changes that gave rise to the 1918 pandemic flu virus," the story says. The mutation indicates adaptation to humans, said Alan Hay, director of the WHO flu laboratory at the NIMR, as quoted in the story. The story goes on to say that the Turkish samples are the first in which the polymerase and hemagglutinin mutations have been found together. "They could make it easier for humans to catch the virus from poultry," it says. "But they might also favor human-to-human transmission." Together, the two mutations help the virus survive and infect cells in the nose and throat, increasing the chance that coughing would spread it via droplets, the story says. However, Hay said it is hard to predict how the mutations will affect the virus's behavior and that "just two changes are unlikely to create efficient human-to-human transmission on their own," according to the report. Jan 12 WHO statement on analysis of H5N1 virus from Turkish patients http://www.who.int/csr/don/2006_01_12/en/index.html" I posted this awhile back PB2 amino acid at position 627 affects replicative efficiency of Hong Kong H5N1 influenza A viruses in mice.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15016548
Shinya K, Hamm S, Hatta M, Ito H, Ito T, Kawaoka Y. Department of Pathobiological Sciences, University of Wisconsin, Madison, WI 53706, USA. A single amino acid substitution, from glutamic acid to lysine at position 627 of the PB2 protein, converts a nonlethal H5N1 influenza A virus isolated from a human to a lethal virus in mice. In contrast to the nonlethal virus, which replicates only in respiratory organs, the lethal isolate replicates in a variety of organs, producing systemic infection. Despite a clear difference in virulence and organ tropism between the two viruses, it remains unknown whether the dissimilarity is a result of differences in cell tropism or the reduced replicative ability of the nonlethal virus in mouse cells in general. To determine how this single amino acid change affects virulence and organ tropism in mice, we investigated the growth kinetics of the two H5N1 viruses both in vitro and in vivo. The identity of the PB2 amino acid at position 627 did not appreciably affect viral replicative efficiency in chicken embryo fibroblasts and a quail cell line; however, viruses with lysine at this position instead of glutamic acid grew better in the different mouse cells tested. When the effect of this substitution was investigated in mice, all of the test viruses showed the same cell tropism, but infection by viruses containing lysine at position 627 spread more rapidly than those viruses containing glutamic acid at this position.
Further analysis showed a difference in local immune responses: neutrophil infiltration in lungs infected with viruses containing lysine at position 627 persisted longer than that associated with viruses lacking a glutamic acid substitution.
Our data indicate that the amino acid at position 627 of the PB2 protein determines the efficiency of viral replication in mouse (not avian) cells, but not tropism among cells in different mouse organs. The presence of lysine leads to more aggressive viral replication, overwhelming the host's defense mechanisms and resulting in high mortality rates in mice.
PMID: 15016548 [PubMed - indexed for MEDLINE]"
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Posted: June 08 2006 at 7:13pm |
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Jhetta - the testing was done in Feb-March, so it wouldn't be the same cluster, but still..... it could have lead to such a consequence, I'm guessing.
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Posted: June 08 2006 at 7:16pm |
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IMHO, what it's saying, in part, is that it has apparently shown to grow at cooler temps, meaning it can grow in your upper resp. system, i.e. throat.
That would mean to me, that with this new strain of H5 one could cough, sneeze and spit H5N1 and pass it on the bus to ten people,..... or something like that. It's mutating, making it more transmittable. Look for an increase in cases. Somebody pluuuueezzz correct me if I'm wrong. : ) Mary Kay |
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Jhetta
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Posted: June 08 2006 at 7:18pm |
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These two statements concern me... I hope that this report is not accurate
11 among them had spesifisitas the receptor 2,6. Meaning that, these viruses had the capacity immediately could infect humankind without must from the poultry before. Moreover, some of the samples had the amino acid lisin in the number 627 proteins PB2, that meaning that the virus could be stable in the temperature of the human body. |
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Posted: June 08 2006 at 7:27pm |
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If I'm correct, Dr. Niman has said that the strains coming out of parts of Indonesia were not avian, that is they didn't match up with any of the viruses from poultry. That leaves pigs, other humans..... I don't know how or where he gets his information, but I'm sure he's not just guessing. It IS concerning, and it just makes even more upset with the lack of transparency (i.e. the WHO's statement that there have been no "significant" mutations of the virus - what does that mean? I think we should be told)
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Jhetta
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Posted: June 08 2006 at 7:29pm |
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If some of the strains in Indonesia have indeed changed receptor specificity from Alpha 2,3 to alpha 2.6. This would not be good news. This would mean that it would be easier for humans to catch.
People infected with H5N1 have a carbohydrate receptor on cells lining their throats. Human influenza viruses, prefer to bind to the receptor called alpha 2,6, which is dominant in humans.
The receptor -- called alpha 2,3 -- is predominantly found in birds and avian influenza viruses like to bind to this class of receptors to replicate and cause disease.
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Posted: June 08 2006 at 7:48pm |
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Jhetta, I'm so glad you're here. I wish I understood this as well as you.
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Jhetta
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Posted: June 08 2006 at 8:04pm |
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Okay to break it all down... Multiple Organ Dysfunction Syndrome (MODS) can make H5N1 more deadly and difficult to treat.
Finding lysine instead of glutamic acid at position 627 of the PB2 protein in the H5N1 virus is not good. More research needs to be done however results in mice show that it converts a nonlethal H5N1 influenza A virus isolated from a human to a lethal virus in mice. And it replicates in a variety of organs, producing systemic infection. The presence of the lysine amino acid at position 627 of the PB2 protein also determines the efficiency of viral replication and leads to more aggressive viral replication, overwhelming the host's defense mechanisms and resulting in high mortality rates in mice.
I think it is importent to note that mouse pathogenicity may not extrapolate directly to humans. However, I find it intriguing that four of the six viruses (highly virulent in mice) reported in one study were isolated from patients who eventually died,
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Posted: June 08 2006 at 8:05pm |
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Thanks Jhetta!
Angie
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Posted: June 08 2006 at 8:18pm |
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Did someone say Wal-Mart was still open??? : )
LOL! MK |
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Jhetta
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Posted: June 08 2006 at 8:30pm |
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"This difficulty was caused by two matters that is receptor relations and spesifisitas the receptor and the difference of the temperature between the person and the poultry also were different." The normal body temperature of a chicken is 106°F to 108°F or 41°C to 45°C degrees, compared to a human's average body temperature 98.6°F or 37°C He was looking for the receptor specificity to see if it was 2,3 or 2,6. He knew that if he found 2,6 it could infect humans and pigs. Note: Swine have receptors to both 2,6 and 2,3.
The sample that I the test came from the poultry, the pig, and humankind. He tested chickens, pigs and humans for H5N1 He found 2,6 receptor specificity which means that this strain of H5N1 could pass from Humans to humans without the need for intense exposure to chickens.
Meaning that, these viruses had the capacity immediately could infect humankind without must from the poultry before. Moreover, some of the samples had the amino acid lisin in the number 627 proteins PB2, that meaning that the virus could be stable in the temperature of the human body." I was not aware of this termperature issue... will look into it more.
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Jhetta
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Posted: June 08 2006 at 11:02pm |
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You are welcome Rodin33 and Angie
Here is more conformation that the change at PB2 627 would not be good.
 A single amino acid in the PB2 gene of influenza A virus is a determinant of host range. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8445709&dopt=Citation Subbarao EK, London W, Murphy BR. Respiratory Viruses Section, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. The single gene reassortant virus that derives its PB2 gene from the avian influenza A/Mallard/NY/78 virus and remaining genes from the human influenza A/Los Angeles/2/87 virus exhibits a host range restriction (hr) phenotype characterized by efficient replication in avian tissue and failure to produce plaques in mammalian Madin-Darby canine kidney cells. The hr phenotype is associated with restriction of viral replication in the respiratory tract of squirrel monkeys and humans. To identify the genetic basis of the hr phenotype, we isolated four phenotypic hr mutant viruses that acquired the ability to replicate efficiently in mammalian tissue. Segregational analysis indicated that the loss of the hr phenotype was due to a mutation in the PB2 gene itself. The nucleotide sequences of the PB2 gene of each of the four hr mutants revealed that a single amino acid substitution at position 627 (Glu-->Lys) was responsible for the restoration of the ability of the PB2 single gene reassortant to replicate in Madin-Darby canine kidney cells.
Interestingly, the amino acid at position 627 in every avian influenza A virus PB2 protein analyzed to date is glutamic acid, and in every human influenza A virus PB2 protein, it is lysine. Thus, the amino acid at residue 627 of PB2 is an important determinant of host range of influenza A viruses. PMID: 8445709 [PubMed - indexed for MEDLINE]
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redcloud
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Posted: June 08 2006 at 11:39pm |
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Is it just me, or does the symptomology discussed in this thread sound like that of the Namibian "mystery disease?"
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If all is not lost, where is it?
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pheasant
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Posted: June 09 2006 at 3:22am |
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ok....has the virus mutated ??? yes or no ...or we dont know ...multiple choice......
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The only thing we have to fear, is fear itself......FDR
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Posted: June 09 2006 at 8:45am |
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pheasant-
Multiple choice, take your pick...
A. Yes
B. No
C. Yes.. wait No.. well, not sure
 D. Maybe
 E. Not telling until it really doesn't matter anymore.
 (feeling a bit cynical today, sorry)
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Posted: June 09 2006 at 8:59am |
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not being an expert in the field of microbiology, there is something I don't understand. Namely this: if the H5N1 virus shows 'no significant' mutations, then what do you call a change in a virus that gives it the ability to more freely infect humans? Is a change in a virus not a mutation? I'm asking this question in sincerity. As a lay person, to me change means mutation. So does the term change mean mutation? |
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Jhetta
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Posted: June 09 2006 at 9:08am |
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I did work in research for a time... I am not a Virologist. I do understand how to find info regarding Dr. Nimons reports and I do understand the reports I find on publicmed to a large degree.
My questions would be... Is his information correct? If they are, I am quite concerned. The changes he has cited would potentially make H5N1 both more contagious to humans and from the research done on mice (which does not necessarily translate to humans) more severe, including systemic infections with the potential to infect the blood, Multiple Organs, etc.
I personally am not looking for conformation regarding this from the WHO. Or the local goverment agencies. I will be looking at the data coming from scientist.
We need to look for info regarding patients that have been documented to have the H5N1 virus with these changes.
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Gimme
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Posted: June 09 2006 at 9:16am |
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Multiple Organ Dysfunction Syndrome (MODS)
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pheasant
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Posted: June 09 2006 at 9:30am |
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i wasn't joking.................has the virus mutated...yes or no ?
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The only thing we have to fear, is fear itself......FDR
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Zondar
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Posted: June 09 2006 at 9:41am |
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That's a good basic question, pheasant. From my layman's point of view, it sounds as though it's mutated. But I'm not entirely sure what constitutes "mutation" to a to a geneticist or a virologist, especially considering (from what I understand) that some degree of mutation is all but continuous in viruses. I don't know what a cleavage receptor site is. If it's "novel," is that a mutation?
I share your curiosity.
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Jhetta
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Posted: June 09 2006 at 10:11am |
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I am a little frusterated here... I spent a good deal of time of digging up info for you. Did you read it?
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Posted: June 09 2006 at 10:16am |
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pheasant, I think that would mean a yes, if the research is valid then yes
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Posted: June 09 2006 at 10:34am |
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The answer is YES! What they uncovered is the fact that some of the viral samples have made the change necessary for Ease of Transmission. What we don't know is how wide spread this mutation is. Was it just limited to that part of Indonesia or is it more widely entrenched? We will know in the next few weeks and months. What I do know is that IT IS COMING. When the sneezing starts, it will travel the oceans in pressurized aluminum cylinders and make itself known the world over. November. |
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Posted: June 09 2006 at 10:40am |
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the virus is always mutating...
it used to just drop people back in 1997,
by lower resp.
it's adapting now.. (they knew human to human in 2005, not so efficient)
now one gets headache, fever, watery diarrhea, (shedding the virus like birds do) 6-7 days before it hits the lower resp..
In 1918... there was bleeding from any/all mucosal sites in serious cases.
and they call this... conjuntivitis...
redness, lacrimation and pain. An eye examination usually reveals conjunctivitis and neovascularization. Also, central dendritic corneal erosions are prevalent. If the patient is not treated,
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Posted: June 09 2006 at 2:23pm |
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well i dont see a rash of new cases in indo so..................more hype
as far as iam comcerned....
i just want the facts not speculation....show me proof........
dont get me wrong i belive it will happen also
but i dont want guess work i want solid info i cant work with...
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Jhetta
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Posted: June 09 2006 at 2:34pm |
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H5N1 Mammalian Receptor Binding in Indonesia
Recombinomics Commentary June 9, 2006 I began research in February-March 2006. This research was sponsored by Tokyo University. The samples that I tested came from poultry, swine and humans. Of the 100 samples, there were 20 that succeeded in being brought to life and actually 11 of them had the receptor specificity 2.6. a portion of those samples had the amino acid lysine at number 627 protein PB2, which means that the virus can be stable at the human body temperature. The above human translation of an interview of Dr CA Nidom from the Avian Influenza Laboratory Tropical Disease Center and the Department of Biochemistry and Molecular Biology from the Faculty of Veterinary Medicine at Airlangga University, Surabaya. Dr Nidom has previously identified H5N1 in swine in Indonesia, including Tangerang, not far from the residence of the first reported H5N1 cluster in Indonesia. The current interview raises a number of important questions that are not easily answered with the information above. Additional information indicates that 3 of the 11 isolates with alpha 2,6 specificity also had PB2 E627K. Since alpha 2,6 linkages are found in mammalian upper respiratory tract, it is likely that those 11 isolates with 2,6 specificity were from swine or humans. The only H5N1 from birds that have E627K are in the Qinghai strain. However, all of the human H5N1 isolates described to date are readily distinguished from the Qinghai strain. This can be seen in the phylogenetic tree generated by China's Ministry of Health. It contains data for the first two H5n1 isolated form humans in Indonesia. The first isolate was Indonesia/5/2005, which was from the father in the Tangerang cluster. The second isolate, Indonesia/6/2005, was from a patient who lived in southwest Jakarta and is thought to have been infected by home fertilizer. These two isolates are at opposite sides of the Indonesia branch, which is distinct from the Qinghai isolates, which are from Qinghai and Turkey in the isolates represented on the tree. All of the other human isolates from Indonesia are similar to the first Indonesian isolate. They have a novel cleavage site, RESRRRKKR, as does a H5N1 from a cat in Jakarta. The samples described by CA Nidom also are from the Jakarta area and the cleavage site does not match the poultry isolates from the region. However, these two named isolates above have been described in WHO updates and there was no mention of the 2.6 receptor specificity. This difference could be explained by isolation procedures. Isolating human H5N1 in chicken eggs will select against H5N1 with alpha 2,6 specificity. Since the 2.6 linkage is found in the upper respiratory tract of humans, H5N1 with that specificity would be more efficiently transmitted from human-to-human. Indonesia has reported a large number of familial clusters, and most have a gap between disease onset dates of the index case and other family members, strongly suggested that most or all are from human-to-human transmission. Thus, more detail on the distribution of alpha 2,6 specificity among human and swine isolates, as well as sequence data from these isolates, would be useful. Media Source Link Phylogenetic Tree |
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Posted: June 09 2006 at 2:42pm |
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again this means nothing to me......
i want to know if its taking off somewhere then we need to concerned..
what it may or may not do is irrelevent...
i am watching indo closely just as everyone else is but till i see it go from indo to austraila to japan i will not be concerned...
whats the point?
i just keep preping and see what happens.....
there is alot more to worry about out there than just h5...
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Jhetta
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Posted: June 09 2006 at 2:49pm |
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I did not post the last post in response to your post.
The more I investigate the more I learn... my feeling is if you do not understand your enemy how can you protect yourself.
Personally sound bites do not cut it for me and I post information for people who want to learn about H5N1 like I do.
Put me on ignore... and wait for someone with a definitive Yes it is stage 6 and spreading... |
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pugmom
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Posted: June 09 2006 at 3:15pm |
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I'm with you Jhetta! For me, there is never enough detail. Other people have limited attention spans, either that or you and I have overactive imaginations.
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jpc
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Posted: June 09 2006 at 3:22pm |
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I did not do well in biology, but my take on this is that the virus is experimenting with it's mutations. Maybe it mutates and falls apart until it has it down correctly. Kind of like a child learning to walk. (Maybe that's why the clusters burn out.)There are bird flu viruses in many parts of the world, all mutating and evolving independently, until one hits that last mutation and decides to stay there for a while, and the pandemic begins. Again, I'm not a scientist, it's kind of how I understand it to be. So how far off am I?
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redcloud
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Posted: June 09 2006 at 4:31pm |
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Pigs are a perfect "nursery" for a virus to recombine into a human infective strain. The next best such nursery is the human body itself.
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If all is not lost, where is it?
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Posted: June 09 2006 at 6:18pm |
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Table 1: 2005 WHO Guidelines for Phases of Influenza Pandemic Inter-pandemic period Phase 1: No new influenza virus subtypes have been detected in humans. An influenza virus subtype that has caused human infection may be present in animals. If present in animals, risk of human infection or disease is considered to be low. Phase 2: No new influenza virus subtypes have been detected in humans. However, a circulating animal influenza virus subtype poses a substantial risk of human disease. Pandemic alert period Phase 3: Human infection(s) with a new subtype, but no human-to-human spread, or at most rare instances of spread to a close contact. Phase 4: Small cluster(s) with limited human-to-human transmission but spread is highly localized; suggesting that delay the virus is not well adapted to humans. Phase 5: Larger cluster(s) but human-to-human spread still localized, suggesting that the virus is becoming increasingly better adapted to humans, but may not yet be fully transmissible (substantial pandemic risk). Pandemic period Phase 6: Pandemic: increased and sustained transmission in general population Thus. although WHO has maintained phase 3, their language in updates, and actions signal pandemic evolution well beyond phase 3, and recent comments indicate the level will not be raised until the pandemic has reached the final phase 6.
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pheasant
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Joined: May 20 2006 Location: Florida Status: Offline Points: 9851 |
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Posted: June 09 2006 at 7:01pm |
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sorry..jhetta...please dont take the question as it sounded,im frustrated too ...and getting grumpy, i did read your posts and took it to mean a change has been seen i realize its not a clean cut thing ...also to you and all the rest here who are working so hard ...thank you..:)
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The only thing we have to fear, is fear itself......FDR
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Posted: June 09 2006 at 7:25pm |
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Jhetta: Thank you for putting it into layman's terms...When a post like that comes up I have to read it at least 3 times and even then I say to myself.
What?? What does that say. Huh...
So thank you for your help....
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Jhetta
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Posted: June 09 2006 at 8:44pm |
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Thank you all... sorry I was grumpy... had some stuff going on in my own life.
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birdlady wrote: