usenet virus

    Taken together, the results indicate  that  the  H5N1  viruses  from
human  infections and the closely related avian viruses isolated in 2004
and 2005 belong to a single genotype, often referred to as  genotype  Z,
and can be traced back to viruses isolated in 1997 in Hong Kong and from
geese in China.

    Thus, viruses from the 1997 H5N1 epidemic may have been  circulating
in  Asia  since  without causing any reported human infections until the
two confirmed cases in Hong Kong in February 2003.  Where and  how  have
they been circulating?


Intensive poultry farming & bird flu

In  an earlier study, researchers found that H5N1 influenza viruses were
isolated from apparently healthy domestic ducks in Mainland  China  from
1999  to  2002\;\s\sand  these  viruses  were  becoming  progressively more
pathogenic for mammals as time passed.

    Twenty-one viruses isolated were confirmed to be H5N1  subtype,  and
antigenically  similar to the virus that was the source of the 1997 Hong
Kong bird flu haemagglutinin gene, and all  were  highly  pathogenic  in
chickens  (most  causing  100% mortality, although the earliest isolates
were less lethal).  The viruses were increasingly  pathogenic  for  mice
the  later  they  were  isolated.  The earliest seven isolates were non-
pathogenic or of low pathogenicity, the next seven  of  relatively  more
pathogenic, and the last four highly pathogenic.  All pathogenic viruses
replicated in the lung.

    The genetic findings suggest that H5N1 had  been  circulating  among
domestic  fowl  in Asia since the 1997 epidemic in Hong Kong.  And while
circulating in domestic  ducks,  H5N1  viruses  gradually  acquired  the
characteristics  that make them lethal in mammals including humans.  One
possible explanation is the transmission of duck H5N1 viruses to humans,
the  selective  evolution of the viruses in humans, and their subsequent
transmission back to ducks.

    Thus, commercial factory farming could be  the  reservoir,  breeding
ground   and  incubator  for  deadly  epidemic  viruses  like  H5N1,  as
consistent with other evidence  (see  "Fowl  play  in  bird  flu",  this
series).


How likely is the bird flu pandemic?

Many experts are saying that the only barrier between a pandemic of bird
flu among birds and one among humans is if the H5N1 mutates its HA  gene
to  recognize  the  human-type  cell surface marker rather than the bird
type.

    As it turned out, human cells deep in the lower respiratory tract do
have  the  bird-type  receptor,  which  is why the virus can enter those
cells and cause severe pneumonia\;\salthough the  progeny  virus  is  less
easy  to  pass  on than if, like human influenza viruses, it could enter
and replicate in the cells of the upper respiratory tract as  well.   Is
that the only barrier that keeps away the bird flu pandemic?

    Things  are not that simple, according to the team of researchers in
Erasmus Medical Center in Rotterdam, the Netherlands.  Left to  its  own
devices,  successful  species jumps in nature are relatively rare.  That
is because complex adaptations are needed for a virus to get established
in  a  new  species  and transmit from host to host within that species.
These  complex  adaptations  including  genetic  differences  constitute
biological  barriers  between  species,  which  can  only be breached by
genetic modification.  That is why genetic modification is dangerous, as
I,  and  others  have been warning since genetic engineering began.  The
SARS virus of the last pandemic did  breach  species  barriers  and  was
highly  infectious  as it passed from one human host to numerous others,
it made many more people ill and caused  many  more  deaths.   There  is
indeed evidence that extensive genetic engineering of corona viruses may
have been contributed to creating the SARS virus.


What are the barriers preventing a virus to get into a new host?

First of all, there are barriers to prevent the virus from entering  the
body,  such  as  mucus, alveolar macrophages, and epithelium (linings of
organs and tissues).  There are specific receptors governing  the  entry
into  cells.   The  HA on the viral coats of the avian influenza viruses
preferentially bind to carbohydrate  chains  attached  to  the  receptor
protein ending in a sialic acid in a-2,3 linkage to a galactose, whereas
the HA on human influenza viruses prefer an a-2,6  linkage.   The  lower
respiratory  tract cells in humans have carbohydrate chains on receptors
ending in SA-a-2,3-gal, however, which is why fatal pneumonia can  occur
in humans infected with the virus.

    Once  within  the  cell,  the  virus  must  replicate.   Many  avian
influenza viruses can  infect  mouse  cells  but  not  replicate\;\s\soften
because  the  viral  polymerase  differs  between  avian  and  mammalian
influenza viruses in residue 627 of the polymerase protein PB2, which is
usually  glutamic acid in avian viruses and lysine in mammalian viruses.
So this might be another barrier.  In experimentally  infected  mice,  a
glutamic  acid to lysine mutation at this position in the PB2 protein of
H5N1 virus results in increased virulence and  in  the  ability  of  the
virus to invade organs other than the lungs.  Both H5N1 virus from human
patients in Asia  and  H7N7  virus  from  a  fatal  human  case  in  the
Netherlands possess a lysine at this site.  Lysine is also in the PB2 in
H5N1 viruses isolated from the thousands  of  dead  wild  water-fowl  in
mid-2005 from Qinghai Lake in China.

    The  replicated  virus must be released from the host cell to infect
more cells or be shed  from  the  host.   In  influenza,  progeny  virus
particles  are  bound to host cell receptor carbohydrate chains by their
haemagglutinin.  Viral neuraminidase cleaves these carbohydrate  chains,
thus releasing the newly produced virus from the cell surface.  Like the
respective haemagglutinins, neuraminidases from avian influenza  viruses
have  a preference for the SA-a-2,3-gal-terminated chains, whereas those
from many human influenza viruses prefer the a-2,6 linkage.

    Even if progeny virus  exits  one  host  cell,  host  innate  immune
responses  may  hinder  the  infection  of other cells.  Interferons may
induce uninfected cells to enter an antiviral state that inhibits  viral
replication.   The  viral  NS1  polypeptide  acts  as  an  antagonist to
interferon induction in infected cells by  sequestering  double-stranded
RNAs  or suppressing host post-transcriptional processing of mRNAs.  NS1
also may help the virus  to  replicate  in  interferon-treated  cultured
cells.

    In  order  to spread from the respiratory tract to other susceptible
tissues, the virus needs to enter the lymph and/or blood system, and  be
successfully   transported   to  other  tissues.   In  poultry,  whether
infection is localised or systemic depends on the amino acid sequence at
the   cleavage   site   of   HA.   The  cleavage  is  required  for  the
haemagglutinin to become fully  functional.   Low  pathogenic  influenza
viruses   require  extracellular  proteases  that  are  limited  to  the
respiratory  and  gastrointestinal  tracts  to  cleave   the   precursor
haemagglutinin,  whereas  highly pathogenic avian influenza viruses have
changes in the cleavage site that allow the precursor HA to be processed
by  ubiquitous  intracellular  proteases,  resulting  in  fatal systemic
infection.  The HAs of H5N1 viruses all have this  change,  which  is  a
motif of basic amino acids.

    From  their  sites of replication, viruses need to be transmitted to
new hosts.  Dissemination of progeny  viruses  form  the  infected  host
occurs   through   shedding   in  respiratory,  enteric,  or  urogenital
secretions.  Human influenza  viruses  replicate  mainly  in  the  upper
respiratory  tract  and  are  usually  readily  transmitted via droplets
formed during coughing or sneezing.  By contrast, H5N1  virus  typically
infects  human  cells  in the lower respiratory tract and so may be less
easily shed from the infected patient.

    Finally, it is well established in epidemiology theory that, as  the
proportion  of  susceptible  hosts  in  the  population,  s,  drops  (as
individuals become infected,  then  recover,  or  die),  the  number  of
secondary  cases  per  infection, R, also drops, R = sR0.  If R<1, as is
currently the case for  H5N1,  an  infection  will  not  cause  a  major
epidemic.  But if R is even modestly greater than one, a novel infection
may spread locally, with potential for further spread in the absence  of
control.

--
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Prof. Joe Cummins

e-mail: [email protected]

�Corona virus genetic engineering and the origin of SARS�
The growing global epidemic of Severe acute respiratory syndrome
(SARS).

Has been pinned down to a Corona virus. The disease has spread rapidly
from its first appearance in China and impacted heavily on Hong Kong ,
Singapore, Thailand and Toronto, Canada. The disease agent was
identified as a Corona virus with a unique RNA sequence not directly
related to known human and animal viruses (1) None of the early
reports have acknowledged the large body of reports on the genetic
manipulation of Coronas viruses in the laboratory nor have they
considered the possibility that the unique virus arose as a laboratory
accident or purposeful experiment. I have searched out a number of
studies on the genetic manipulation of Corona viruses and describe a
few such studies below.

Corona virus from a disease of pigs that produces symptoms similar to
SARS has been manipulated to create a viral vector to propagate
foreign genes (2). The Corona virus coat protein genes have been
manipulated to alter the tropism (species attacked by the virus) of
the virus (3). The gene for the pig corona virus coat protein
(controlling viral tropism) was propagated in tobacco plants (4).
Prodigene, a company specializing in production of crop
biopharmaceuticals also produced an edible vaccine for swine corona
virus (5) and information on whether or not that product was the one
being field tested in a disastrous field test has been deemed
confidential information.

These brief comments are musing on an ongoing investigation but might
provide some useful background information to others.

References

1)http://www.who.int/en/
Coronavirus never before seen in humans is the cause of SARS
Unprecedented collaboration identifies new pathogen in record time 16
April 2003

2)Journal of General Virology (2002), 83, 567�579.
In vitro and in vivo expression of foreign genes by transmissible
gastroenteritis coronavirus-derived minigenomes
Sara Alonso, Isabel Sola, Jens P. Teifke, Ilona Reimann, Ander Izeta,
Mo! nica Balasch,Juan Plana-Dura! n, Rob J. M. Moormann4 and Luis
Enjuanes

3)JOURNAL OF VIROLOGY, Apr. 2003, p. 4528�4538 Vol. 77,
Switching Species Tropism: an Effective Way To Manipulate the Feline
Coronavirus Genome Bert Jan Haijema, Haukeliene Volders, and Peter J.
M. Rottie

4)Immunogenicity of porcine transmissible gastroenteritis virus spike
protein expressed in plants
T. Tubolya, W. Yub, A. Baileyb, S. Degrandisc, S. Dub, L. Ericksonb,
E� . Nagya,
Vaccine 18 (2000) 2023�2028

5) http://www8.techmall.com/techdocs/TS000215-6.html
sept 2001
ProdiGene is First to Demonstrate Vaccination With Edible Vaccines
�Clinical trials Conducted by ProdiGene, a biopharmaceutical company
in College tation, Texas, have demonstrated for the first time that an
oral vaccine expressed in plants gives protection against a virulent
viral pathogen in livestock. The trials were conducted on swine using
an edible form of a vaccine for transmissible gastroenteritis virus
(TGEV).�


-----









-------
"Colin Trunt" <[email protected]> wrote in message
news:[email protected]...
> Serious question.
>
> I imagine smokey bacon would be safer but I have no
> scientific proof.
>
Generally Viruses need a living host, they die quickly in a dead one,
and are vulnerable to heating. So unless you are eating raw pig
that's alive, or has just been killed, you should be OK?

The real problem with this new outbreak of Swine flu
is it has jumped to being human to human infectious.
So watch out for people who look unwell and avoid contact

Good thing about quickly mutating viruses like this one,
is they tend to mutate to a safe form within 6 months

Steve Terry

-----
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From: %steve%@malloc.co.uk (Steve Firth)
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Subject: Re: Can you catch swine flu from bacon?
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Steve Terry <[email protected]> wrote:

> "Colin Trunt" <[email protected]> wrote in message
> news:[email protected]...
> > Serious question.
> >
> > I imagine smokey bacon would be safer but I have no
> > scientific proof.
> >
> Generally Viruses need a living host, they die quickly in a dead one,
> and are vulnerable to heating.

Generally, you're far from correct.

Viruses have a range of thermal stability and those which have
Archaebacteria as hosts have been found to be stable at temperatures
closer to boiling than to 37C. SARS-associated corona virus has been
determined to be infective up to 51 days post-mortem, and SVD, foot and
mouth, bluetongue and other significant veterinary viruses have been
discovered in pasteurised serum and cooked meats.

> So unless you are eating raw pig
> that's alive, or has just been killed, you should be OK?

I wouldn't make such a statement, not even with the addition of a
question mark, presumably indicating your real uncertainty about the
apparently definitive statements you are making.

> The real problem with this new outbreak of Swine flu
> is it has jumped to being human to human infectious.
> So watch out for people who look unwell and avoid contact
>
> Good thing about quickly mutating viruses like this one,
> is they tend to mutate to a safe form within 6 months

Bullshit.

--


From: [email protected] (Crystalviolent)
Newsgroups: bionet.microbiology
Date: 20 Apr 2003 00:26:46 GMT
References: <[email protected]>
Organization: AOL http://www.aol.com
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In article <[email protected]>, [email protected]
(Christopher) writes:
>the news about this virus I was just wondering that if a cure wasn't
>found, could it kill off most of the entire human race,
The mortality rate of SARS (a Corona virus) worldwide is 4.8%. (USA is 0%)
Pandemics of viral influenza (a Myxo virus) are much higher and IT hasn't wiped
out the human race.
Simian herpes, on the other hand, is 99% fatal to humans. Good thing the
manufacturers have great quality control/assurance on the green monkey kidney
cells we use in the lab. ;-)





---
From: [email protected] (Jeffrey Rice)
Subject: HIV-1 Adaptation to host/various musings
Date: 1995/10/18
Message-ID: <[email protected]>#1/1
X-Deja-AN: 117752365
organization: Pomona College
newsgroups: bionet.immunology
	I was reading Robin Henig's _A Dancing Matrix_, and came across a
couple ideas that didn't seem to work.  (BTW- has anyone else read this
book?  I'm loving it...)
	Dr. Henig says that HIV-1 shows signs that it may have existed in a
human host for several generations, as opposed to HIV-2 which shows signs of
a recent cross-over.  He bases this on comparisons to SIV, as well as case
studies dating to the 50's, as well as historical suggestions.
	HIV-1 is also more lethal than HIV-2, in that I guess most patients
infected with HIV-2 can be unaffected for two decades or more.
	Here's my thought/question:
	Since the viruses adapt to their hosts via mutation, selection,
ect., why would HIV-1 become more lethal across generations?  I guess I am
making the assumption it originated with something like SIV, which causes
symptoms more like HIV-2.  Wouldn't natural selection favor a less virulent
strain, to prolong host life and therefore transmission opportunities?  Or
can we guess from this that HIV-1 was MORE virulent historically than it is
now?
	What got me started on this topic was the (correct) idea that the
intention of a virus is not cell death, but replication.  If that includes
cell death of the host, this can be acceptable, assuming enough replication
is a result and transmission to a new host is possible.  Host death kills
the parasite, usually.  (Obviously we see with viruses like Ebola, ect. that
much transmission occurs after death, since the victims have bled-out.  This
seems a less secure method to me, though...)
	Anyway, I'd be interested to hear people's thoughts on this.  If you
are interested in immunology or virology, I'd recommend Henig's book.  It
really is facinating, not only in its coverage of the emergence of HIV but
also in other viruses.
					Jeff Rice
---


From: [email protected] (Howard Olson)
Subject: Re: Why  HIV-2 is less lethal than HIV-1?
Date: 1996/11/07
Message-ID: <[email protected]>#1/1
X-Deja-AN: 194994520
references: <[email protected]>
newsgroups: bionet.molbio.hiv
Umnarj Paeratakul <[email protected]> wrote:
>Dear friends,
>I read an article saying that the HIV-2 is not
>as "potent" as HIV-1.  People do get sick and
>die, but at the lower rate.
>Do you know why?
>Umnarj Paeratakul
>Thailand
      Viruses sometimes evolve less lethality against their host as
competition against another strain that is more lethal. By not killing
the host as quickly they have more chance to spread their genes versus
those of a more lethal strain.
---


From: [email protected] (Ian A. York)
Subject: Re: Just another comment on purpose
Date: 1996/09/13
Message-ID: <[email protected]>#1/1
X-Deja-AN: 180486786
references: <[email protected]>
organization: Panix
newsgroups: bionet.virology
In article <[email protected]>,
Martin Hewlett  <[email protected]> wrote:
>
>I think that this is the key point of the "balance" argument.  It seems
>to me that a successfull virus must somehow allow for the presence of
>"further hosts" in order to propagate.  Therefore, it is difficult to
>see how case fatality rates approaching 100% are consistent with this
>need.
Not so.  First, as far as many non-fatal viruses are concerned, a host is
a one-shot case anyway (i.e. after a host is infected, it becomes immune,
and the virus's progeny have no practical chance of re-infecting it; that
individual host is out of the pool of susceptible individuals).  Since
that host is of no more use to the virus, it cares not whether she lives
or dies - it can't even detect the difference between a dead host and an
immmune host.  (Sorry for the anthropomorphizing.  You know what I
mean.)
If the host dies, it leaves no more progeny; this might present a virus
with a problem in the long run, but that's not necessarily the case.
Hosts die anyway; individuals produce a more-than-replacement number of
progeny.  The key is that the virus maintains a roughly steady level
within the population over time.  A population can replace the ravages of
a 100%-fatal virus.
Analogy time: mice are preyed upon by owls.  Damn few mice survive an owl
attack - owls are close to 100% fatal for mice.  But there is no selection
pressure on owls to become less lethal on an individual basis; there is
pressure on the owl population as a whole to not become more abundant
than the mouse population can support - if they do, the owls starve to
death, the mouse population recovers, and the status quo is restored.
The situation is exactly the same for viruses.  If a virus is 100% fatal,
and it becomes too abundant, then each individual it infects is less
likely to encounter (and re-infect) a new host; the virus becomes less
abundant, the population recovers; now infected individulas are more
likely to infect new hosts, the virus bounces back, and so forth.
One strategy for the virus is to allow the host to survive longer, and
that may let it encounter more potential new hosts.  But there are many
other also potentially successful strategies: it could survive longer
outside the host, it could become more infectious (enhance the chance of
infecting those new hosts it does encounter), it could cause the host to
run around more to enhance the chance of meeting new hosts, and so on.
Rabies is close to, if not at, 100% fatal.  It's a highly successful
virus, and its strategy hasn't changed over the centuries.  Rabid animals
run around a lot, increasing their chances of meeting new hosts; they
tend to be exciteable and snap at things, enhancing the infection of the
virus in the salivary glands; and so on.
You're exactly right to say that the key point is one of balance.  You're
exactly wrong to assume that there is only one way of balancing things,
and that that way is to become less lethal.
Ian
--
      Ian York   ([email protected])  <http://www.panix.com/~iayork/>
      "-but as he was a York, I am rather inclined to suppose him a
       very respectable Man." -Jane Austen, The History of England
---


Very good point, Ian.  I stand corrected.  I especially appreciate the
example of rabies.  I was being much too simplistic in my approach.
Martin Hewlett
Dept. of Molecular and Cellular Biology
University of Arizona

---


[email protected] (Ian A. York) wrote:
>Not so.  First, as far as many non-fatal viruses are concerned, a host is
>a one-shot case anyway (i.e. after a host is infected, it becomes immune,
>and the virus's progeny have no practical chance of re-infecting it; that
>individual host is out of the pool of susceptible individuals).  Since
>that host is of no more use to the virus, it cares not whether she lives
>or dies - it can't even detect the difference between a dead host and an
>immmune host.  (Sorry for the anthropomorphizing.  You know what I
>mean.)
Also, a virus being non-fatal is not necessarily a viral virtue,
rather a feature of the host's immune system.
>If the host dies, it leaves no more progeny; this might present a virus
>with a problem in the long run, but that's not necessarily the case.
>Hosts die anyway; individuals produce a more-than-replacement number of
>progeny.  The key is that the virus maintains a roughly steady level
>within the population over time.  A population can replace the ravages of
>a 100%-fatal virus.
Would you say that a finely balanced population (low early- and
mid-life mortality, roughly equal birth and death rate) is at at
particularly high risk of being decimated by aggressive pathogens?
Modern humans spring to mind, they are also very slow reproducers,
compared to viruses..
>One strategy for the virus is to allow the host to survive longer, and
>that may let it encounter more potential new hosts.  But there are many
>other also potentially successful strategies: it could survive longer
>outside the host, it could become more infectious (enhance the chance of
>infecting those new hosts it does encounter), it could cause the host to
>run around more to enhance the chance of meeting new hosts, and so on.
This is very well, what I have a problem understanding is how a virus
lineage can adapt to, or even maintain, a less aggressive (wrt. host
survival time or rate) strategy, at least if a reduced rate of virus
replication is the way to go.
Unless we have a cloning situation, i.e., all virus progeny within the
host is produced from one (slow-replication mutant) infectious unit,
then a slower-replicating genotype will lose out to its more
aggressive cousins infecting the same individual and have a lower
---


Olav Hungnes <[email protected]> wrote:
>
>Would you say that a finely balanced population (low early- and
>mid-life mortality, roughly equal birth and death rate) is at at
>particularly high risk of being decimated by aggressive pathogens?
The way you phrase that, I don't think you can make that statement.  At
some timescale, just about every population is finely balanced - you may
have to juggle with the scale a bit, though.  (Snowshoe hare populations
flucutate greatly, but within certain limits, over a moderately regular
cycle [I think I've read that somewhere]); if you compare one year to the
next, the population may be quite different, but if you take 7-year
averages, the population might be quite constant.)
I think I know what you mean, though: a population without the great
swings in population numbers.  I think that they might indeed be more
susceptible to this, but I also think that the species with this
characteristic tend to be ones with relatively small numbers anyway.  (If
there are lots of the individuals, then a boom/bust approach to population
turnover is more safe, because the odds are that some one individual will
survive the bust.  If there aren't many individuals, then a
slightly-higher-than-average bust cycle will put the population numbers
too low to keep going.)  So that boils down to the suggestion that if
there aren't many individuals, the loss of some of those individuals is
significant to the population as a whole - not very surprising.
I don't think that either statement applies well to humans.
>This is very well, what I have a problem understanding is how a virus
>lineage can adapt to, or even maintain, a less aggressive (wrt. host
>survival time or rate) strategy, at least if a reduced rate of virus
>replication is the way to go.
Think of it in terms of spread from one host to another, not in terms of
spread within an individual host.
Simplistic example:  Aggressive virus "A" infects a host.  It replicates
rapidly and rapidly kills the host.  Let's say it causes the host to shed
10 million viral particles over a period of one week.  During that week
the host comes into contact with one other susceptible individual and
infects it.  Host is now dead, and the virus has maintained its population
level.
Less aggressive virus "B" infects a different host.  It doesn't kill the
host; it causes the host to spread particles for two weeks - the same
number of particles, but this host meets two new ones and infects them.
By being less lethal, it has infected twice as many new hosts.
Other things to think about:  A healthier-feeling host might travel around
more.  Some species shun sick-looking individuals.  And I'm sure there are
lots of other points I'm missing as well - I know diddly about
evolutionary theory.
>Unless we have a cloning situation, i.e., all virus progeny within the
>host is produced from one (slow-replication mutant) infectious unit,
That's probably true, in many cases - I think that quite often a host is
infected with a single infectious unit.  It depends on the virus, of
course.
>then a slower-replicating genotype will lose out to its more
>aggressive cousins infecting the same individual and have a lower
I see no reason to assume that "slow-replicating" has anything at all to
do with "lethality".  There's no particular reason why the two should be
linked.  Some viruses which replicate very rapidly in vitro aer very
innocuous (eg rhinovirus).  But even if they are, it doesn't change the
overall picture: the selection on the virus at any long-term level is at
the level of spread between hosts, as well as within hosts.  And the two
are not necessarily tightly linked: those factors which enhance spread
between hosts don't necessarily have a lot to do with the factors that
enhance replication within a host.  So the viruses which have adapted to
replication in the host, are probably at a disadvantage compared to those
who are adapted to spread between hosts.
I do see your point, but don't think it really affects the overall
situation.
>cloning events, i.e., haploid gamete stages. Our scenario will often
>be more like cancer, where a majority of cells with a "good strategy"
>of controlled growth can be overthrown by a single cell lineage that
>has escaped such control.
But cancer is *only* adapted to replication *within* a host, so there's no
longer-term selection for spread *between* hosts.  That means it's a poor
analogy for viruses.
>Could one conceive an STD scenario with a virus/bacterium producing a
>factor that stimulates mating behaviour? This could even result in
>synergy.. Perhaps a virus could be the source of the ultimate
>aphrodisiac?  :-)
I've sen this speculated by, I *think*, Richard Dawkins - the suggestion
was that viruses are really good at inducing itches (nudge nudge wink
wink).  Maybe it wasn't Dawkins, but it's within that strict adaptationist
philosophy.  Cetainly it's possible, but I do think it's unlikely - I
think that some things just happen (the "spandrels" theory proposed by
Gould).
Ian
---


newsgroups: bionet.virology
In article <[email protected]>, [email protected] (Ian A. York) wrote:
> In article <[email protected]>,
> Hans Andersson <[email protected]> quoted:
> >Ebola, like other RNA viruses, has an error-prone replication process,
> >which would boost the frequenzy of mutations and thus the emergence of new
> >strains. Sanchez says that the high mutation rate increases the chance
> >that the disease could someday adapt a more contagious form."
>
> Which is equally true for *every other RNA virus around*, of course, and
> there are thousands - hundreds of thousands or millions - of them.
> Including such things as influenza virus, which killed, 20,000,000 (that's
> twenty million) people in one winter (European Journal of Epidemiology.
> 10(4):455-8, 1994); but of course that's not an Exciting
> New Virus that kills people in Excitingly Photgenic Ways, is it, so we
> won't worry about that at all.
>
> Come on, Hans, think a little, would you?
>
> Ian
>
Ian.
I just thought a little and this is the result:
I believe that health authorites all around the world, including CDC, have
their eyes on the possibility of a new and more lethal influenza virus
strain. There's two chapters about it in Stephen Morse's "Emerging
Viruses" and many others have brought up this concern. There's also
international research, surveillance and prevention efforts for that
possibility.
Joshua Lederberg are discussing "the resurgence of a 1918-like flu
pandemic", and other threats, in his article "Infection Emergent" in last
weeks JAMA.
This is what he says about Ebola:
"There is an outside chance of a zoonosis like Ebola escaping more
broadly, with increasing adaption to person-to-person spread, and perhaps
some muting of mortality that would keep the virus from burning out before
it spread further."
JAMA, Vol. 275, No.3, Jan. 17, 1996, p. 244 (Editorial)
It wasn't Joshua Lederberg who said that we shouldn't cover a
"hypothetical mutation scenario" or that he "do not want to see money
thrown at Ebola". It was
you, Ian - and you're wrong! ("Re: The return to The Hot Zone", Jan. 18, 1996)
Hans
---

From -7050536341627706118
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From: [email protected] (Ian A. York)
Subject: Re: The Hot Zone & The New Republic
Date: 1996/01/17
Message-ID: <[email protected]>#1/1
X-Deja-AN: 135757942
references: <v01530501ad2201f8595c@[166.84.199.117]>
organization: Panix
newsgroups: bionet.virology
In article <v01530501ad2201f8595c@[166.84.199.117]>,
Hans Andersson <[email protected]> wrote:
>
>You have been downplaying the risks with filoviruses and trying to build a
>case where newly emerging and highly fatal viruses aren't much of a
>problem.
Hans, please read what Ed has to say.  The lethality of a virus has
little or nothing to do with the potential public health problem.  For
example, diseases such as Creutzfeld-Jacob disease are lethal, but they
are not of concern to the population as a whole because they're not
particularly infectious.
The worst case for an Ebola virus outbreak would be the appearance of the
disease in an urban center in the third world, where identification and
isolation of patients is difficult.  Well, pay close attention: That's
pretty much what happened in Zaire, and if you'll notice the world is
still alive.
>"These viruses could be on our doorstep tomorrow", as one virologist said in a
>magazine article about budget cuts for CDC and USAMRIID.
Look, nobody argues that we should not be paying attention to emergning
viruses.  But you've lost sight of the diseases that have already
emerged.
Should we ignore the risks of a highly contagious, air-spread disease with a
long infectious period?  Tuberculosis is predicted to kill thirty million
people in the next decade.  Why aren't you wetting your pants about
that?  That's infinitely more frightening than the Ebola scenarios you've
proposed.
How about a virus that is much, much more lethal than Ebola?  That's
widespread in North America, readily spread between animals (the
reservoir) and humans?  Rabies virus kills between 20,000 and 50,000
people each year; it has a fatality rate of 99.999%.
How about an immensely contagious viral disease ("the most
transmissible disease known to man":  Archives of Internal Medicine.
154(16):1815-20, 1994) that kills around one million children per year?
Measles is a controllable disease; why aren't you lobbying to get the
vaccine to the places that need it?  And isn't it terrifying that people
in North America think of measles as a mildly amusing childhood nuisance?
These are not emerging diseases, Hans.  These are diseases that have
emerged.  These three alone kill millions of people every year, and we
don't have to postulate mysterious and hypothetical mutations.  Ebola
virus has killed some 500 people in the past ten years; that includes the
worst-case outbreak last year.
No realistic mutation you can propose for filoviruses can make it a worse
killer than any one of these diseases.
>From a virology point of view, I think that it's perfectly valid to express
>support for virus research and surveillance.
Absolutely.  It helps to understand which diseases are more important.
Everybody on this newsgroup agrees that virology funding should be
increased.  Until it is, let's use our knowledge to identify true
menaces, not the flavour of the month.
Ian
--
                      Ian York   ([email protected])
      "-but as he was a York, I am rather inclined to suppose him a
       very respectable Man." -Jane Austen, The History of England

---

From -6540797387061517408
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From: [email protected] (Ian A. York)
Subject: Re: The return to The Hot Zone
Date: 1996/01/18
Message-ID: <[email protected]>
X-Deja-AN: 135803743
references: <v01530502ad236bb2b2c4@[166.84.199.117]> <[email protected]>
organization: Panix
newsgroups: bionet.virology
I'm replying to Frank Eldredge's followup to Andersson's article, since
the original hasn't hit my news spool - baffling since we're both on the
same ISP.  (I checked to see if Hans had cancelled his article, but didn't
see his name in 'control', so I guess it's just Panix weirdness.  Unless
Andersson is using the mailing list instead of the Usenet groups for this
discussion?)
Frank says that both Hans and I have overstated our arguments.  To be
entirely honest, I don't know what Andersson's argument is.  I went back
and reread this thread (thanks to alta vista and dejanews) and, frankly,
I'm not much further ahead - although I gather Andersson is a
professional journalist, I'm quite honestly unclear on what he's trying
to say here. So let me first explain my interpretation of Andersson's
point, and then explain where I disagree with him.
HA says that the filoviruses are deadly viruses on an individual basis.
Nobody here has disagreed with that, so we have no argument there.  If
you get it, it's bad news for you.
Where we do seem to disagree is two other points:  (1)  The present
public-health risk of Ebola; (2)  The risk of Ebola mutating to become a
public-health risk at some time in the future.
I maintain that Ebola *as it is now* is not a major public health risk.
It certainly is of some concern, but our present knowledge of Ebola, and
the Kikwit outbreak (and I repeat, that was the worst-case scenario)
assure us that an Ebola outbreak is not going to destroy civilization;
it's not going to destroy a city, even.  The reason is that Ebola is
simply not a particularly infectious virus, and the reason for that is
that it kills people - and causes symptoms in people - too quickly.  There
is not a long contagious period during which the victims get around and
spread the disease.
HA doesn't address this, as far as I can see.  He keeps repeating that
Ebola is deadly, which is true but irrelevant.  He says, "It's only in a
world of theories that the lethality of a virus has little or nothing to
do with the potential public health problem."  But this isn't just theory,
it's theory that's been confirmed by observation; Ebola burnt itself out
in Kikwit, as predicted.  All the 'theory' is coming from Hans.
Let's look next at his concern about mutation.  He seems to feel that
because Ebola has been shown to spread by aerosol then it might mutate to
become as infectious as flu - or something like that.
Well, let's look at a virus that's not as exciting right now as Ebola.
And let's take HA's two main arguments: That a lethal virus is a major
public health concern, and that things that have been shown to spread by
aerosol are likely to mutate to spread like influenza.
There are quite a few articles demonstrating that rabies virus can be
spread by inhalation, and rabies is vastly more lethal than Ebola (see,
Hans, I read quite a bit later than Jane Austen; you might actually try to
read a little more yourself, to get a real understanding of the
situation).
Furthermore, there are tens of thousands of cases of rabies in North
America each year (in animals - I put this in so that Hans won't be able
to misinterpret as he did with my CJD example) - providing plenty of
opportunities for mutation to respiratory spread.  In case you missed it,
it hasn't happened.  Should we put the CDC on alert and throw money at the
problem for fear that it will mutate to respiratory spread?  -Or mutate so
the vaccine doesn't neutralize it (more likely, since there's some
selection pressure there)?  I can come up with rabies scenarios all day
that more more plausible than any of your Ebola scenarios.
Of course, Richard Preston hasn't written any scary books about rabies;
perhaps he doesn't care about the 50,000 people (and their families) who
die of it, in excruciating pain, every year?
In other words, I don't think anyone says that Ebola cannot possibly
mutate to become a threat.  (Read that carefully.) But the likelihood of
that is the same as any of a thousand other viruses mutating to become
threat.
What if human cytomegalovirus incorporates a mutant p53 in its genome,
Hans?  Shouldn't we be preparing for that possibility?  It's at least as
likely as an airborne Ebola - Richard Preston's claim that "Ebola is a
virus trying to break out - out of the jungle, out of the monkey species,
and out of Africa" notwithstanding, Ebola is a virus: it doesn't have
goals or intentions.
But I do think (I won't speak for Ed here, my wrist is still sore from the
last slap he gave it) that we have to assign our non-infinite resources -
money, time, and manpower - rationally.  That means assessing where the
most likely risks are, and addressing them.
If the only virus you know anything about is Ebola, then it's going to
look like the biggest threat.  But if you look at some of the established
killers like TB (and yes, Hans, I know you said "*This* discussion just
happens to be about Ebola", but you're wrong; this discussion is about
public health risks, of which Ebola is one), measles, and polio, then it's
hard to argue that resources should be withdrawn from them in order to
cover the hypothetical risk of a hypothetical mutation.  And if you do
want to cover that hypothetical mutation scenario, than you should also
cover the risk of rabies mutating, polio mutating, TB mutating, measles
mutating ...
Let me say it again:  We KNOW that TB kills millions of people per year.
We KNOW that measles kills another couple of million people per year.
Ebola has killed about 400 people in the time these two diseases have
killed some 40,000,000. There's no theory here, Hans, just facts.
I'll tell you what I, personally, would like to see done.  I'd like to
see funding of a much better infectious disease surveillance program,
worldwide - probably heavily based on the CDC, since they seem to have
the most experience at it. Basically, an expansion of the programs the
WHO is already working on.
I do not want to see journalists advocating research on the latest flavour
on the month. I do not want to see money being thrown at Ebola, because
that money will come from somewhere else - and it will probably come from
somewhere in the health care/research system, and people will die because
they didn't get the measles vaccine that money was originally going to
cover.
And, as long as we're dreaming here, I wish that the CDC didn't have to
use scare tactics based on the latest mobies in order to get some funding.
I think this will be my last post on the subject of Ebola, so feel free to
insult me some more, Hans; you'll have the last word.
Ian
---


New York Times
April 27, 2003
>From China's Provinces, a Crafty Germ Spreads
By ELISABETH ROSENTHAL
SHUNDE, China - An hour south of Guangzhou, the Dongyuan animal market
presents endless opportunities for an emerging germ. In hundreds of
cramped stalls that stink of blood and guts, wholesale food vendors
tend to veritable zoos that will grace Guangdong Province's tables:
snakes, chickens, cats, turtles, badgers, frogs. And, in summer,
sometimes rats, too.
They are all stacked in cages one on top of another - which in turn
serve as seats, card tables and dining quarters for the poor migrants
who work there. On a recent morning, near stall 17, there were
beheaded snakes, disemboweled frogs and feathers flying as a
half-alive headless bird was plunked into a basket.
If you were a corona virus, like the one that causes severe acute
respiratory syndrome, known as SARS, it would be easy to move from
animals to humans in the kitchens and food stalls of Guangdong, a
province notorious for exotic cuisine prepared with freshly killed
beasts.
Indeed, preliminary studies of early SARS victims here in Guangdong
have found that an unusually high percentage were in the catering
profession - a tantalizing clue, perhaps, to how a germ that
genetically most resembles chicken and rodent viruses has gained the
ability to infect thousands of humans.
One of the earliest cases, last December, was a seller of snakes and
birds here who died at Shunde's First People's Hospital of severe
pneumonia. His wife and a several members of the hospital staff
contracted it as well, setting off an outbreak that now sounds eerily
familiar.
"Oh yes, I heard that a guy here died of that pneumonia," said Li
Songyu, a 40-year-old wearing a neat tan blouse, as she filleted live
frogs and dumped them into a basket. "But it is very safe and sanitary
now."
Around the same time in December, Huang Xinchu, a chef, was admitted
to the Heyuan People's Hospital, 100 miles to the north, ultimately
infecting eight doctors there. On Jan. 2, another desperately ill chef
was hospitalized in the city of Zhongshan, south of Shunde, setting
off an outbreak.
But if such early outbreaks present scientific hints about the origin
of SARS, they also provide painful political lessons in how a disease
that has spread worldwide could have been prevented.
In early January, alarmed health departments in Shunde, Heyuan and
Zhongshan all reported the strange pneumonia clusters to Guangdong
provincial authorities, who concluded that they were facing a highly
infectious pneumonia caused by a previously unknown agent.
It is unclear whether that conclusion was passed on by provincial
officials to the Ministry of Health in Beijing, or ever reported to
international health agencies that might have conducted an early
investigation into the problem. Instead, it would be another two and a
half months before the strange pneumonia had a name, coined only after
an Italian doctor working in Hanoi, Vietnam, alerted the World Health
Organization about a similar new pneumonia he was seeing there.
And it would be three and a half months before China's leaders would
admit that their country had an epidemic of SARS. From January through
the middle of March, doctors in Asia and Canada were encountering
patients carrying a virulent and highly contagious germ, unaware that
they were facing potentially lethal infection.
During that period, hundreds of health workers fell ill. During that
period, well-meaning doctors were placing SARS patients in ordinary
wards - as they would patients with normal pneumonia - and those
patients were passing the infection on to hundreds of others.
Origins in Food Trade
Scientists have always considered the teeming farms of southern China,
where animals and people crowd together as ideal breeding grounds for
new human viruses, which can jump between species under such
conditions. So it was no surprise in March when the World Health
Organization said it believed that SARS originated in Guangdong.
But when a World Health Organization delegation went to look at data
on the earliest SARS cases, they found few farmers among the victims.
Instead what jumped out was an odd preponderance of food handlers and
chefs - about 5 percent of the first 900 patients, as opposed to less
than 1 percent among patients with normal pneumonia.
So far, studies are in their early stages and have yielded few
specific conclusions. Even if food handlers turn out to be the
conduits through which SARS passed from animals to humans, all
evidence points to human-to-human transmission now.
Still, for much of December and January, several small cities around
Guangzhou were fighting - and often winning - localized battles with
the strange pneumonia that would later be named SARS.
In December, the 32-year-old chef from Heyuan was admitted to the
Heyuan People's Hospital, having falen sick with pneumonia on his job
near the boom town of Shenzhen. His family had him transferred to
Guangzhou when his condition deteriorated despite medication. But when
eight doctors and nurses fell ill with a similar untreatable pneumonia
in Heyuan just a few days later, hospital officials became alarmed.
On Jan. 1, they told the local health department of the cluster of
cases. "On Jan. 2, we reported a new infectious disease to the
provincial health bureau," said Dr. Ouyang Songhua, deputy chief of
the Heyuan Public Health Department. "They immediately sent out an
expert team to investigate it, deciding it was a pneumonia of
previously unknown cause."
Word of the disease spread among local doctors so that when another
chef with pneumonia arrived at Zhongshan Hospital on Jan. 2, short of
breath and feverish, doctors isolated him in intensive care.
But not soon enough: 13 medical staff members were infected, who in
turn infected 15 others in Zhongshan as well. Outbreaks in Shunde,
Heyuan and Zhongshan peaked in January, and by February the virus was
poised to move on.
By early February, sick and frightened patients from small cities like
these were traveling to more advanced hospitals in the provincial
capital of Guangzhou - and that is when the surge of cases really
began.
>From Feb. 2 through Feb. 4, a very sick man from Zhongshan made the
rounds of emergency rooms in Guangzhou as treatment failed to improve
his condition, leaving dozens of health workers infected. At the time,
emergency room staff members understood little about the new pneumonia
that had been cropping up around the province. At first, they did not
isolate the man and were wearing no protective gear.
Unfortunately, the man was what is now known as a "super-spreader" -
one of a small group of SARS patients who is highly infectious. Dozens
of doctors and nurses fell sick at the Zhongshan No. 2 Hospital, where
he was finally admitted.
"He was very sick, but who knew there was something so terrible going
around?" said a nurse named Mo at the Zhongshan No. 2 Hospital,
recalling the long, frightening quarantine that followed in February,
when nurses and doctors spent long weeks living in their units waiting
to see if they will start to cough. In China and in much of Asia, more
than 30 percent of SARS victims have been hospital workers.
Hong Kong as a Gateway
On Feb. 21, Dr. Liu Jianlun, a 64-year-old lung specialist from the
Zhongshan hospital, attended his nephew's wedding in Hong Kong, even
though he was running a fever. With what is now known about the
disease, health care providers like Dr. Liu with such extensive
exposure to SARS would be quarantined and forbidden to travel. But no
such guidelines existed then.
At the Metropole Hotel, where he stayed, he passed SARS on to a number
of other guests, including two Canadians, an American businessman en
route to Hanoi, a Hong Kong man, and three young women from Singapore.
SARS, until then confined to the Chinese mainland, was unleashed on
the world.
At the Kwang Wah Hospital in Hong Kong, where Dr. Liu went when his
breathing became labored, he advised shocked doctors and nurses of the
mystery pneumonia that was ravaging his hometown, insisting that they
isolate him behind double panes of glass and don protective gear
before his exam. The doctor died several days later; no one at the
hospital was infected.
But the grisly story was not shared with other doctors in Hong Kong or
the rest of the world. And, with the new corona virus silently
breeding in their bodies, the nine guests at the three-star Metropole
Hotel dispersed on airplanes like bees carrying a deadly pollen,
seeding SARS locally and to far corners of the world.
The woman from Toronto, Kwan Sui-chu, died in a Toronto hospital on
March 5, but not before infecting her son and at least five health
workers. Canada now has identified at least 140 SARS cases, 15 fatal.
Johnny Chen, the American businessman, fell ill at a hospital in Hanoi
in late February, where he ultimately infected 20 health workers,
including Dr. Carlo Urbani, an Italian medical researcher who alerted
the W.H.O. about a new type of pneumonia and who also eventually died
of the disease. The Hong Kong man was admitted to a general ward at
the Prince of Wales Hospital, setting off a huge outbreak.
The three friends from Singapore fell ill after returning home in late
February and were admitted to three different hospitals from March 1
to March 3. While two of the women infected no one else, the third,
Esther Mok, another super-spreader, set off a chain of infection based
at the Tan Tok Seng Hospital, from which over 90 people fell ill,
accounting for more than half the cases in Singapore. Ms. Mok has
recovered, but many members of her family became ill, including her
mother and father, who both died.
On March 14, the World Health Organization formally issued its
worldwide alert about the new disease, which it called SARS.
A Focus on Prevention
Since then, countries visited by this new plague have taken
increasingly severe steps in order to control further spread of a
disease that has eluded many conventional infection barriers. Because
the disease remains difficult to treat and has a death rate of 5 to 10
percent, by far the most effective way to deal with it is to stop its
spread.
"On an individual level it is relatively low risk, but the proportion
of people who have a severe course is quite high," said Rob Breiman, a
virology expert who has worked for the World Health Organization on
the outbreak. "Until we know more about this disease, protecting
against exposure is extremely important."
In Canada, for example, even healthy travelers arriving from affected
areas are advised to go into a 10-day voluntary quarantine, where they
are advised to stay at home, take their temperature frequently and
sleep in a separate room from other family members. Ontario alone now
has 7,000 people under various types of quarantine.
But some people have resented the restrictions for what most often
proves to be nothing more than a fever from a common cold. On Easter
Sunday, one health care worker who had been exposed refused to stay at
home, attending church services and a funeral in Toronto. Health
officials are now considering a court order to keep him isolated.
Companies and governments in the West are drastically curtailing
travel to SARS-affected regions. Some are also are requiring employees
to stay at home for 14 days after visiting SARS-infected areas.
"I'm not too worried about the disease," said Jane Cowells, a resident
of New Zealand, as she arrived this week, unmasked, at Beijing Capital
Airport. "But the whole thing is a headache, since when I go home I
can't go back to work for 10 days."
In Vietnam, where the epidemic is now under control, officials said
they were considering sealing off the entire 800-mile border with
China to prevent sick tourists from reintroducing the germ.
In many Asian countries, airports have come to resemble bioterrorism
labs, as nurses in protective gear assess arriving passengers for
signs of disease. No place is more vigilant than Singapore.
Singapore's Drastic Steps
"Welcome to Singapore! Are you feeling well today?" chimes a chorus of
nurses, their faces covered by masks, their eyes by goggles, their
bodies by yellow hospital gowns. Passengers coming from other
countries with SARS are guided to pass through a high-tech thermal
scanner that picks up temperatures over 100. A bevy of masked soldiers
in camouflage uniforms are there to escort away those with fever.
Those who pass muster are given a card warning that they might have
been exposed to a deadly disease. Those who are feverish are whisked,
without apology, into a 10-day quarantine, and Singapore means
business. Video cameras will be installed in the home by a security
firm, to make sure patients do not stray. Those few who do are tagged
with an electronic wristband that records their movements.
But even in a small country, placing thousands on quarantine has been
a strain. Last Monday, after a case of SARS was discovered in a vendor
at Singapore's largest vegetable market, the Ministry of Health
ordered all 2,400 food sellers to report for quarantine, up from a
total of 467 quarantined before. Since 80 percent of the country's
vegetables pass through the Pasir Panjang Market, restaurants were
bracing for a shortage of greens.
"We do what we have to," said Dr. Balaji Sadasivan, a neurosurgeon who
is Singapore's minister of state for health. "I don't think we've seen
anything like this before and it is a global problem. For now this is
a battle that is being fought with the thermometer and quarantine."
Because of elaborate contact tracing, the Singapore outbreak is by far
the best defined in the world. All but 4 of the 188 victims were
infected in the hospital or by a family member at home. The four
exceptions are a child who got the disease from a classmate with an
infected parent, a flight attendant who served an infected doctor from
Singapore on a flight in Europe, a cab driver and a vegetable
salesman.
Dr. Sadasivan is unapologetic as he describes the increasingly
draconian measures his department has adopted to halt the spread of
the germ.
When the three young women from the fateful Hong Kong hotel brought
SARS to three different hospitals in Singapore in early March,
Singapore doctors were unaware of the odd pneumonia that was
hospitalizing dozens of patients each day in Guangdong and so admitted
them to ordinary wards. If the Chinese had publicized their severe
pneumonia in Guangdong, or if the Hong Kong doctors had more
aggressively reported the information about Dr. Liu, their response
almost certainly would have been different.
Two of the women did not pass on the germ, but one infected more than
20 people, both patients and hospital workers. One of the nurses she
infected also proved to be a super-spreader, passing SARS to 26
others. One of the 26 was a patient in the cardiac intensive care unit
whose SARS was not recognized because of many other medical problems.
Within a month, 90 people at the Tan Tok Seng Hospital had the
disease. The Health Ministry dug up an old law that allowed them to
impose mandatory quarantines, with fines of 5,000 Singapore dollars
for those who disobey. They also essentially closed the 1,000-bed
hospital to other patients - hoping to contain the virus within its
walls.
But it escaped all the same. Some patients who had been at Tan Tok
Seng in March contracted the disease and later went to other hospitals
when they developed coughs - setting off secondary outbreaks. One went
to Singapore General for an endoscopy and was screened for SARS, but
did not run the telltale fever because he was on steroids that
suppress the body's response. Ninety people at the hospital were
infected.
After this resurgence, the Health Department instituted a policy that
every patient at every hospital be considered a potential SARS
patient. Nurses are always masked when seeing patients, who are
allowed only one visitor a day. Confirmed SARS patients are allowed no
visitors at all, though they can talk to friends and family on their
cellphones. Nurses may not work on more than one unit and patients may
not transfer from hospital to hospital.
"We used to have a health care system organized for efficiency," said
Dr. Sadasivan. "But now our hospitals are organized for SARS
prevention."
Outside of the hospitals, the ministry closed all schools for two
weeks to halt potential transmission of the virus. All cab drivers now
take their temperatures twice a day. Temperature checks and health
questionnaires are standard for those entering buildings.
At Tan Tok Seng Hospital last Monday, an ambulance arrived carrying a
vegetable seller who came under the market quarantine. Although he
felt well, the man said he had a fever, and so the driver told him he
might have to remain in the hospital. Approaching a cordoned-off
screening area, he was resigned, saying, "I don't think I could have
the disease, but I know I have to do it."
China's Slow Response
But Singapore's aggressive, open confrontation with a viral enemy is a
lesson that some other countries have been slow to learn, especially
China, the world's most populous country, where SARS emerged almost
half a year ago.
Although doctors in Guangzhou were well aware of the problem as early
as January, information about an epidemic was suppressed for months,
and only started dribbling out at the beginning of April, under
intense international pressure.
Only in the last week have numbers begun to emerge elsewhere in China,
and the task is still not complete. In Beijing, they already paint an
alarming portrait of an epidemic that is likely to dwarf that in
either Guangdong or Hong Kong.
At a news conference on April 10, He Xiong, the deputy director of the
Beijing Centers for Disease Control, was still delivering a calm
message, endorsing numbers that the government released at the time:
that in Beijing there were only 27 SARS cases, so people should not
worry.
"Of course they can travel, we think it's very safe," he said,
referring to an approaching national vacation when tens of millions of
Chinese would normally be expected to travel.
But that misinformation only fueled the spread of SARS, as people -
with fevers and coughs - continued to go to school and work, passing
the disease on to others. As the number of cases increased well into
the hundreds, the illusion proved hard to maintain in a city with a
world-class gossip network that spread rumors of overflowing SARS
wards.
By last weekend, everyone was skeptical, as a smattering of schools
and hospitals mysteriously closed. One People's Armed Police hospital
in Beijing was closed after five patients were infected. The
Zhongguancun No. 1 Primary School closed when a relative of a student
came down with SARS. The Beijing University Institute of Economics put
several dozen people on quarantine after a secretary's mother got
pneumonia.
More than a dozen of Beijing's universities had reported suspected
cases. At the Economics and Finance University alone, more than a
dozen students and faculty members were listed as suspected SARS
cases, resulting in the suspension of classes from April 17.
That day, the main gate of the Northern Construction University was a
panic scene, as masked students made arrangements to flee to their
hometowns in the wake of suspected SARS cases on campus. "I want to
get out of here as soon as possible," said one alarmed student, making
calls on her cellphone to borrow money for the trip home.
Then, last Sunday, the Chinese government fired both the health
minister and the mayor of Beijing, and started releasing alarming data
that confirmed these fears. As of Friday, there were close to 900
confirmed cases in Beijing, a number that is certain to strain the
resources of city hospitals and will make SARS far difficult to
control.
But can the lessons of prevention learned in a tiny, authoritarian
country like Singapore be applied in other countries, particularly in
a vast, chaotic place like China, with far more cases and a highly
mobile population?
In Singapore, with its aggressive system of identifying and isolating
SARS patients, no health care worker has been infected for over three
weeks. But in Hong Kong, 2 to 10 doctors and nurses are falling ill
each day, in part, health officials there say, because doctors are
still not identifying them as SARS victims early enough and are
admitting them to ordinary wards.
"There is so much we don't know about this virus - how long it will be
with us? Will it mutate and become more easily transmitted?" Dr.
Breiman said. "But it is a little frightening that something which
started in one location could spread so quickly around the world."
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