Re: GAH! Pandemic fears excuse for power grab!

In article <1129258344.548418.279850@xxxxxxxxxxxxxxxxxxxxxxxxxxxx>,
jmdrake_98@xxxxxxxxx says...
>
> Strider wrote:

Material Cut

> >> So, now ush decided to get out front on this one and suddenly the
> > >> bashers are accusing him of overthrowing the government.
> > >
> > >The "bird flu" pandemic is a paper tiger. The real threat is
> > >the 1918 Spanish flu that scientists have resurrected and put
> > >it's gene sequence on the web for any rogue nation to see.
> > Like you know your ass from a hole in the ground......
>
> I know more than you which isn't saying much. Anyway this was
> reported in the journal Nature. I know. They disagree with
> what you wish to believe so you'll just dismiss them as
> "leftist".
>

The Spanish flu was avian.
For a general overview see:
http://www.nature.com/nature/focus/avianflu/timeline.html

Misses the Russian outbreak in 1977, but is but succient.

And the home page for avian flu on Nature:
http://www.nature.com/nature/focus/avianflu/index.html

Not sure how much you could access from the net, but worth checking out
(I get full access, but that is through a federal hospital link).

Matthew

Additional information below is cut from Clinical Microbiology Reviews,
2001, Horimoto & Kawaoka.

INFLUENZA PANDEMICS AND OUTBREAK OF H5N1 VIRUS IN HONG KONG IN 1997
Origin of Pandemic Viruses That Emerged in the 20th Century

Four human influenza pandemics have occurred in this century. Here we
briefly review the salient aspects of these global outbreaks, focusing
on the origin and biological properties of the causative viruses.

Spanish influenza. The biological properties of the virus responsible
for "Spanish influenza" (H1N1) in 1918 to 1919 have not been studied,
owing to the lack of viral isolates. Phylogenetic and seroarcheological
studies suggest that all genes of the 1918 pandemic strain were closely
related to those of H1N1 swine viruses, although sequence data to
support this notion were lacking until 1997, when Taubenberger et al. ,
using reverse transcription-PCR, succeeded in obtaining nucleotide
sequences of this pandemic virus from a formalin-fixed, paraffin-
embedded, lung tissue sample from an influenza victim. Phylogenetic
analysis of sequences encoding the HA, NA, NP, M1, and M2 proteins
disclosed a genetic relationship between the pandemic strain and H1N1
human and swine influenza A viruses. Further study of the HA gene
indicated the absence of multiple basic amino acids at the cleavage site
in contrast to findings in virulent avian viruses. Although the virus is
most probably derived from birds, it will be difficult to determine
whether pigs served as an intermediate host, at least until sufficient
sequence information on early swine H1N1 viruses becomes available. The
only virulence determinants of influenza virus that we understand
involve genes encoding HA (high cleavability due to multiple basic amino
acids at the cleavage site), NA (plasminogen-binding activity), or NS1
(interferon-counteracting activity). Thus, unless sequence analyses of
the HA, NA, and NS1 genes of this H1N1 virus suggest some unique
features about these activities, it is unlikely that the extreme
virulence of the 1918 strain will ever be understood.

Asian and Hong Kong influenza. The human pandemic viruses, such as those
responsible for Asian influenza (H2N2) in 1957 and Hong Kong influenza
(H3N2) in 1968, share two defining features: they first emerged in
southeastern Asia, and they were antigenically distinct from the
influenza viruses then circulating in humans. Genetic studies, together
with biochemical analyses, indicated that the Asian and Hong Kong
pandemic strains were generated by reassortment between human and avian
viral genes (Fig. 4). The causative virus in the 1957 pandemic possessed
three genes (PB1, HA [H2], and NA [N2]) from an avian virus and all
remaining genes from a circulating human H1N1 virus, which disappeared
soon after the H2N2 virus emerged. The pandemic H3N2 virus identified in
Hong Kong in 1968 was a reassortant with avian PB1 and HA (H3) genes and
six other genes from a human H2N2 virus. The latter virus could no
longer be detected in humans after the H3N2 strains appeared.
Phylogenetic studies indicated that the avian viral genes in these
pandemic strains were derived from viruses of Eurasian lineage, in
accord with epidemiological findings suggesting that the viruses
originated in southern China. Why the viruses previously circulating in
the human population vanished with the emergence of the new viruses
remains uncertain. Although many people died during these pandemics, the
causative viruses do not seem to be extraordinarily pathogenic, unlike
the 1918 strain. The increased death rate associated with these viruses
was probably a result of the lack of immunity to these viruses in human
populations.

Figure 4.
Phylogenetic studies suggest that an avian influenza virus was
transmitted to humans, leading to the 1918 pandemic. A reassortant virus
possessing its PB1, HA, and NA genes from a Eurasian avian virus, with
the remainder coming from an H1N1 human virus, caused the Asian pandemic
of 1957. The H1N1 virus subsequently disappeared from humans. In 1968, a
reassortant possessing its PB1 and HA genes from a Eurasian avian virus
and the remainder from an H2N2 human virus emerged, followed by the
disappearance of the H2N2 virus. In 1977, a virus genetically almost
identical to those circulating in humans in 1950 appeared and spread
among children and young adults. The H1N1 and H3N2 viruses are now
cocirculating in humans.

Russian influenza. The causative agent of the Russian influenza pandemic
in 1977 was essentially identical to viruses circulating among humans in
the 1950s (Fig.. 4). Given that influenza viruses continually evolve in
animals, it is highly unlikely that this virus was maintained in an
animal host for over 20 years without changes. Thus, one logical
conclusion is that the virus was maintained in a freezer until it
somehow was introduced into human populations. The relatively low death
rate in this pandemic can be attributed to the immunity of persons over
20 years of age who had been infected with the virus when it circulated
earlier in the century.

Outbreak of H5N1 Virus in Hong Kong in 1997

In May 1997, an H5N1 influenza virus (A/Hong Kong/156/97) was isolated
from a 3-year-old boy in Hong Kong 34, 184. The patient died of
extensive influenza pneumonia complicated by Reye's syndrome. By the end
of 1997, a total of 18 Hong Kong residents were infected with H5N1
influenza viruses, 6 of whom died 31. Because human populations lacked
immunity to the H5 influenza virus subtype, there was great concern
about the possibility of a major pandemic due to this unusual virus. The
human H5N1 isolates were not reassortants like the 1957 and 1968
pandemic strains; instead, all of the viral genes had originated from an
avian virus 34, 184.

Patients. The 18 human cases were not confined geographically or to a
specific age group. Rather, they developed in both children and adults
with ages ranging from 1 to 60 years 31. In 7 of the 18 cases, there
were histories of possible exposure to poultry: the patients either had
bought chickens before they became ill or had worked in proximity to
chicken stalls near their homes 121. The clinical features of the first
12 cases included onset with fever and upper respiratory tract
infection, typical of classic influenza 222. Seven of the patients had
severe complications, most prominently pneumonia, gastrointestinal
manifestations, elevated liver enzyme levels, and renal failure. In
general, children fared better than adults. With one exception, patients
younger than 13 years recovered from their illness whereas older
patients had severe disease that resulted in five deaths.
Epidemiological studies suggested mainly direct transmission of the
virus from birds to humans; serological evidence of human-to-human
transmission was limited to a few cases only 121. Serologic surveillance
also indicated limited transmission of H5N1 virus in Hong Kong residents
161. Although isolates from cousins were genetically very similar (only
4 nucleotide differences out of approximately 6,000 nucleotides
compared) 48, it is not clear whether one cousin acquired the virus from
the other or whether they both were infected with virus from a common
source. The lack of evidence for human-to-human transmission of this
virus in the majority of cases suggests that the virus had not fully
adapted to its human host. Most probably, additional mutations
introduced through continued replication in humans or perhaps
reassortment with a currently circulating human virus will be required
to produce a highly virulent and contagious virus.

Where did the 1997 Hong Kong virus originate? From late March to early
May 1997, an H5N1 influenza killed more than 6,500 chickens (75%
mortality rate) on three farms in the New Territories, Hong Kong SAR
(Special Administrative Region), China 219. Epidemiological and
phylogenetic analyses suggested that the human H5N1 isolates had
originated from an avian virus prior to this outbreak in poultry 34,
182. Surveillance of Hong Kong poultry markets for H5N1 viruses in
December 1997 detected the virus in approximately 20% of fecal samples
from chickens and 2% of fecal samples from ducks and geese (176). One
virus-positive market that served as a wholesale outlet for the city may
have been responsible for the contamination of other live-poultry
markets. Each of the H5N1 isolates was lethal when tested in chickens.
These findings implicate virus-contaminated birds in live-poultry
markets as the source of the H5N1 influenza outbreak in Hong Kong.

A potential lead to the origin of the H5N1 virus came from isolation of
a similar virus from geese dying of an influenza-like disease in
Guandong Province, China 176, 219. However, experimental infection of
geese with this isolate did not reproduce the disease, indicating that
the H5N1 virus was not the causative agent in the outbreak. Phylogenetic
studies showed that the HA of this isolate, but not other genes, shares
an immediate ancestor with the Hong Kong H5N1 virus 219. The HA of
another H5N1 virus isolated from a waterfowl in a wholesale live-poultry
market in Hong Kong in the beginning of 1999 was genetically closely
related to the H5N1 viruses isolated from patients in Hong Kong in 1997.
These findings suggest a precursor role for these viruses, at least for
the HA. An ancestral nonpathogenic strain for the 1997 Hong Kong
outbreak has not been isolated, as found in the Pennsylvania and the
1993 Mexican outbreaks.

Properties of the causative virus. Sequence analysis of the human H5N1
isolates indicated that all of the genes have an avian origin and are
not reassortants 34, 184. They contain multiple basic amino acids (R-E-
R-R-R-K-K-R) at the HA cleavage site and thus fulfill one of the
requirements for high virulence in chickens. However, they are
biologically heterogeneous in terms of the plaque sizes they produce in
MDCK cells, as well as their pathogenicity in mice 48, 112. Some of the
human H5N1 isolates were highly lethal in mice (the dose required to
kill 50% of mice [LD50] was approximately 0.3 PFU) and could replicate
in a variety of organs, including the brain 48, 112. Other isolates
showed moderate virulence (LD50 103 PFU) and replicated only in
respiratory organs. Nonetheless, all human and avian H5N1 isolates from
Hong Kong were lethal to chickens (LD50 102 PFU) and replicated well in
a variety of organs, including the brain and endothelial cells 182, a
property shared by other virulent avian influenza viruses 105.

In an effort to gain insight into the molecular basis of viral
adaptation in humans, sequences of the Hong Kong isolates were compared
with those of H5 chicken, duck, and goose viruses from live-poultry
markets 176. Like the human viruses, all of the avian isolates contained
multiple basic amino acids at the HA cleavage site, but there were no
amino acid differences that immediately suggested the basis for viral
adaptation in humans. Further analysis with monoclonal antibodies
disclosed two discrete antigenic groups, which correlated with genetic
findings and the presence or absence of a carbohydrate at residue 158
adjacent to the receptor-binding site on HA 176. However, the results of
antigenic and genetic studies did not correspond to virus
classifications based on virulence in mice 48. Also, both the index
human and avian isolates preferentially bound to NeuAc2,3Gal- rather
than NeuAc2,6Gal-containing receptors 116, although epithelial cells
lining the human trachea contain mainly NeuAc2,6Gal glycoconjugates 38.
Thus, there appears to be some "leakiness" of the receptor specificities
of influenza viruses in host range restriction. This finding is not
unexpected, since the receptor specificity of influenza viruses is only
"preferential" and conventional human viruses do bind NeuAc2,3Gal
(although they do so only poorly). Since the earliest isolates from the
1957 and 1968 pandemics preferentially recognize NeuAc2,6Gal over
NeuAc2,3Gal 155, 157, even though their HAs were derived from an avian
virus, the findings with the H5N1 Hong Kong viruses suggest that
conversion of the receptor specificity of the avian virus HA from
NeuAc2,3Gal to NeuAc2,6Gal is a necessary step leading to the efficient
transmission of avian-like influenza viruses in human hosts.
.

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