-------- Original Message --------
6 May 2009
Contact: Stephen M.
Apatow
Founder, Director of Research & Development
Humanitarian Resource Institute (UN:NGO:DESA)
Humanitarian University Consortium Graduate Studies
Center for Medicine, Veterinary Medicine & Law
Phone: 203-668-0282
Email: s.m.apatow@humanitarian.net
Internet: www.humanitarian.net
Pathobiologics International
Internet: www.pathobiologics.org
IDIN:
Pathobiologics
International: Biodefense
Threat Analysis & Communication Center
Subject: Pandemic Influenza: Contingency Planning Discussion
Dear Colleagues:
The swine flu outbreak that began in Mexico and
continues to spread around the globe may be particularly dangerous for
young, otherwise healthy adults because it contains genetic components
of the H5N1 avian influenza virus, which can induce a "cytokine storm,"
in which a patient's hyper-activated immune system causes potentially
fatal damage to the lungs. -- Does New Swine Flu Virus Kill By Causing A 'Cytokine
Storm'?: ScienceDaily, 6 May 2009.
In
the
context of Phylogenetic analysis and reassortment history of
Human/Swine
H1N1 (tree.bio.ed.ac.uk) and specific H5N1 determinants in the lineage
of
Novel A/H5N1, I would like to direct your attention to Human/Swine H1N1: Phylogenetics (all segments)
with
additional swine isolates (Gavin Smith, Vijaykrishna Dhanasekaran,
Justin
Bahl 02 May 2009):
PB1 gene – HKU 02 May 2009 (PDF)
Avian Gene Pool
-- AF144301 Goose/Guangdong/1/1996 (H5N1)
PA gene – HKU 02 May 2009 (PDF)
Avian Gene Pool
-- AF144302 Goose/Guangdong/1/1996 (H5N1)
M gene – HKU 02 May 2009 (PDF)
Eurasian avian gene pool
-- SCk/HK/SF189/2001 H5N1
-- AF144306 Gs/GD/1/1996 H5N1
-- Gs/GD/1/1996 H5N1
-- DQ997259 Sw/Guangxi/wz/2004 H5N1
Evolution of H5N1 into a human to human pandemic strain (Novel A/H1N1),
is now realized. The cytokine storm is the variable that makes
the present pandemic strain a serious concern.
Because proinflammatory cytokines are markedly elevated
during H5N1 influenza virus infection, the “cytokine storm” is
hypothesized to be the main cause of mortality. Here, we demonstrate
that mice deficient in the hallmark inflammatory cytokines TNF-α, IL-6,
or CC chemokine ligand 2 succumb to infection with A/Vietnam/1203/04
(H5N1) virus, as do wild-type mice treated with glucocorticoids for
suppression of cytokines. Because cytokine inhibition does not protect
against death, therapies that target the virus rather than cytokines
may be preferable. -- Inhibition
of the cytokine response does not protect against lethal H5N1 influenza
infection: National Academy of Sciences, 5 June 2007.
Interactive Figure. Proposed Mechanism of the
Cytokine Storm Evoked by Influenzavirus. Supplement to: Osterholm MT. Preparing for the Next Pandemic. N Engl J Med
2005;352(18):1839-42.
Now as the virus continues to spread throughout the United States and
across the globe, we should be shortly gaining a grasp of the clinical
consequences of spread with a 1-7 day incubation period.
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