pretty much inevitable IMO. The guy who DID get to Dallas did so as a result of a MAJOR fuckup in quarantine procedures back in West Africa and a complete breakdown by the much-vaunted TSA and the Department of Homeland Security >>SNICKER, SNICKER<<. However, unlike everybody screaming thhat we should head for the hills, I'm actually GLAD we got it NOW in the way we did. Right now, the virus seems to be breaking out into the human population and being more and more able to go directly from human to human - just based on numbers. As much as I've tried - and believe me, I've been shaking every branch I know of, and if I DO get something I WILL post it here! However, as hard as I can, I can't get ahold of the raw data regarding the R0 rate and whether it's increasing or is stable - which REALLY scares me because I have a sneaking feeling based SOLELY on the numbers available from the most recent WHO survey that the R0 IS increasing. This number, R0, refers to the transmissibility of the virus, in other words, how many people get sick from any one person being sick. With diseases like smallpox and polio - yes, I know, everybody flamed me for pointing out that Ebola is more deadly than smallpox on a per capita basis (which is true but let's not start that up again - let's be serious for a second here and discuss this epidemic. You all can go back to flaming me later to your heart's content). However, smallpox and polio have R0 of around 5-7. The MOST transmissible pathogens we know of are whooping cough - pertussis - and the measles - well, noroviruses too but they're a special case in that they can infect EVERY mammalian species and therefore are almost benign in their effects - have an R0 of around 12-15. This means that for every person who gets polio, they will, on average, give it to 12-15 people. For all the damage that the Black Death caused, Y.Pestis has an R0 of only about 2.5-3 and it killed half the population of Europe in the 1380s. However, the current Ebola epidemic has an R0 value of around 1.4 - or, rather, that's the last hard number I have for this current outbreak (Ebola is an emerging virus and generally requires a host - which carries the virus but does not get sick from it - to pass on to humans. However, from time to time, Ebola, which mutates VERY quickly, HAS managed to jump from animal to animal (for example, the current strain, Ebola Zaire, can be observed jumping from bats to pigs without the two species ever coming into contact with one another) and achieve an R0 of up to 4*.
I know, I know, and before I get labelled as some kind of nihilistic sociopathic conservative monster who wants to see the black people of Africa all killed off to create a white Eden or some other such nonsense, allow me to expand on that "I'm actually GLAD we got it NOW in the way we did" remark before others on this board do it for me. The reason I'm glad we got it now is because we seem to have gotten ONE patient who had very little contact with the outside world before he presented at the hospital - ideally we'd have somebody who came here, had NO contact with anybody, covered himself with the proper precautions and barriers before calling 911, and insisting that the paramedics and doctors glove up and suit up with BL3+ protection barriers before responding to his/her 911 call, however, the perfect is the enemy of the good and the chances of the above ideal Ebola patient just showing up stateside are practically zero. So, given what DID happen, it could've been much, much, worse. Like I've said before and try to say in this post, given the nature of Ebola, IF it truly DOES make the jump from the jungle to a human-to-human transmissibility route, then it will have to become MUCH less lethal and will have to turn itself into basically a bad cold or a flu. However, if it continues to use whatever host it's using to pass itself along - see below - then it will be under no such evolutionary pressure. In fact, IF it DOES manage to jump into infecting the general human population by using another species as a host vector, THEN, the evolutionary pressure will be precisely the opposite. When the virus was confined to villages in the Congo of a couple-hundred people, when it broke out, the surrounding villages closed off and quarantined the infected village, allowed it to die off, and then - after burning the infected village to the ground - repopulated it with a new population. What was going on in previous outbreaks was that the virus was accidentally released into a very limited human population. Ebola isn't designed to live in humans so when it DOES get accidentally released into a closed population in some up-country village, it kills everybody - or almost everybody - and then retreats to whatever ecological niche it once inhabited. There were only a limited number of humans to kill and it was obvious when a person WAS sick, so there was a very limited chance of having this bug move into the general population. However, this current epidemic HAS released the virus into a MUCH larger population. As a result, the virus has NO need to keep those it's infecting alive so that it can spread - and, in fact, the more deadly the strain, the more packed the patient's blood will be with virus, meaning the greater the chance that the virus will be passed along. Therefore the evolutionary pressure, over time, will be for the virus to become even MORE deadly and even MORE transmissible. THIS is what I meant by saying that I'm glad it happened here the way it did. A couple of doctors and a nurse who willingly put themselves into harm's way get sick it's NOT going to cause a general alarm in the population. However, when the population discovers that somebody can just waltz onto a plane with this bug, get sick, and show up at the neighborhood hospital with Ebola-Zaire, that WILL wake the population up, and HOPEFULLY they'll DEMAND the proper precautions be taken so the rest of us don't get sick. However, as I mentioned above, over time the evolutionary pressure on this virus is to become even deadlier and more transmissible. So, if instead of the virus coming here NOW, it didn't come here 'till, say, February, by that time the R0 for the epidemic might be as high as 5 or even 7 and might be 90-95% fatal - and the symptoms associated with this virus are absolutely horrible! I really hope this shakes up the people who need to be shaken up so we can begin putting measures into place NOW rather than later when it'll be too late! THAT'S what I was talking about!
Does that make sense?
***************************************************************************************************************************************************************************************
*Most think that the natural carrier for Ebola is fruit bats, but that makes NO sense - mainly because the bats die when infected with Ebola - just not at the same rate that humans do. Also, Ebola is one of the oldest and simplest viruses in the world - it's so basic that it doesn't even package itself in distinct units. Generally, RNA viruses are among the oldest in the world and are remnants of the "RNA world" of the early Hadean Period when life as we know it consisted of a bunch of RNA strands that carried out metabolic functions and reproduced themselves and were packaged in a soap bubble, protein shell, or tidal pool. This was before protein or DNA came along. Viruses and cells diverged around the time that amino-acids became incorporated into life - first as a way to purify the closed area containing the RNA, and then later to perform cellular functions - and viral proteins are some of the oldest proteins on earth next to metabolic proteins. This was about 3 billion years ago, and given the divergence of Ebola and the next living genetic viral relatives (a line of ancient bacteriophages that behave nothing like Ebola or filoviruses in general) we find that this virus is very, very old and is likely a "living fossil" virus).
Being so old, this virus should either have as it's host some organism that is ALSO extremely old OR it should have mutated and adapted to infect just about every lifeform on the planet. In the case of Ebola, in what is yet another head-scratcher, it's done neither. The oldest cellular, and therefore infective, lifeforms are bacteria while the youngest are mammals - and in particular simians and hominids. Filoviruses - the genus that Ebola belongs to - have been found to infect just humans/simians and a handful of other mammals either domesticated BY humans or that live in close proximity TO humans, and even then there's a VAST difference in transmissibility and mortality between various Filoviruses - from an R0 of between 0.5-4.5 and can kill between 0 and 100% of animals infected. These things can present with all the hallmarks of an airborne virus - like you, I really don't think Ebola can actually BE an airborne virus in the sense that Measles can, BUT I think it can APPEAR to be an airborne virus - and can kill ALL the animals of some genus or species it comes in contact with (Ebola Reston infecting monkeys) to being completely refractory to other genuses of animals that it contacts, like humans in the case of Ebola Reston or monkeys in the case of Ebola Gabon - maybe not Gabon, but one of those sub-strains of Ebola is the opposite of Reston in that it kills humans but is completely refractory to monkeys. My guess - and again, this is just an educated guess at this point, but it DOES support Pete's data (he's a good friend of mine who works BL4 at USAMRIID and specializes on Ebola and Lassa viruses) is that the natural host of Filoviruses are dust mites. While some mites are territorial and tend to live on just one type of animal, others are gregarious and just live on a warm body and they could care less what body. Moreover, they're microscopic, meaning that even though what appears to be an airborne disease is really just a bunch of mites seeking another host because their current one is dying. Moreover, it would explain why the virus has to concentrate itself to such a high-titer in the host and kill the infected patient - mites don't eat much, just a few flakes of skin. So, the virus really needs to pack itself into each potential cell the mites could eat so that it would get passed to another patient. Since Ebola just isn't a respiratory bug - it doesn't do much with the lungs but rather eats up the blood and capillaries - it would be odd for it to gain the proper mutations necessary to become an honest-to-God airborne virus. However, it could very easily manage to obtain a handful of mutations necessary to pass itself on to one of the more gregarious dust-mite species, AND be able to remain viable for longer within these mites. This would make the virus more transmissible - which is precisely what we're seeing currently.
Once it enters the body, it produces a positive strand of RNA which attaches to, and permanently hijacks the cell's ribosomes and pumps out massive quantities of the five viral proteins that the Ebola genome codes for. While those proteins are being produced, one of them, the polymerase makes negative strand copies of the positive strands of RNA floating about in the cell - once ALL the cell's ribosomes have been hijacked there's nothing for the positive strands of RNA to do so they just hang out and act as templates for Ebola virus polymerase to run negative copies of itself off. It produces a negative strands of RNA which the viral coat proteins - which are produced from the RNA on the ribosomes - then surround as the polymerase runs off the RNA. The coat proteins look like half-pipes - the kind you see the skate-rats using at the local skate park. They're also palindromic - meaning that one side is the inverse of the other and the top is the inverse of the bottom (in this case, the top part is greasy and the bottom part is charged on one side of the half-pipe while the opposite holds true of the other side of the half-pipe. This means that they fit together perfectly when one half covers one side of the RNA strand and the other flips around and covers the other side of the RNA strand so that greasy meets greasy and opposite charges meet as well. This same configuration holds true of the top and bottom of the coat proteins so they can snap together like curved Lego blocks. Now the RNA is protected from the outside. One of the things that makes this virus so simplistic is that the polymerase doesn't just run off ONE copy of the genome, stop, and then go back to the beginning and start all over. It'll just keep on running off strand after strand after strand by simply turning around and continue adding nucleotide bases 'till they run out of bases to add or fall off because the strand breaks or whatever. Finally, there's a sugar-coated receptor protein that's attached to the front of the string and acts to bind to a receptor and gain entry into the next cell and a combination protease and polymerase protein bound to the back-end of the protein. This makes a mature virus that's ready to infect other cells. This is why this virus looks like long strings of different lengths. When the virus is mature, it buds out of the dying cell - taking a bit of the cell's membrane with it to coat the virus and prevent it from being seen by the body's immune system - and goes on to find a new cell to invade. Also, there's one other protein that's coded for in the Ebola virus genome, some kind of excreted protein that somehow down-regulates or turns down the immune response (and, Ebola being extremely simple, this protein is actually coded for from the same piece of RNA that makes one of the coat proteins. Ebola uses the cell's own DNA repair enzymes in some as yet not very well understood way to break the positive strand in half, insert an adenine base - an "A" in the genetic code - and once this happens, the gene goes from coding for a coat protein to some kind of immune modulation protein. Since the modulation protein is NOT a normal cellular protein and is, in fact, toxic TO the cell, but at the same time appears to be a signaling protein that's ubiquitous in ALL multicellular life, the cell simply pushes it out and into the blood stream where it somehow turns down the immune response. It's THAT protein that turns what would otherwise be a virus barely capable of causing a fever and chills into SUCH a dangerous and deadly pathogen. The more virus, the weaker the immune response, meaning the virus becomes capable of attacking more and more cells and producing more virus until the virus simply overwhelms the body and the patient dies.
On Tuesday, September 30, 2014 8:15:23 PM UTC-6, Herman Adler wrote:
-- I know, I know, and before I get labelled as some kind of nihilistic sociopathic conservative monster who wants to see the black people of Africa all killed off to create a white Eden or some other such nonsense, allow me to expand on that "I'm actually GLAD we got it NOW in the way we did" remark before others on this board do it for me. The reason I'm glad we got it now is because we seem to have gotten ONE patient who had very little contact with the outside world before he presented at the hospital - ideally we'd have somebody who came here, had NO contact with anybody, covered himself with the proper precautions and barriers before calling 911, and insisting that the paramedics and doctors glove up and suit up with BL3+ protection barriers before responding to his/her 911 call, however, the perfect is the enemy of the good and the chances of the above ideal Ebola patient just showing up stateside are practically zero. So, given what DID happen, it could've been much, much, worse. Like I've said before and try to say in this post, given the nature of Ebola, IF it truly DOES make the jump from the jungle to a human-to-human transmissibility route, then it will have to become MUCH less lethal and will have to turn itself into basically a bad cold or a flu. However, if it continues to use whatever host it's using to pass itself along - see below - then it will be under no such evolutionary pressure. In fact, IF it DOES manage to jump into infecting the general human population by using another species as a host vector, THEN, the evolutionary pressure will be precisely the opposite. When the virus was confined to villages in the Congo of a couple-hundred people, when it broke out, the surrounding villages closed off and quarantined the infected village, allowed it to die off, and then - after burning the infected village to the ground - repopulated it with a new population. What was going on in previous outbreaks was that the virus was accidentally released into a very limited human population. Ebola isn't designed to live in humans so when it DOES get accidentally released into a closed population in some up-country village, it kills everybody - or almost everybody - and then retreats to whatever ecological niche it once inhabited. There were only a limited number of humans to kill and it was obvious when a person WAS sick, so there was a very limited chance of having this bug move into the general population. However, this current epidemic HAS released the virus into a MUCH larger population. As a result, the virus has NO need to keep those it's infecting alive so that it can spread - and, in fact, the more deadly the strain, the more packed the patient's blood will be with virus, meaning the greater the chance that the virus will be passed along. Therefore the evolutionary pressure, over time, will be for the virus to become even MORE deadly and even MORE transmissible. THIS is what I meant by saying that I'm glad it happened here the way it did. A couple of doctors and a nurse who willingly put themselves into harm's way get sick it's NOT going to cause a general alarm in the population. However, when the population discovers that somebody can just waltz onto a plane with this bug, get sick, and show up at the neighborhood hospital with Ebola-Zaire, that WILL wake the population up, and HOPEFULLY they'll DEMAND the proper precautions be taken so the rest of us don't get sick. However, as I mentioned above, over time the evolutionary pressure on this virus is to become even deadlier and more transmissible. So, if instead of the virus coming here NOW, it didn't come here 'till, say, February, by that time the R0 for the epidemic might be as high as 5 or even 7 and might be 90-95% fatal - and the symptoms associated with this virus are absolutely horrible! I really hope this shakes up the people who need to be shaken up so we can begin putting measures into place NOW rather than later when it'll be too late! THAT'S what I was talking about!
Does that make sense?
***************************************************************************************************************************************************************************************
*Most think that the natural carrier for Ebola is fruit bats, but that makes NO sense - mainly because the bats die when infected with Ebola - just not at the same rate that humans do. Also, Ebola is one of the oldest and simplest viruses in the world - it's so basic that it doesn't even package itself in distinct units. Generally, RNA viruses are among the oldest in the world and are remnants of the "RNA world" of the early Hadean Period when life as we know it consisted of a bunch of RNA strands that carried out metabolic functions and reproduced themselves and were packaged in a soap bubble, protein shell, or tidal pool. This was before protein or DNA came along. Viruses and cells diverged around the time that amino-acids became incorporated into life - first as a way to purify the closed area containing the RNA, and then later to perform cellular functions - and viral proteins are some of the oldest proteins on earth next to metabolic proteins. This was about 3 billion years ago, and given the divergence of Ebola and the next living genetic viral relatives (a line of ancient bacteriophages that behave nothing like Ebola or filoviruses in general) we find that this virus is very, very old and is likely a "living fossil" virus).
Being so old, this virus should either have as it's host some organism that is ALSO extremely old OR it should have mutated and adapted to infect just about every lifeform on the planet. In the case of Ebola, in what is yet another head-scratcher, it's done neither. The oldest cellular, and therefore infective, lifeforms are bacteria while the youngest are mammals - and in particular simians and hominids. Filoviruses - the genus that Ebola belongs to - have been found to infect just humans/simians and a handful of other mammals either domesticated BY humans or that live in close proximity TO humans, and even then there's a VAST difference in transmissibility and mortality between various Filoviruses - from an R0 of between 0.5-4.5 and can kill between 0 and 100% of animals infected. These things can present with all the hallmarks of an airborne virus - like you, I really don't think Ebola can actually BE an airborne virus in the sense that Measles can, BUT I think it can APPEAR to be an airborne virus - and can kill ALL the animals of some genus or species it comes in contact with (Ebola Reston infecting monkeys) to being completely refractory to other genuses of animals that it contacts, like humans in the case of Ebola Reston or monkeys in the case of Ebola Gabon - maybe not Gabon, but one of those sub-strains of Ebola is the opposite of Reston in that it kills humans but is completely refractory to monkeys. My guess - and again, this is just an educated guess at this point, but it DOES support Pete's data (he's a good friend of mine who works BL4 at USAMRIID and specializes on Ebola and Lassa viruses) is that the natural host of Filoviruses are dust mites. While some mites are territorial and tend to live on just one type of animal, others are gregarious and just live on a warm body and they could care less what body. Moreover, they're microscopic, meaning that even though what appears to be an airborne disease is really just a bunch of mites seeking another host because their current one is dying. Moreover, it would explain why the virus has to concentrate itself to such a high-titer in the host and kill the infected patient - mites don't eat much, just a few flakes of skin. So, the virus really needs to pack itself into each potential cell the mites could eat so that it would get passed to another patient. Since Ebola just isn't a respiratory bug - it doesn't do much with the lungs but rather eats up the blood and capillaries - it would be odd for it to gain the proper mutations necessary to become an honest-to-God airborne virus. However, it could very easily manage to obtain a handful of mutations necessary to pass itself on to one of the more gregarious dust-mite species, AND be able to remain viable for longer within these mites. This would make the virus more transmissible - which is precisely what we're seeing currently.
Once it enters the body, it produces a positive strand of RNA which attaches to, and permanently hijacks the cell's ribosomes and pumps out massive quantities of the five viral proteins that the Ebola genome codes for. While those proteins are being produced, one of them, the polymerase makes negative strand copies of the positive strands of RNA floating about in the cell - once ALL the cell's ribosomes have been hijacked there's nothing for the positive strands of RNA to do so they just hang out and act as templates for Ebola virus polymerase to run negative copies of itself off. It produces a negative strands of RNA which the viral coat proteins - which are produced from the RNA on the ribosomes - then surround as the polymerase runs off the RNA. The coat proteins look like half-pipes - the kind you see the skate-rats using at the local skate park. They're also palindromic - meaning that one side is the inverse of the other and the top is the inverse of the bottom (in this case, the top part is greasy and the bottom part is charged on one side of the half-pipe while the opposite holds true of the other side of the half-pipe. This means that they fit together perfectly when one half covers one side of the RNA strand and the other flips around and covers the other side of the RNA strand so that greasy meets greasy and opposite charges meet as well. This same configuration holds true of the top and bottom of the coat proteins so they can snap together like curved Lego blocks. Now the RNA is protected from the outside. One of the things that makes this virus so simplistic is that the polymerase doesn't just run off ONE copy of the genome, stop, and then go back to the beginning and start all over. It'll just keep on running off strand after strand after strand by simply turning around and continue adding nucleotide bases 'till they run out of bases to add or fall off because the strand breaks or whatever. Finally, there's a sugar-coated receptor protein that's attached to the front of the string and acts to bind to a receptor and gain entry into the next cell and a combination protease and polymerase protein bound to the back-end of the protein. This makes a mature virus that's ready to infect other cells. This is why this virus looks like long strings of different lengths. When the virus is mature, it buds out of the dying cell - taking a bit of the cell's membrane with it to coat the virus and prevent it from being seen by the body's immune system - and goes on to find a new cell to invade. Also, there's one other protein that's coded for in the Ebola virus genome, some kind of excreted protein that somehow down-regulates or turns down the immune response (and, Ebola being extremely simple, this protein is actually coded for from the same piece of RNA that makes one of the coat proteins. Ebola uses the cell's own DNA repair enzymes in some as yet not very well understood way to break the positive strand in half, insert an adenine base - an "A" in the genetic code - and once this happens, the gene goes from coding for a coat protein to some kind of immune modulation protein. Since the modulation protein is NOT a normal cellular protein and is, in fact, toxic TO the cell, but at the same time appears to be a signaling protein that's ubiquitous in ALL multicellular life, the cell simply pushes it out and into the blood stream where it somehow turns down the immune response. It's THAT protein that turns what would otherwise be a virus barely capable of causing a fever and chills into SUCH a dangerous and deadly pathogen. The more virus, the weaker the immune response, meaning the virus becomes capable of attacking more and more cells and producing more virus until the virus simply overwhelms the body and the patient dies.
On Tuesday, September 30, 2014 8:15:23 PM UTC-6, Herman Adler wrote:
What do you think about Dallas, xtal?
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