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- 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.
- --
- ;From -8066292221520757068
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- om!news.compuserve.com!news-master.compuserve.com!not-for-mail
- From: marcus@myrealbox.com
- Newsgroups: uk.business.agriculture
- Subject: Re: SARS update
- Date: Tue, 22 Apr 2003 09:52:47 +0100
- Organization: CompuServe Interactive Services
- Lines: 71
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- Prof. Joe Cummins
- e-mail: jcummins@uwo.ca
- �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" <colin@trunt.com> wrote in message
- news:uKQIl.89545$ga.53197@newsfe01.ams2...
- > Serious question.
- >
- > I imagine smokey bacon would be safer but I have no
- > scientific proof.
- >
- Generally Viruses need a living host, they die quickly in a dead one,
- and are vulnerable to heating. So unless you are eating raw pig
- that's alive, or has just been killed, you should be OK?
- The real problem with this new outbreak of Swine flu
- is it has jumped to being human to human infectious.
- So watch out for people who look unwell and avoid contact
- Good thing about quickly mutating viruses like this one,
- is they tend to mutate to a safe form within 6 months
- Steve Terry
- -----
- From 1250770940491672925
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- net!not-for-mail
- From: %steve%@malloc.co.uk (Steve Firth)
- Newsgroups: uk.legal,uk.misc,uk.people.health
- Subject: Re: Can you catch swine flu from bacon?
- Date: Sun, 26 Apr 2009 14:44:01 +0100
- Organization: Firth Consulting
- Lines: 36
- Message-ID: <1iysayo.ohv697z7t5l2N%%steve%@malloc.co.uk>
- References: <uKQIl.89545$ga.53197@newsfe01.ams2> <gt1le9$em4$1@news.albasani.net
- >
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- Steve Terry <gFOURwwk@tesco.net> wrote:
- > "Colin Trunt" <colin@trunt.com> wrote in message
- > news:uKQIl.89545$ga.53197@newsfe01.ams2...
- > > 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: crystalviolent@aol.com (Crystalviolent)
- Newsgroups: bionet.microbiology
- Date: 20 Apr 2003 00:26:46 GMT
- References: <3ea17dc5.10926114@news.dsl.pipex.com>
- Organization: AOL http://www.aol.com
- X-Newsreader: Session Scheduler (Queue Name: usenet_offline-m07)
- Subject: Re: The SAR's virus?
- Message-ID: <20030419202646.18828.00000167@mb-m07.aol.com>
- Xref: archiver1.google.com bionet.microbiology:3323
- In article <3ea17dc5.10926114@news.dsl.pipex.com>, coroscant@hotmail.com
- (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: jrice@pomona.edu (Jeffrey Rice)
- Subject: HIV-1 Adaptation to host/various musings
- Date: 1995/10/18
- Message-ID: <4629pj$h07@epcot.pomona.edu>#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: holson@california.com (Howard Olson)
- Subject: Re: Why HIV-2 is less lethal than HIV-1?
- Date: 1996/11/07
- Message-ID: <3280d922.0@seashell.california.com>#1/1
- X-Deja-AN: 194994520
- references: <54uf66$ib4@chopin.inet.co.th>
- newsgroups: bionet.molbio.hiv
- Umnarj Paeratakul <umnarj@mozart.inet.co.th> 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: iayork@panix.com (Ian A. York)
- Subject: Re: Just another comment on purpose
- Date: 1996/09/13
- Message-ID: <51cv8c$1lc@panix.com>#1/1
- X-Deja-AN: 180486786
- references: <51cp4h$pnk@net.bio.net>
- organization: Panix
- newsgroups: bionet.virology
- In article <51cp4h$pnk@net.bio.net>,
- Martin Hewlett <hewlett@brahms.biosci.arizona.edu> 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 (iayork@panix.com) <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
- ---
- iayork@panix.com (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 <olavhung@idgonline.no> 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 <4elafv$1rn@panix.com>, iayork@panix.com (Ian A. York) wrote:
- > In article <hasse-2901962357370001@hasse.dialup.access.net>,
- > Hans Andersson <hasse@panix.com> 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
- X-Google-Language: ENGLISH,ASCII-7-bit
- X-Google-Thread: 103cc5,fda7f8b81815fa22
- X-Google-Attributes: gid103cc5,public
- From: iayork@panix.com (Ian A. York)
- Subject: Re: The Hot Zone & The New Republic
- Date: 1996/01/17
- Message-ID: <4dj6ij$860@panix.com>#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 <hasse@PANIX.COM> 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 (iayork@panix.com)
- "-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
- X-Google-Language: ENGLISH,ASCII-7-bit
- X-Google-Thread: 103cc5,47f37c78567b14be
- X-Google-Attributes: gid103cc5,public
- From: iayork@panix.com (Ian A. York)
- Subject: Re: The return to The Hot Zone
- Date: 1996/01/18
- Message-ID: <4dmsjj$6gc@panix.com>
- X-Deja-AN: 135803743
- references: <v01530502ad236bb2b2c4@[166.84.199.117]> <4dm7mc$k4m@ixnews6.ix.netcom.com>
- 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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