- The study below states exactly what Dr. Henry Niman said
a year ago. This H1N1 virus is the closest pandemic virus to the 1918
Spanish Flu Virus of any pandemic since then.
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- Here is a Chinese study below confirming Henry's work.
I certainly hope Henry gets due credit.
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- Patty
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- INFLUENZA PANDEMIC (H1N1) - MUTATION ANALYSIS
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- Date: Mon 8 Mar 2010 Source: PLoS ONE 5(3): e9549. doi:10.1371/journal.pone.0009549
[edited]
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- Title: Genomic Signature and Mutation Trend Analysis
of Pandemic (H1N1) 2009 Influenza A Virus
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- Introduction
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- The causative agent of the 2009 (H1N1) influenza pandemic
was proved to be a novel swine-origin pandemic influenza A (H1N1) virus
(H1N1pdm, also referred to as S-OIV). Its hemagglutinin (HA), nucleoprotein
(NP), and nonstructural (NS) protein genes belong to the classical swine
lineage, while its neuraminidase (NA) and matrix (M) protein genes derive
from a Eurasian swine influenza lineage which entered pigs from avian hosts
around 1979, and its polymerase gene segments, PA, PB1 and PB2, descended
from the North American triple reassortant swine lineage.
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- This unique genetic combination may contribute to the
improved fitness of the H1N1pdm in humans and its human-to-human transmissibility,
although none of the molecular features previously shown to confer increased
human-to-human transmissibility has so far been identified in the 2009
H1N1pdm. Since there is a serious concern that the virus may further mutate
into a more dangerous form, it is critical to monitor the evolutionary
trends of the 2009 H1N1pdm virus.
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- Previously Shih and colleagues developed an entropy-based
computational scheme to identify host-specific genomic signatures of human
and avian influenza viruses. Most recently, they used this method to compare
the protein sequences of the 2009 H1N1pdm strains collected before 28 May
2009, with those of avian, swine and human influenza A viruses (IAVs).
Among the 47 avian-human signatures, they found that 8 (one in PB1, one
in PB2, 2 in PA and 4 in NP) showed human-characteristic signatures, which
may serve as a molecular marker for monitoring adaptive mutations in the
influenza viruses.
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- In the present study, we compared the protein sequences
of 2009 H1N1pdm strains collected from 1 Apr 2009 to 31 Dec 2009, with
the corresponding protein sequences of the human, avian, and swine IAVs
and those causing past influenza pandemics. We then conducted an analysis
to gain insight into 1) the mutation trend of the residues at the signature
and non-signature positions in the proteins of H1N1pdm during the pandemic
of 2009 and 2) the potential roles of the mutated residues in human adaptation
and virulence of the 2009 H1N1pdm influenza virus.
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- Abstract and summary: --------------------- A novel swine-origin
pandemic influenza A(H1N1) 2009 virus (H1N1pdm, also referred to as S-OIV)
was identified as the causative agent of the 21st century's 1st influenza
pandemic, but molecular features conferring its ability of human-to-human
transmission have not been identified. Here we compared the protein sequences
of 2009 H1N1pdm strains with those causing other pandemics and the viruses
isolated from humans, swine and avians, and then analyzed the mutation
trend of the residues at the signature and non-signature positions, (i.e.,
those that are species- and non-species-associated), respectively, in the
proteins of H1N1pdm during the pandemic of 2009.
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- We confirmed that the host-specific genomic signatures
of 2009 H1N1pdm, which are mainly swine-like, were highly identical to
those of the 1918 H1N1pdm. During the short period of time when the pandemic
alert level was raised from phase 4 to phase 6, one signature residue at
the position of NP-100 mutated from valine to isoleucine. A total of 4
non-signature residues, at positions NA-91, NA-233, HA-206, and NS1-123,
also changed during the epidemic in 2009. All these mutant residues, except
that at NA-91, are located in the viral functional domains, suggesting
that they may play roles in the human adaption and virulence of 2009 H1N1pdm.
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- Our study confirms that the 2009 H1N1pdm virus has much
closer linkage to the 1918 H1N1pdm than any other pandemic influenza viruses.
We identified one dominant mutation at the signature position (NP-100)
and 4 dominant mutations at the non-signature positions (NA-91, NA-233,
HA-206, and NS1-123). Except NA-91, all these mutant residues are located
in the viral functional domains, suggesting that they may play roles in
the human adaption and virulence of 2009 H1N1pdm.
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- Byline: Chungen Pan(1,2), Byron Cheung(1), Suiyi Tan(1,3),
Chunling
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- Li(4), Lin Li(1,3), Shuwen Liu(3), Shibo Jiang(1,3) 1
Lindsley F. Kimball Research Institute, New York Blood Center, New York,
New York, United States of America, 2 College of Life Sciences, Peking
University, Beijing, China, 3 Southern Medical University, Guangzhou, Guangdong,
China, 4 Institute of Veterinary Medicine, Guangdong Academy of Agricultural
Sciences, Guangzhou, China
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- http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0009549
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-
- Communicated by ProMed-mail <mailto:promed@promedmail.org>promed@promedmail.org
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- The data, analysis and references cannot be abstracted
easily and interested readers are referred to the original text for further
enlightenment. - Mod.CP
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- see also: 2009 ---- Influenza pandemic (H1N1) 2009 (116):
origin 20091126.4052
- .......................
- cp/ejp/lm
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-
- Patricia A. Doyle DVM, PhD Bus Admin, Tropical Agricultural
Economics Univ of West Indies Please visit my "Emerging Diseases"
message board at: http://www.emergingdisease.org/phpbb/index.php Also
my new website: http://drpdoyle.tripod.com/ Zhan le Devlesa tai
sastimasa Go with God and in Good Health
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