Viruses

THIS IS MATERIAL FROM THE ICE CAVE. IT HAS NOT YET BEEN FORMATTED.

Date: Sun, 27 Sep 1998 11:49:22 -0400 (EDT)
From: "Andrew D. Gable"

What exactly is Creutzfeld-Jakob Disease? As far as I understood from some references on the CDC website, I believe it might be sort of the human variation of Mad Cow, but I'm not sure.

For that matter, does anyone know exactly what Marburg is? I found listings for articles about it, but no real information. I gather it's some kind of fungal infection, maybe something similar to Hantavirus?

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Date: Tue, 08 Sep 1998 13:24:17 -0500
From: Mark Carroll

far as I understood from some references on the CDC website, I believe it
might be sort of the human variation of Mad Cow, but I'm not sure.

For that matter, does anyone know exactly what Marburg is? I found
listings for articles about it, but no real information. I gather it's
some kind of fungal infection, maybe something similar to Hantavirus?

Ahhh, pathology. All right, short and sweet:

Creutzfeld-Jakob Disease — dead on the money here. CJD is, as I recall, a viral infection, usually leading to many of the same symptoms of Mad Cow Disease. One of the reasons for the big beef scare awhile back, if I'm remembering right. You guys in the UK, chime in on this; I'm a bloody Yank.

Marburg is named for the town in Germany where it first appeared. Pathologically, it most resembles Ebola, with many of the same symptoms, albeit with a much, much lower fatality rate — something like 25 percent, with proper medical treatment. Marburg was instrumental in diagnosing some of the first occurrences of Ebola. It also appeared (like Ebola-Reston) in a monkey-handling facility.

For more info on Marburg, and the associated filovirii, check out 'The Hot Zone', one of the definitive scare-books on Ebola and its cousins.

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Date: Sun, 27 Sep 1998 15:09:46 -0500
From: Jeff McSpadden
Mark Carroll wrote:

Creutzfeld-Jakob Disease — dead on the money here. CJD is, as I recall, a
viral infection, usually leading to many of the same symptoms of Mad Cow
Disease. One of the reasons for the big beef scare awhile back, if I'm
remembering right. You guys in the UK, chime in on this; I'm a bloody Yank.

One of the few ways you can get Creutzfeld-Jakob Disease is eating squirell brains in the U.S. (Mad Squirrell Disease?) I believe this is a favored food in Kentucky, or somewhere in Appalachia. see http://gema.library.ucsf.edu:8081/emedl/archive/n/no_no__not_more_on_brains.html

for a news clipping.

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Date: Mon, 28 Sep 1998 08:29:42 -0700
From: Alan L. Krause

When this thread came up a few months back, I recall someone mentioning a NOVA episode which talked about Mad Cow disease, and it's theorized cause, PRIONS.

PRIONS are not viruses, but some sort of mutant protein IIRC. Therefore, you could take the brain of a cow which is infected, incinerate it to ashes, and then consume the ashes and still contract the 'disease' since the proteins are still in tact.

Pretty F'ing creepy. For more information, visit www.pbs.org/search and enter the following in the basic search text box:

NOVA, PRION

You'll get a list of about 20 matches. Select the "NOVA Online | The Brain Eaters " link and prepare yourself.

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Date: Wed, 30 Sep 1998 10:13:25 -0400
From: "Randall L. Orndorff"
I saw a very interesting speaker at my university last night (Kent State University, motto: "No Students Killed Since 1997"). Colonel Nancy Jaax, Chief Pathologist for the the United States Army Medical Research Institute of Infectious Disease (I think that is the whole name, of course many on this list would know it as USAMRIID). I learned quite a lot from her presentation, especially about the incident in Reston, Virginia. Although I did not read "The Hot Zone", she was one of the doctors who was there throughout the incident.

Luckily for me, they did not have any pictures of those infected with Ebola Zaire, only monkeys with Ebola Reston (transmitable to humans, but luckily not dangerous). They are part of the order of Fiboviri (?) which only contains Marberg and Ebola viruses to this date. What really scared the hell out of me is that Colonel Jaax mentioned that all viruses with RNA, like Ebola, are highly mutable and very susceptible to change. Whenever Ebola Zaire shows up (approx. 4 times since 1976) it is exactly the same. Which leads to one of two conclusions (from her standpoint): either the virus's carrier makes it impossible for it to survive except under certain extrordinary conditions (i.e. an extremely selective environment) or it was developed and has be reintroduced several times by humans.

Colonel Jaax said that she hoped that the first was true, but since the carrier for the virus has not yet been found (not a single trace so far) she said the second is still a possibility.

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From: "G. Wyckoff"
Date: Wed, 30 Sep 1998 09:47:11 -0500 (CDT)

which only contains Marberg and Ebola viruses to this date. What really
scared the hell out of me is that Colonel Jaax mentioned that all
viruses with RNA, like Ebola, are highly mutable and very susceptible to
change. Whenever Ebola Zaire shows up (approx. 4 times since 1976) it
is exactly the same. Which leads to one of two conclusions (from her
standpoint): either the virus's carrier makes it impossible for it to
survive except under certain extrordinary conditions (i.e. an extremely
selective environment) or it was developed and has be reintroduced
several times by humans.

I'm gonna chime in here, and I'll look up some of the details on this later. Maybe Graeme (where is Graeme, anyway?) could help as well.

The statement that "all viruses with RNA are highly mutable" leads me to believe that this is an generalization made on the basis of the study of known retroviruses. Things like HIV, although there are lots of retroviruses. And lots of the retroviruses studied aren't necessarily studied in humans. So, if they are finding that, through direct sequencing, large portions of the Ebola Zaire virus are _exactly the same_ with no mutations from one outbreak to the next, that is suspicious, but there are two other possibilities (more likely, IMHO) that the speaker didn't raise.

1) Ebola Zaire has a far more efficient and reliable method of replication than most other RNA-based viruses. (I don't know if that's true)

2) The virus is in a stable host population, and is not replicating with the same frequency in the host population as it is in a susceptible infected population. (I also don't know if this is true.)

The suggestion by a Military Doctor that Ebola Zaire was _developed_ by humans and reintroduced into populations several times (leading to the outbreaks) seems particularly alarmist and unfounded. The other thing is that I highly question their methods of judging similarity if they are saying that the viruses are "the same" from one outbreak to the next. There are even some portions of the HIV virus which are relatively stable from one generation to the next; I would guarantee that Ebola is the same way. If they are looking at a particular, essential gene it would make some sort of sense that the gene was not evolving quickly at the molecular level.

I'll do a little research on this. Meanwhile, anyone with more knowledge of viruses in general and Ebola in particular please chime in; viruse evolution is a little outside of my normal field of expertise. The Doctor quoted, though, seems like they are making a dangerous logical leap.

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Date: Wed, 30 Sep 1998 11:29:57 -0400
From: "Randall L. Orndorff"

The suggestion by a Military Doctor that Ebola Zaire was
_developed_ by humans and reintroduced into populations several times
(leading to the outbreaks) seems particularly alarmist and unfounded. The
other thing is that I highly question their methods of judging similarity
if they are saying that the viruses are "the same" from one outbreak to
the next. There are even some portions of the HIV virus which are
relatively stable from one generation to the next; I would guarantee that
Ebola is the same way. If they are looking at a particular, essential
gene it would make some sort of sense that the gene was not evolving
quickly at the molecular level.

Doh… The "human re-introduction" theory was just what happened to frighten me. She made it pretty clear that what she believed was the virus "lived" in a environment that continuously selected for its particular traits.

I'll do a little research on this. Meanwhile, anyone with more
knowledge of viruses in general and Ebola in particular please chime in;
viruse evolution is a little outside of my normal field of expertise. The
Doctor quoted, though, seems like they are making a dangerous logical
leap.

You may be right, but bear in mind she also did and is doing some of the first work on the subject, and is most likely one of if not the only authorities on the Ebola virus. She has been at all of the recent outbreaks of Ebola and has first hand knowledge that most of us will never possess. I'm sorry if my post led you to believe otherwise, but her talk was neither alarmist nor irrational, which is really something when you consider the subject matter.

She only discussed the threat of engineered diseases very briefly, but when she did, she said that the most danger we face from terrorists (with regards to biological warfare) is that of diseases like smallpox or the flu. They apparently are easy to use as deadly weapons. Then again, I guess it is not too hard to envision a great flu epidemic, as it has already happened in this century.

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Date: Wed, 30 Sep 1998 11:18:56 -0700
From: Alan L. Krause
It seems as if they may have found a way to quickly identify the presence of mad cow disease in slaughtered cows. Now, just who 'they' are. I leave up to you! :>

Check out http://cnn.com/TECH/science/9809/28/madcow.test.ap for more information..


Date: Wed, 30 Sep 1998 13:46:53 -0500 (CDT)
From: Don Juneau

She only discussed the threat of engineered diseases very
briefly, but when she did, she said that the most danger we face from
terrorists (with regards to biological warfare) is that of diseases like
smallpox or the flu. They apparently are easy to use as deadly weapons.
Then again, I guess it is not too hard to envision a great flu epidemic,
as it has already happened in this century.

One fictional speculation was that during/prior to WWI, German scientists noticed Ebola in their colony (German East Africa, forget what it became), brought it back, and married it to the influenza, for a pneumatically <?> transmitted disease. (ARCHANGEL, forget the authour offhand. "Fiction" for certain, and pushing it a *lot* with that level of skill at that time.)

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Date: Tue, 29 Sep 1998 18:59:22 -0300
From: "Roberto L. Vargas"

Creutzfeldt-Jakob Disease.

For some weird reason I've always found the Spongiform Encephalopathies very interesting. Among them are Creutzfeld Jakob, kuru, and specific animal forms like scrapie, mad cow, and a transmissible encephalopathy in minks and raccoons. They are called spongiform because of a special pathologic finding on microscopy post-mortem. The grey matter of the brain has these little holes of different sizes which kind of look like a sponge.

The easiest form of transmission is direct intracerebral inoculation (I know it sounds a bit hard, but I'll explain later) but a variety of parenteral modes of transmission will do, like eating monkey brains for kuru. After about 18 months latency, the disease explodes with full force.

Attempts at demosntrating nucleic acids, either DNA or RNA, which would have been inevitable in a virus or any other classic infectious agents as understood today, have been unsuccesful so a protein has been implicated as the causative agents. This is called a prion, and it is an abnormal form of a protein normally encountered in cells, which develops immunity to enzyme digestion. CJD even apparently has some sort of heredable aspect, as the gene for the abnormal protein has been characterized, it is found on chromosome 20, and the mutation that probably causes the disease may be hereditable, in sharp disregard for natural selection principles.

Experiments using animals with transplanted genes shows that the disease is transmisible to any individual with the gene for the original normal protein. The exact relationship between the protein and the disease is not understood very well, but it probably corrupts the integrity of normal structures.

CJD presents as a rapidly deteriorating dementia, and is extremely rare, in spite of the proven infectibility (about 1/1,000,000 worldwide). In humans, it has been transnmitted through the use of "infected" tissues and instruments, specially in neurosurgery and corneal transplant. The thing isn't alive, so you cannot kill it. Sometimes it even holds for the high pressures and heat in autoclaving surgical instruments.

The clinical picture is classic. Mild memory and behavioral disturbances at first, with a quickly progressing dementia and startle myoclonus (involuntary twitching of muscles). There is no cure or treatment, and it is invariably fatal (usually within 7 months).

I'm not very familiar with Marburg, but I do know it is a virus, I believe of the same family as Ebola and Dengue (flavivirus, I think).

I think it is deadly, and extremely rare. That's about as much as I can say. Could find out more, if anyone is interested, but we have a resident microbiology Ph D, so I'm sure he knows loads about it.

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Date: Wed, 30 Sep 1998 16:04:00 -0500
From: William Timmins

Then, either you get the abnormal protein from exogenous source
(transmitted) or the mutation kicks in and you get a different
conformation in your protein. This abnormal form then facilitates,
in cooperation, the transformation of other normal molecules of the
protein into the abnormal form or prions, which presumably goes in and out
of cells just like the normal protein does, but dirupting everything in it's
path.

Ah ha! This is what I was curious about. How does a protein transform other proteins

Date: Tue, 29 Sep 1998 23:29:04 -0300
From: "Roberto L. Vargas"

When speaking of the Spongiform Encephalopathies, specially of the mechanism of disease, we are dealing on the fringes of medical knowledge. Most things are conjecture (not on my part, of course) but it is educated conjecture based on some evidence and fairly plausible. With that disclamer, I feel confident in strutting forward.

These are two different questions. The form of spreading the prion depends on how you got it in the first place. If you had it through the most effective transfer method, intracerebral inoculation, it is already in it's target organ and does not need to go any further.

Arguably, when the prion is ingested it is absorbed from the gut and once in the blood stream simply crosses the hematoencephalic barrier into the brain. There are 2 huge problems with this.

Proteins are usually not absorbed whole, but divided into small chains or individual amino acids (the building blocks of proteins) and then absorbed. So that should effectively render our prion ineffective. Turns out the little sucker resists enzymatic degradation into smaller blocks and it just needs a break, since it is a small (about 30 kd) protein to get in. This is rare, but so is getting infected this way. The second is that the hematoencephalic barrier (the one dividing the brain from the stream of blood) is notably impermeable to proteins. So it probably needs two breaks in the natural defenses of the body to get to it's target organ.

The answer to the second question, apparently it does not "invade" cells per se (like viruses do). It is normal constituent of the cell, just mutated impairing the integrity of the cell and presumably lysing them. That is the reason why only a species which has the normal form of the protein can get the disease. The mutations in the gene are usually hereditable, so you are born with them, not infected.

Not if the model postulated is correct. You are born with the mutation, since actually getting the exact mutation through regular means is very very improbable ( since there are so many possibilities for mutations the chance of getting a random mutation that is exactly like the one associated with SE is extremely slim).

This is how the thing supposedly works. You have the gene for the normal protein, so chances are you have the protein circulating. Then, either you get the abnormal protein from exogenous source (transmitted) or the mutation kicks in and you get a different conformation in your protein. This abnormal form then facilitates, in cooperation, the transformation of other normal molecules of the protein into the abnormal form or prions, which presumably goes in and out of cells just like the normal protein does, but dirupting everything in it's path.

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From: "G. Wyckoff"
Date: Wed, 30 Sep 1998 15:15:46 -0500 (CDT)

Ah ha! This is what I was curious about. How does a protein transform other proteins?

THAT is part and parcel of the $64,000 question. I've seen talks on yeast prions where they were talking about the modified prion acting like a chaperone protein and adjusting the conformation of other proteins. Chaperone proteins are proteins that aid in keeping other proteins in the proper conformation for function in "extreme" conditions (where the protein might lose it's configuration, for example) or aid in transporting proteins through channels which they would otherwise not be able to go through.

It makes sense that a prion, therefore, can change the configuration of another protein; chaperones do it, other types of proteins do it, ad nauseum. But exactly why and how it manages this conformational switch is an open question, as far as I know.

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From: "G. Wyckoff"
Date: Wed, 30 Sep 1998 15:24:56 -0500 (CDT)

Doh… The "human re-introduction" theory was just what happened to
frighten me. She made it pretty clear that what she believed was the
virus "lived" in a environment that continuously selected for its
particular traits.

Alright, I see what you mean, I guess I mis-read what you wrote.

However, in doing some quick searches, there is an article in Molecular Biology and Evolution which might be helpful (if you have access to a good library).

Molecular Biology and Evolution, 14(8):800-806 (1997)
"The Origin and Evolution of Ebola and Marburg Viruses."
Suzuki, Y. and T. Gojobori

Brief synopsis (my words); Ebola and Marburg evolve at the molecular level 100 times more slowly than human influenza A and other retroviruses, and the rate of evolution was at about the same level as hepatitis B. Also, the _types_ of molecular changes suggests that the virus is constrained in how it can evolve.

Worth a read.

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Date: Wed, 30 Sep 1998 17:19:20 -0400
From: Graeme Price

OK, I've gotten in a little late on this one - I've been monitoring the thread via the archive (server finally blew up a fortnight ago and has only just come back - hence my prolonged absence from the list: that and a stupid amount of work).

Roberto Vargas wrote lots of very useful clinical stuff on CJD, which I won't repeat due to bandwidth (slightly off target on one thing though: Kuru was transmitted by consumption of human [not monkey] brains by Fore natives in Papua New Guinea during ritual burial ceremonies: a form of ancestor worship - men got to eat muscle and other "choice cuts", women and children got the viscera and brains, which explains why they Kuru was much more prevalent in women and children than adult males… These practices ceased in the late 60's due to government pressure).

The question as to how one protein transforms another is _exactly_ what the big scientific question is in the prion field: there are at leat 2 Nobel prize winners working on this, and they don't know the answer! The probable pathway likely involves another protein, or group of proteins called the heat shock proteins (and related molecules called chaperonins). These proteins bind to denatured (ie. misfolded) proteins and help put them back together again in their proper form (conformation). If the chaperonins refold the prion protein into the wrong (pathogenic) form, perhaps using the abnormal prion protein as a template , then this could lead to the propogation of more abnormal prions.. which would lead into a vicious circle as the new abnormal prions could be used as a template for misfolding new prions and so on…. One key factor will be where the folding of the abnormal prions occurs within (or outside) the cell.

Of course, this is all theory and is a long way from being proved. It is an attractive hypothesis though, as it implies that simply being exposed to an abnormal prion isn't enough to trigger the disease, and that there can be other genetic susceptibilities (perhaps mutations in the heat shock protein genes) which predispose towards prion disease. A comforting thought for millions of Brits like me who grew up during the BSE epidemic.

Sorry for the hard (cutting edge) science involved here…. all research scientists tend to talk quickly using lots of long words when they don't really know what's going on, and I'm no exception!

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Date: Wed, 30 Sep 1998 21:47:04
From: Davide Mana

For more fictional accounts of Ebola-like viruses, German scientists and then all hell breaks loose, I recommend James Herbert's novel "48" . A book that screams to be made into a movie, and quite good overall.

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Date: Wed, 30 Sep 1998 17:56:19 -0400
From: Graeme Price
Roberto Vargas wrote:

Hmm. That would be me then. Virologist to the stars!

Actually Roberto, I'm glad you're not very familar with Marburg virus, as if you were you would have roughly a 75% chance of being dead right now.

Right. Marburg virus is a filovirus (genome is negative sense, single stranded RNA), reasonably closely related to Ebola. Many people say that Marburg is less pathogenic than Ebola, and this may be true (but whether you can say that a 60-80% case fatality rate [Marburg] in people who are treated with western medicine is less deadly than a 70-95% case fatality rate [Ebola] in people who generally aren't treated is another matter). Marburg virus was first documented in 1967 in the town of Marburg, West Germany (still the site of one of Europe's premier virology institutes). The initial outbreak here was in workers at the BehringWerke (IIRC) vaccine plant where monkeys were used for the production of polio vaccine. The monkeys (which had been imported from Uganda) which were the source of the infection died, and then so did the workers (who contracted the virus from the monkeys). In the initial outbreak there was a 60% death rate. There was also secondary transmission: one infected worker (who recovered and was subsequently discharged from hospital) spread the virus to his wife: presumably via semen (this is not a well known fact) 6 _weeks_ after his initial infection. Death was from multipe organ failures as the virus generated a massive haemorrhagic fever (bleeding from all orifices and pores of the skin) and normally occurred within a fortnight of initial infection (days normally). Clinically, Marburg and Ebola present with almost identical patterns of disease (for the hypochondriacs out there, hiccups are one of the first signs of disease: worried yet?). Almost simultaneously, there was a second outbreak in Blegrade, Yugoslavia from monkeys imported from the same source. Sporadic outbreaks have occured in frequently since (IIRC there was [almost] nothing between 1967 and 1976 - when Ebola first hit: Ebola was first thought to be anew outbreak of Marbug, but the two viruses were shown to be different via their surface features).

The scary thing with Marburg in '67 was that this was the first time anything like it had been seen. The level of panic (and fear) in the medical staff who were suddenly confronted with a disease that no one had ever seen before, that was particularly gruesome and especially deadly, with no treatment and no cure (or vaccine) can only be guessed at. Note, there is still no vaccine for Marburg or Ebola: the Russians say they have one and USAMRIID has one that works in guinea pigs, but (not surprisingly) no one is especially eager to volunteer to have it tested in them…. Today, treatment is supportive (treat the symptoms: blood loss and fever mostly, rather than the cause) and still not very effective.

With Marburg and Ebola, no one knows what the true source of the infection is. It cannot be a virus normally found in monkeys, as it kills them too fast. Smart money is on bats (one study has shown that experimentally infected bats can enter a relatively asymptomatic state, but no infected bats have ever been found in the wild: the CDC, USAMRIID and the Special Pathogens Branch of the South African Institute for Virology (in Witwatersrand, South Africa IIRC) have looked for them. A lot!).

Dengue is quite a different beast which is much better understood. Briefly, it is a Flavivirus (Flavi for yellow: Yellow Fever Virus is the classic example of a Flavivirus, so called because of the jaundice associated with Yellow Fever) which are spread by mosquitoes. Whilst there is an excellent vaccine against YF, due to various problems there is not one against dengue. Clinically, dengue is nasty (flu like, with excruciating joint pains - leading to it's alternative name of breakbone fever) but recovery is almost always complete. Problems occur with re-infections by a second (different) strain (there are 4) of dengue virus. Antibodies against the first strain bind, but don't neutralize the virus. This means that the virus can now enter white blood cells macrophages) which have receptors for antibody. These macrophages produce massive amounts of cytokines (immune system hormones) which trigger shock and all sorts of nastiness - this results in two disease patterns called Dengue Shock Syndrome and Dengue Haemorrhagic Fever which are often fatal (see symptoms of haemorrhagic fevers described above - although bleeding out is less common). I have described this a little on the list before, and much of the earlier discussions can be found in the ICE CAVE.

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Date: Wed, 30 Sep 1998 18:18:50 -0400
From: Graeme Price
Jerry Wycoff (Hi Jerry!) wrote:

Yeah, but pretty thin data. Comparisons with Flu A (my own pet virus) are meaningless due to the sheer amount of data available for flu (a virus found in several species), and the sheer lack of data available for Marburg and Ebola. Retroviruses (flu isn't one) theroretically mutate at amazingly high rates, but every time you sequence you are by necessity getting a consensus (quasispecies: mixture of different viral sequences all potentially different at one or two points through the entire genome: I'm an "RNA virologist" and this is a real pain in the arse for guys like me!).

Hep B mutates much more slowly than RNA viruses as it is a DNA virus (no proofreading for RNA polymerases remember) - you cannot reliably compare RNA and DNA viruses in this way.

One thing which may be relevant regarding the apparent genomic stability of Filoviruses (note "apparent": we still don't have enough data) are the findings with avian influenza viruses. Birds are the natural reservoir of influenza virus strains, but the virus seems to be in "evolutionary stasis" within birds (no net changes in sequence over the course of several long term studies: in comparison with major changes in man and pigs where the viruses are continually evolving). The probable reason for this is that influenza virus has acheived a genetic optimum (adaptation) in birds, and that any sequence changes will not provide an advantage (note that because of the quasispecies phenomenon, changes can still occur, but they will not be selected for either within a population or an individual as they provide no advantage - hence no _net_ change). Such a thing is possible with Filoviruses, and provides a better explanation than the much posited "high fidelity RNA polymerase", but to be sure we would have to find the host (not easy) and sequence lots of isolates in that host (not easy) rather than go on studies in man and monkeys.

Anyway, I've probably overlooked something (not having been party to the initial discussion) so don't flame me for trying to help! Also sorry about the technical terms… I hate it when I get carried away with long words!

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Date: Tue, 29 Sep 1998 19:48:21 -0500
From: William Timmins

How exactly do prions spread in a body? That is, how do they manage to 'infect' a cell and tell it to make more prions?

From Roberto L Vargas' message, it was mentioned that prions are a variant form of a natural protein coded by chromosome 20 (in CJD). Does the prion interfere with or modify DNA replication or something?

Curious minds want to know (and not get all spongiform)

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From: "G. Wyckoff"
Date: Wed, 30 Sep 1998 17:49:59 -0500 (CDT)

Yeah, but pretty thin data. Comparisons with Flu A (my own pet virus) are
meaningless due to the sheer amount of data available for flu (a virus
found in several species), and the sheer lack of data available for Marburg
and Ebola. Retroviruses (flu isn't one) theroretically mutate at amazingly
high rates, but every time you sequence you are by necessity getting a
consensus (quasispecies: mixture of different viral sequences all
potentially different at one or two points through the entire genome: I'm
an "RNA virologist" and this is a real pain in the arse for guys like me!).
Hep B mutates much more slowly than RNA viruses as it is a DNA virus (no
proofreading for RNA polymerases remember) - you cannot reliably compare
RNA and DNA viruses in this way.

<nice discussion of evolutionary stability in hosts snipped>

Actually, what intrigued me about this was the attempt in the paper to date the initial divergence of the viruses. But, as you explained rather thoroughly, there are lots of problems with the study.

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Date: Tue, 29 Sep 1998 15:37:39 -0500
From: Mark Carroll
FYI, and a heads-up, check out this article:

http://www.cnn.com/TECH/science/9809/28/madcow.test.ap/

Not only does it give a few details, but there's links to other info sources as applies to CJD.

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Date: Wed, 30 Sep 1998 20:36:35 -0300
From: "Roberto L. Vargas"

<loads of viral goodness snipped>

Absolutely great work Graeme!

On a note about Dengue, I'm REALLY familiar with this one, since we are right in the middle of a huge epidemic (although it seems to be in a lull after the hurricane, but mosquitoes should be back on their feet in no time at all) and I know what the books say about the Dengue Fever, but believe me it is far more tricky than advertised. People with just malaise symptoms, suddenly start bleeding through their teeth (literally as their gums start bleeding) and I've seen at least six people die from it, mostly children for some reason. It seems that the three recognized clinical presentations are simply a progression from the simple viremia (Breakbone) which sometimes (like you said, related to different types of the virus and mercifully in small percentages) progresses into the hemorrhagic which sometimes cannot be controlled and the patient goes into shock.

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