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Human to Human? Mystery intensifies on how H7N9 is spreading; most had no contact with poultry
This entry was posted in Civilizations unraveling, Dark Ages, Disease outbreak, Earth Changes, Earth Watch, Environmental Threat, High-risk potential hazard zone, Human behavioral change after disaster, New virus reported, Pestilence Watch, Prophecies referenced, Time - Event Acceleration. Bookmark the permalink.
I THINK THIS VIRUS IS EASY TRANSMITED TO HUMANS FROM ANY SOURCE AIR OR WATER, ANIMAL OR HUMAN, BIRD OR FISH ,,,,
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Hey, Alvin, well, I wouldn’t call it a term paper, but, it ain’t short either; I post and submit to your discretion. If nothing else, PLEASE add the last link to your own list; it is a site that tracks outbreaks worldwide.
A virus, from the Latin for “poison”, is not considered an actual life-form, because all viruses lack cellular structure (the standard to meet in order to be considered “life”), their own metabolism, the ability to self-reproduce, and cannot survive (for long) outside of a host organism, which means that they are primitve parasites. Though the range of hosts is limited for each type of virus, as an order, viruses are able to infect everything, bacteria, fungi, worms, sponges, catfish, lizards, oak trees, etc. They are adaptable and hardy; while science recognizes the existence of millions of them, only five thousand or so are known in detail. Of all life-forms/sub-life-forms, the classification system for viruses is the most complex in science, complicated to understand (my head would explode) and even harder to explain with brevity (your head would explode, at least if I tried), so I’m skipping that part. Influenza viruses, specifically, are “negative-sense single-strand RNA” [(-)ss-RNA] viruses; the ss-RNA is the important part, because these guys are extra-primitive. Upon infection, they begin to replicate in the cytoplasm (the goo inside all cells wherein the other parts float); they borrow some proteins from the ribosome and start spitting out copies, a process which (unlike other classes of virus) is unchecked and unregulated; in the process, they often glean pieces and parts from other viruses, and by this “random” nature of reproduction, they create mutations more often than any other form/sub-form of life, almost by design.
http://en.wikipedia.org/wiki/Virus
http://en.wikipedia.org/wiki/Orthomyxoviridae
The published information contained in the study by Chinese officials represents just seven (7) isolate samples that were collected from three connected provinces. Two came from avian donors, one chicken and one pigeon (both from Shanghai), another was an environmental sample, collected from a marketplace in Shanghai, and the other four were taken from victims of the disease. Of them, the first (Shanghai1) is from an 87 year old man who died on 4 March; the second (Shanghai2), collected from a 27 year-old pork seller who died 10 March; sample three (Anhui1) is from a 35 year-old woman from Anhui province (west of Shanghai) who became ill on 15 March and remains hospitalized in critical condition; the fourth isolate (Hangzhou1) was taken from a 38 year-old man who died on 27 March in Zhejiang province, south of Shanghai.
According to genetic analysis, this H7N9 virus shares (H) genes with the low-pathogenic H7N3, (N) genes with the low-pathogenic H11N9 (isolated in the Czech Republic, 2010), and remaining sequences with H9N2, which circulated recently in Shanghai, Zhejang, and Jiangsu. This suggests that the viruses are reassortants; their H7 and N9 genes are derived from avian viruses and the remaining genes from poultry viruses. Of the four human isolates, all are similar at the amino-acid and nucleotide level, which suggests a common ancestor, BUT, where Shanghai2, Anhui1, and Hangzhou1 share 99% identity and differ by no more than 3 nucleotides per gene (though they were gathered from 3 different provinces, several hundred kilometers apart); Shanghai1 differs from Shanghai2 by 52 nucleotides, even though these cases were identified in the same city around the same time. In combination with the other three samples, the findings suggest that Shanghai2, Anhui1, Hangzhou1, Chicken, and Environment share a closely related source of infection while Shanghai1 and Pigeon are likely to have originated from other SOURCES. (For a total of THREE)
Similarities/differences of note:
The amino-acid sequence of the receptor-binding site (H) determines preference for human/avian type receptors; Shanghai1 contains an H3 mutation, while Shanghai2, Anhui1, Pigeon, Chicken, Environment show two other mutations; any of the three could increase binding to human receptors. More alarming is the finding in regards to Hangzhou1, which contains the same amino-acid as SEASONAL H3N2.
In another position that contributes to binding, all seven samples share a mutation, an H3 trait, of increased binding to human receptors.
In a position that is responsible for replication of avian influenza in humans, Lysine is essential; it is present in all four human cases, while it is absent from the avian and environmental samples.
All seven isolates share resistence to ion-channel inhibitors (amantadine and rimantadine), but six show sensitivity to neuramindase inhibitors (tamiflu). The exception is Shanghai1, which registers resistance, thus the newly-discovered Shanghai1 is already treatment-resistant.
Conclusion:
While the low-pathogenic viruses have not devastated bird populations, the viruses have had time to intermix, recombine, and mutate; evidence supports THREE sources for seven samples, in an outbreak (for humans) that is less than 90 days old. And none of the information herein answers the question that got me started on this: if the avian samples do not contain the amino-acid that is critical for replication in humans (Lysine, so at least I did learn the name of the responsible compound), where did the human isolates get it?
From another source, one that provides the missing link that allows the virus to cross species (and flourish), a source that is not isolated here. Which means . . . there may be four sources for seven samples. Also, if the resistance of Shanghai1 resurfaces, or if the H3N2 component of Hangzhou1 spreads, the chances of it crossing species greatly increases. And one more thing: of over 1000 close-contacts to victims who are being monitored by the Chinese none have shown any signs of illness. Which means that it is not contagious, person-to-person. Yet. Just don’t let a pigeon sneeze on you.
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=20453
http://www.cbc.ca/news/technology/story/2009/04/27/virus-mutate.html
http://en.wikipedia.org/wiki/H7N9
http://www.timescolonist.com/world-s-in-new-territory-with-challenging-new-flu-virus-who-expert-says-1.109715
http://www.cidrap.umn.edu/cidrap/content/influenza/avianflu/news/apr1613china.html
EXCELLENT SITE that tracks outbreaks worldwide:
http://healthmap.org/en/?gclid=CNGsjIn3yrYCFQzNnAodalQAQA
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Finally… (just in the last few hours) they are acknowledging the possibility, which has been obvious for some time now…
“H7N9 Flu: China Investigating Possible Human-To-Human Spread”
http://www.huffingtonpost.com/2013/04/18/h7n9-flu-human-spread-china-_n_3106038.html?1366295872
Chinese Government Suspects Human-to-Human Transmission of H7N9 Bird Flu
http://www.usnews.com/news/articles/2013/04/18/chinese-government-suspects-human-to-human-transmission-of-h7n9-bird-flu
If you are really curious about the possibilities of this, read about the 1918 pandemic, otherwise known as the Spanish Flu. Starts small, but can then explode.
On April 4, Recombinomics wrote, “Q226L Signals Recent H7N9 Human Adaptation”
http://www.recombinomics.com/News/04041301/H7N9_Q226L_Adapt.html
“[In 2003, I think] When new H5N1 bird flu cases were reported, agencies would claim that the H5N1 couldn’t transmit human to human (H2H) because the two key changes, Q226L and G228S, were not present… The recent appearance [in H7N9] of Q226L, as well as D225G on H7 and E627K on PB2, raises concerns that the number of severe and fatal cases will spike higher…The presence of Q226L in most recent cases is expected, and the appearance of additional receptor binding domain changes, such as G228S would be catastrophic.” This change relates to its ability to transmit more easily.
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It is person to person so stop killing animals. AND IT WAS ENGINEERED TO BE AIRBORNE
NSABB KNOWS ABOUT THE RESEARCH DONE OVER THE PAST NINE YEARS SINCE THEY VOTED TO APPROVE THE PUBLISHING OF DR RON FOUCHER’S RESEARCH. THE PUBLIC WAS NOT TOLD ABOUT IT, THEY KEPT IT SECRET
MY COMMENTS WERE DELETED BY THIS WEBSITE
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Investigate Virologist Ron Fouchier,Ph.d., a.k.a. Ron Foucher, the virus creator who has modified lethal pandemic viruses and made them more lethal, made them airborne, and able to transmit from humans to humans!! Maybe he spread one of his new lab-made viruses to China and then deliberately got himself hired by China to investigate their H7N9 which he probably created!
It is criminal to not destroy these manmade pandemic viruses or to hold onto them and spread them selectively to test them “in the field”. He became the”world’s foremost expert on viruses” because he makes them and spreads them and pretends to be the hero to stop them, but fails to publish any antidotes to his viruses.
HEY CHINA:This virologist is NOT AMERICAN!! HE IS FROM THE NETHERLANDS AND RUNS ERASMUS MEDICAL CENTER.
REVIEW ALL HIS GENETICALLY MODIFIED VIRUS RESEARCH FROM 2007 TO PRESENT. HE INFECTED FERRETS WITH H1N1 VIRUS, AND OVER 7 YEARS WITH NIH FUNDING CHANGED THE VIRUS TO DELIBERATELY SPREAD IT TO HUMANS AND THEN FROM HUMANS TO HUMANS BY AIR. HE MADE AN AIR-BORNE BIO-WEAPON AND SHOULD BE PROSECUTED BY INTERNATIONAL LAWS
THE POULTRY ARE NOT THE SOURCE OF THE VIRUS. THE CHICKENS WERE THE “COVER STORY” TO MISLEAD THE COUNTRIES INFLICTED WITH THE VIRUS, SO PLEASE STOP KILLING ALL THOSE UNINFECTED BIRDS AND CHICKENS AND ONLY KILL THE INFECTED ONES.
IF THERE IS A WAY TO CHANGE BACK OR BLOCK THE FIVE GENETIC MUTATIONS MADE BY RON FOUCHIER, THEN DEMAND HE REVEAL THE WAY TO CHANGE THE MUTATIONS, HE KNOWS ABOUT ALL FIVE MUTATIONS AND THERE ARE NOT JUST THREE WHICH HE FALSELY CLAIMED!
DEMAND HIS ANTIDOTE AND VACCINE WHICH HE MUST BE WITHHOLDING FROM THE VIRUS VICTIMS. HE KNOWS HOW TO KILL THIS VIRUS SINCE HE WAS THE ONE WHO MADE IT. ARREST HIM AND FULLY INVESTIGATE HIS ACTIVITIES. HE PUBLISHED HIS PANDEMIC VIRUSES IN SCIENCE JOURNALS AND NO ANTIDOTES, AND SHOULD BE IMPRISONED FOR LIFE. HE IS “ARGUABLY AND ALLEGEDLY” GUILTY OF CREATING PANDEMIC BIO-WEAPONS.
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