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#1 of 31 Old 10-25-2006, 01:50 PM - Thread Starter
 
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DH had to get the Flu Mist vax about a week ago (mandatory military vax--although he said he "accidentally missed his nose" with most of it). Now I think I am getting the flu. Does the Flu Mist vax shed?
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#2 of 31 Old 10-25-2006, 01:55 PM
 
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Oh, yeah. And it sheds not one, but three flu viruses.
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#3 of 31 Old 10-25-2006, 02:05 PM - Thread Starter
 
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Oh joy. Feeling cold, achy, exhausted, and dizzy are flu symptoms, right?
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#4 of 31 Old 10-25-2006, 02:06 PM
 
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Originally Posted by caedmyn View Post
Oh joy. Feeling cold, achy, exhausted, and dizzy are flu symptoms, right?

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#5 of 31 Old 10-25-2006, 05:42 PM
 
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Yep.

hope you feel better soon!

-Angela
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#6 of 31 Old 10-25-2006, 05:47 PM
 
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ugh, that sucks. My dh is military too but he came home and told me he had the option of getting the shot or the nasal spray one. He thought it sounded cool not to have to get a shot until I told him all about it. He chose the shot...well, ok, I chose the shot for him because I told him otherwise if he came home and got us all sick because of flumist then he was going to take care of us too and stay up all night with a sick toddler and I wasn't going to lift a finger...he decided the shot didn't sound so bad after all

Rachel, mom to Jake (5/04) and Alexia (7/07) a surprise UC thanks to hypnobabies!
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#7 of 31 Old 10-25-2006, 06:32 PM
 
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...because I told him otherwise if he came home and got us all sick because of flumist then he was going to take care of us too and stay up all night with a sick toddler and I wasn't going to lift a finger...he decided the shot didn't sound so bad after all
...and that, my dear, is probably one of the best vaccines against flu for men out there... (The threat of screaming toddler all night would definitely keep my dh from getting the flu... not to mention giving the flu. )
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#8 of 31 Old 10-25-2006, 06:44 PM
 
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: I have the flu too..no fun...:
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#9 of 31 Old 10-25-2006, 06:44 PM
 
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My DH is military too and I am so glad he remembered me telling him about the flu mist and it shedding! They told him he needed it but since we have our baby and he is our preemie, he let them know and they said they'll look into the shot or he won't need to get it this year.
Whew, I'm so glad they are more relaxed here on the island.
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#10 of 31 Old 10-25-2006, 10:27 PM
 
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#11 of 31 Old 10-26-2006, 12:14 AM - Thread Starter
 
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I would have thought the Flu Mist was the better choice of flu vaccines since it seems to more closely mimic a "natural" exposure to the flu. Maybe not if it sheds, though. I wonder which version DH has got in the past--I didn't get the flu last year but I'm not sure if he had the shot or the mist.
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#12 of 31 Old 10-26-2006, 12:27 AM
 
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Originally Posted by caedmyn View Post
I would have thought the Flu Mist was the better choice of flu vaccines since it seems to more closely mimic a "natural" exposure to the flu. Maybe not if it sheds, though. I wonder which version DH has got in the past--I didn't get the flu last year but I'm not sure if he had the shot or the mist.
It would be, if it didn't shed three living flu viruses. The way the flu mutates is that it reassorts and swaps genetic info with other flu viruses.
A live flu vaccine with three viruses in it is a really, really stupid idea.
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#13 of 31 Old 10-26-2006, 12:58 AM
 
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Oh joy. Feeling cold, achy, exhausted, and dizzy are flu symptoms, right?
Nonsense. Those are "side effects" of the vaccine. Not the flu. :

Sorry you feel gross. Even sorrier your hubby has to put up with that.

: : :
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#14 of 31 Old 10-26-2006, 10:12 AM
 
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The terms "attenuated" and "cold adapted" really need to appear somewhere in this discussion.

The strains that are shed by a person who has recieved the live vaccine are the same ones that were in the vax. They have been tweaked to make them unable to replicate efficiently enough to produce serious infection (attenuated), and to make them poorly tolerant of the higher temperatures found in the lower respiratory tract (cold adapted). Reassortment between the strains in the vaccine would not solve these problems for the virus. A mild form of the illness is not a side-effect of the vaccine, it is precisely the desired result. The idea is to give the immune system an opportunity to develop antibodies against viral antigens without the risk of serious complications from full-blown infection.

The concept shouldn't be that much of a stretch for anyone willing to consider deliberately exposing their child to, say, chicken pox -- the main difference being that in the latter case, nothing insures that a given child will not be among the small number who will develop serious complications (such as pneumonia, or encephalitis, or eye lesions leading to permanent blindness).
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#15 of 31 Old 10-26-2006, 10:39 AM
 
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Nonsense. Those are "side effects" of the vaccine. Not the flu. :

Sorry you feel gross. Even sorrier your hubby has to put up with that.

: : :
How could SHE have an adverse reaction to a vaccine her husband took unless she caught the virus from it. That doesn't make sense.
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#16 of 31 Old 10-26-2006, 01:29 PM
 
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Reassortment between the strains in the vaccine would not solve these problems for the virus.
What? Where in the world are you getting that from?
How do you think OPV loses it's attenuation? And polio is stable compared to influenza. And doesn't even reassort at all.

ETA:
And I was under the impression they weren't even sure where all the attenuating nucleotides were located on all three strains.
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#17 of 31 Old 10-26-2006, 02:09 PM
 
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What? Where in the world are you getting that from?
How do you think OPV loses it's attenuation? And polio is stable compared to influenza. And doesn't even reassort at all.
Again... thank you for saying what I was thinking so concisely!!!

Methinks you deserve an award for the continual ability to say what I (and I'm sure others) are thinking but can't articulate as eloquently or succintly!
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#18 of 31 Old 10-26-2006, 02:20 PM
 
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From the FDA website:

What are the most common side affects of FluMist?

Nasal congestion
Runny nose
Sore throat
Headache
Irritability
Decreased activity
Muscle ache and
Cough
are the most common adverse events associated with the vaccine.
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#19 of 31 Old 10-26-2006, 02:37 PM
 
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I was making a joke...the known side effects , as LI just posted are so strikingly similar to the flu it's absurd.

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Originally Posted by dymaniac
They have been tweaked to make them unable to replicate efficiently enough to produce serious infection (attenuated), and to make them poorly tolerant of the higher temperatures found in the lower respiratory tract (cold adapted).
Source ? from a peer reviewed journal please , not an acronym agency.
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#20 of 31 Old 10-26-2006, 02:45 PM
 
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I was making a joke...the known side effects , as LI just posted are so strikingly similar to the flu it's absurd.
Doy sorry I need some coffee before I read...:
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#21 of 31 Old 10-26-2006, 02:46 PM
 
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Reassortment between the strains in the vaccine would not solve these problems for the virus.
I believe this bit of naivety is best addressed by Orgel's second law:
Evolution is smarter than you.
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#22 of 31 Old 10-26-2006, 02:53 PM
 
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It's really ironic that the same people who argue that birdflu is impending, while acknowledging that it would require a series of unlikely mutuations and coincidences, for a virus that infects relatively few humans to begin with, are the same people who scoff at the idea of the living, replicating, reassorting amongst themselves viruses in FluMist being able to take off on their own in any of the millions and millions of people who recieve the vaccine.
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#23 of 31 Old 10-27-2006, 01:50 PM
 
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It's really ironic that the same people who argue that birdflu is impending, while acknowledging that it would require a series of unlikely mutuations and coincidences, for a virus that infects relatively few humans to begin with, are the same people who scoff at the idea of the living, replicating, reassorting amongst themselves viruses in FluMist being able to take off on their own in any of the millions and millions of people who recieve the vaccine.
There's a difference, and it's an important one.

The influenza viral genome comes packaged in eight segments. Six of these code for a protein each, and two for two each. The segments are replicated independently, then assembled into a complete virus just prior to budding from the cell wall. Where a single host cell is infected with multiple strains of virus, the segments can get mixed up during the assembly. Happens all the time. Most of the time, the resulting virus is not viable -- but once in a while it not only produces viable virus, but one with new characteristics due to the mixing.

In the vaccine, all of the "internal" gene segments have been deliberately modified by sustained forced selection to make them poor replicators, particularly at higher temperatures. These "master donor" strains are then reassorted with wild type virus to aquire the genes for the two surface glycoproteins (hemagluttinin and neuraminidase), and it to is these that antibody response develops. There are jillions of sources on this.
Here's one.

It is true that the precise nucleotide sequences involved are not clearly known -- which matters not one whit where we're talking about reassortment, because this involves the exchange of whole segments.

Let's say you and a dozen or so of your cousins each have an old Dodge Dart collecting dust out in the barn or rotting away in a field somewhere, and one day you all get together and decide to swap parts around to see if you can get one of them running. Maybe one of them has a good starter, and one has a tranny that'll probably work in a couple of gears, and by taking a fender here and a hood there, you might come up with something that looked okay on the outside -- but if every single one of those cars has a cracked head, a ruined carb, and a frozen water pump, then you can swap parts around till the cows come home, and you still ain't going very far in any one of 'em. Knowing the exact nature and location of each flaw isn't going to change things; broke is broke.

Evolution could find a way to fix the virus by random mutation (small-scale changes in nucleotide sequences: insertions, deletions etc), but to accomplish this, it would require a chain of continuous transmission long enough to permit the damage (done to it by the vaccine developers) to be undone in the same manner that it was inflicted: in a series of small steps. It isn't going to happen by reassortment between the strains in the vaccine. No way. The challenge that the virus would face in reverting through a series of small steps is this: the attenuation is spread out over multiple genes. If any one of them doesn't work, the completed package doesn't work, and if the completed package doesn't work, the virus doesn't get replicated and transmitted efficiently, and if the virus doesn't get replicated and transmitted efficiently, it loses the opportunity to evolve further, because it ceases to exist as a viable, competitive, pathogenic entity. With this in mind, it is unsurprising that the appearance of escape mutants has never been observed.

The situation as far as avian influenza is concerned is very much different. We don't know how unlikely it is for H5N1 to evolve efficient human-to-human transmissibility, though we can be fairly confident that it isn't going to happen in a single step. But the H5N1 virus has a couple of things going for it that the attenuated strains in the live seasonal vaccine don't. One is that its potential reassortment partners include a large number of highly efficient strains which are happily infecting enormous numbers of birds even as we speak, and some other animals as well, including a few humans. Another is that it has already demonstrated the ability to replicate efficiently in human cells (across a broad range of different types of human cells, in fact), and to produce continuous chains of transmission between humans. Every one of those "clusters" represents an increased level of opportunity for evolution to "find a way"; one which is not available to the strains in the attenuated vaccine.

Whew! I was shooting for an early-morning quickie here, but these things have a way of taking on a life of their own. Responding to the other thread may have to wait.
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#24 of 31 Old 10-27-2006, 02:29 PM
 
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Let's say you and a dozen or so of your cousins each have an old Dodge Dart collecting dust out in the barn or rotting away in a field somewhere, and one day you all get together and decide to swap parts around to see if you can get one of them running. Maybe one of them has a good starter, and one has a tranny that'll probably work in a couple of gears, and by taking a fender here and a hood there, you might come up with something that looked okay on the outside -- but if every single one of those cars has a cracked head, a ruined carb, and a frozen water pump, then you can swap parts around till the cows come home, and you still ain't going very far in any one of 'em. Knowing the exact nature and location of each flaw isn't going to change things; broke is broke.
But Dymanic, MoPar parts don't spontaneously evolve and replicate themselves, with the selective advantage in favor of the ones that "work".
(although the "leave it alone and see if the problem resolves itself" method does seem to be freakishly effective with my Duster. )

It's the reassortments plus the random mutations that make the idea of three "living", replicating, reassorting, randomly mutating viruses in one person, or especially lots of people around each other at the same time, a bad idea.

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With this in mind, it is unsurprising that the appearance of escape mutants has never been observed.
It's never been observed because no one's looking! It says so on the package insert! Do you want me to find it for you?
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#25 of 31 Old 10-27-2006, 02:42 PM
 
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Me and my unscientific brain were under the impression that attenuated and even killed were only so to a percentage, such that it's still completely possible that the viruses replicate and mutate - just that the likelyhood is figured to a "satisfactory" risk by deciding what percentage the attenuation or killed organisms will be??
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#26 of 31 Old 10-27-2006, 10:58 PM
 
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But Dymanic, MoPar parts don't spontaneously evolve and replicate themselves, with the selective advantage in favor of the ones that "work".
You wouldn't believe how many times I've argued the point myself.

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although the "leave it alone and see if the problem resolves itself" method does seem to be freakishly effective with my Duster.
"Turn up the radio" sometimes works too. For a while.

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It's the reassortments plus the random mutations that make the idea of three "living", replicating, reassorting, randomly mutating viruses in one person, or especially lots of people around each other at the same time, a bad idea.
Forget about reassortment. If none of the strains revert through random mutation, reassortment between them accomplishes squat, for the same reason swapping one broken car part for another accomplishes squat. If dual infection with a wild strain occurred in a vaccinated individual, reassortment might produce a strain more viable than the attenuated strain, but probably not by enough to enable it to get any traction, and it certainly isn't going to produce one more pathogenic than the wild strain. (And it wouldn't matter anyway, because that individual would already have the flu). It also isn't going to result in a novel strain, because the master donor strains are all derived from strains already in circulation.

The question then is entirely one of whether the virus can revert by random mutation alone. Let's look at that. The cold adaptation (again) doesn't reside in a single gene, and it isn't achieved in one big leap -- for the same reason that the vertebrate eye and the primate brain didn't evolve in one big leap. One of the fundamental principles of modern evolutionary theory is that complex function never evolves in one big leap. Goldschmidt's "hopeful monsters" was the second biggest flop in the history of the modern synthesis (the biggest being Lamarck's "inheritance of aquired characteristics").

Successive generations of virus are subjected to gradually colder temperatures, the survivors among the progeny of each round of replication becoming the parents for the next round. If you simply took the entire population of virus and subjected it to the lowest temperature, they would all die. The vaccine developers don't have to concern themselves with what precise nucleotide changes are required to permit the virus (some) to survive the selective pressure they are subjecting it to; random mutation takes care of that (or doesn't, and the whole population does die, and they have to start over).

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It's never been observed because no one's looking!
Once you grasp the fact that the strains can't revert by reassortment (because it wouldn't do any good), nor by a series of random mutations (because there isn't a continuous chain of transmission to support it), there doesn't seem to be much point.
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#27 of 31 Old 10-28-2006, 12:22 AM
 
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Forget about reassortment. If none of the strains revert through random mutation, reassortment between them accomplishes squat, for the same reason swapping one broken car part for another accomplishes squat.
But we're talking about millions of virons both randomly mutating and reassorting.

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If dual infection with a wild strain occurred in a vaccinated individual, reassortment might produce a strain more viable than the attenuated strain, but probably not by enough to enable it to get any traction, and it certainly isn't going to produce one more pathogenic than the wild strain. (And it wouldn't matter anyway, because that individual would already have the flu). It also isn't going to result in a novel strain, because the master donor strains are all derived from strains already in circulation.
It could easily be novel for whomever caught it. If we're all simply immune to all the strains presently in circulation, then why do we catch the flu?
The nuts and bolts of antigenic drift and immunity to influenza is hardly an exact science at this point. And how pathogenic it is compared to the wild strain has just as much, if not more, to do with the host factors than it does to the virus in and of itself.

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The cold adaptation (again) doesn't reside in a single gene, and it isn't achieved in one big leap -- for the same reason that the vertebrate eye and the primate brain didn't evolve in one big leap.
Remember that we're talking about millions and millions of virons, here...
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One of the fundamental principles of modern evolutionary theory is that complex function never evolves in one big leap.
Well, no joke.
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Successive generations of virus are subjected to gradually colder temperatures, the survivors among the progeny of each round of replication becoming the parents for the next round. If you simply took the entire population of virus and subjected it to the lowest temperature, they would all die.
And then take the virus that's attenuated, and give it to people, and it gives them flu-like symptoms several days to a week later. I'd say it's pretty reasonable to assume the descendants of the cold adapted virons who are causing the flu-like illnesses a week later in the vaccinees are a bit better at living in the tropics than their Inuit forefathers, no?
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The vaccine developers don't have to concern themselves with what precise nucleotide changes are required to permit the virus (some) to survive the selective pressure they are subjecting it to; random mutation takes care of that (or doesn't, and the whole population does die, and they have to start over).
Yes, random mutation allows it to adapt, but if the attenuating nucleotides are located in different places for the different strains, reassortment could certainly accelerate a reversion to virulence.
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Once you grasp the fact that the strains can't revert by reassortment (because it wouldn't do any good),
Might or might not.
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nor by a series of random mutations (because there isn't a continuous chain of transmission to support it),
What do you mean? That Flumist doesn't shed?
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there doesn't seem to be much point.
In even looking for reversions to virulence?
Well that makes this the first live vaccine I've ever heard of where a reversion to virulence wasn't considered and closely studied before the possibility was written off.
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#28 of 31 Old 10-28-2006, 11:24 AM
 
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Remember that we're talking about millions and millions of virons, here...
As was the case during the attenuation process. If it took umpity-ump generations to produce the cold adaptation, why should we expect it to take fewer to reverse the process? If the time it takes for the typical (healthy) immune system to respond is significantly less than the time it takes for those umpity-ump viral replication cycles... game over.

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What do you mean? That Flumist doesn't shed?
No, that secondary cases from exposure to vaccinated individuals are extremely rare, and tertiary cases (from exposure to secondary cases) are non-existant. Viral replication in the attenuated strains is not efficient, and viral load in a vaccinated individual never reaches anything like what it does in one infected with a wild strain; therefore, the chances of contracting the virus from a vaccinated person are far (FAR) less than with a wild strain. A study in a Finnish daycare center estimated those chances at 0.58%--2.4%. Unless the typical vaccinated person passes the virus on to at least one other, the virus loses its chance to evolve back to pathogenicity. At one out of two hundred, or even two or three out of one hundred, the bug is history.

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In even looking for reversions to virulence?
Well that makes this the first live vaccine I've ever heard of where a reversion to virulence wasn't considered and closely studied before the possibility was written off.
In the interest of thoroughness, you can look for something even though theory indicates that you shouldn't find it, and that has been done with Flumist -- but beyond a certain point, it becomes a questionable use of resources.
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#29 of 31 Old 10-28-2006, 12:19 PM
 
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Originally Posted by dymanic
As was the case during the attenuation process. If it took umpity-ump generations to produce the cold adaptation, why should we expect it to take fewer to reverse the process? If the time it takes for the typical (healthy) immune system to respond is significantly less than the time it takes for those umpity-ump viral replication cycles... game over.
Why do any in vitro findings not necessarily reflect the in vivo experience?
How do the viruses that should, in theory, always die off extremely quickly manage to essentially give people the flu?
Heck, for that matter, how do they replicate at all in the human body if the in vitro tests say they should just die?

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If the time it takes for the typical (healthy) immune system to respond is significantly less than the time it takes for those umpity-ump viral replication cycles... game over.
And I'm sure it goes just like that a lot of the time. But surely you're not saying everyone who gets flumist is the picture of perfect health?
There's a pretty delicate balance going on there, with a lot of variables, and many of those variables are unknowns.

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A study in a Finnish daycare center estimated those chances at 0.58%--2.4%.
I'd have to look at the study, but one or two in 50 isn't exactly "impossible" as you're claiming.
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Unless the typical vaccinated person passes the virus on to at least one other, the virus loses its chance to evolve back to pathogenicity. At one out of two hundred, or even two or three out of one hundred, the bug is history.
Ahh...see...you're math is off there because you're assuming the shed virus is as attenuated as it was in the vaccinee when it was originally introduced.
It's far more likely that those strains that do manage to mutate/reassort/ and replicate their way out of their hosts are already significantly more virulent and "warm adapted".

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In the interest of thoroughness, you can look for something even though theory indicates that you shouldn't find it, and that has been done with Flumist -- but beyond a certain point, it becomes a questionable use of resources.
What theory indicated that you shouldn't find it? Real life experience says that you will find it, but not "all that often".
It's only a questionable use of resources if your goal it to be able to use ambiguous phrases like "has not been observed".
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#30 of 31 Old 10-28-2006, 04:00 PM
 
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Originally Posted by dymanic
As was the case during the attenuation process. If it took umpity-ump generations to produce the cold adaptation, why should we expect it to take fewer to reverse the process?
Ah yes, the argument from personal incredulity. Dymanic can't fathom how evolution could produce a virulent strain faster than scientists were able to attenuate it, therefore it can not happen. The fundamental reality that has so far escaped his argument is that once the vaccine is sprayed into the nasal passage of the recipient, those vaccine strains are not restricted to reassort only with each other.


Quote:
Originally Posted by dymanic
Forget about reassortment.

Once you grasp the fact that the strains can't revert by reassortment...
Whoa, hold on a second. Before we go ahead and forget about reassortment why don't we consult a more credible source of mainstream, pro-vaccine opinion - the Journal of the American Medical Association (JAMA). Here's an excerpt from JAMA:

Quote:
One major concern has dogged live virus flu vaccine development from the beginning: the possibility that the attenuated vaccine virus could reassort with virulent wild-type virus and produce a new agent to which the population is susceptible. The result, some scientists hold, could well be an influenza pandemic paralleling that of 1918-1919.

The German workshop report discussed this possibility. “It is difficult if not impossible to assess the probability for such an adverse reassortment in nature,” it said, noting that human infection with H5N1 chicken virus in Hong Kong has renewed the concern. “In the end, the conclusion was, at least on the evidence so far, that this is not likely to occur,” said Kurth. But, he said, “One does have to watch,” adding that the possibility should be followed with continuing surveillance.

The issue is far from settled. A few weeks before the German workshop was held, the FDA held an information session on the live virus vaccine. At that meeting, Brian Murphy...who has done much of the recent work with the influenza virus, said the cold-adapted virus is genetically stable. “The virus has been given to thousands of individuals and we’ve not seen a reassortment, as far as we could tell,” said Murphy. But responded Edwin Kilbourne, MD, research professor at NY Medical College in Valhalla, “That’s the virus that goes into people, not the virus that may come out of people or may recombine in the field, where intergenetic interactions may occur that can not be predicted.” In an interview, Kilbourne added, “I am very worried about categorical statements that mutations will not happen. The phenotype of the vaccine virus may be stable but we have to be concerned about the possibility of interactions in the field. If you vaccinate using a trivalent vaccine with two different live influenza A strains, and then look at the viruses that come out of the recipient, there is a recombination rate of 50%. This indicates that there is a great possibility for generating something novel. This issue hasn’t been addressed very well.”
Okay, now we know that reassortment should not be forgotten, and that scientists rightly grasp the fact that strains can indeed revert by reassortment. It should also be restated that there are more things for the vaccine strains to reassort with in a person's body than in the cell culture lab. Each virus produces a thousand progeny and each of those progeny can in turn infect a new cell and produce a thousand more progeny, resulting in more co-infected cells and more reassortments. Evolution has ample opportunity to get the job done in just a single host. But don't take my word for it, let's once again consult the rabidly pro-vaccine literature to see if anyone's published a mathematical model for estimating the appearance of adverse reassortments. The following is an excerpt from a 2002 research paper published in a scientific journal that is so ardently pro-vaccination that it's simply called Vaccine.

Quote:
It is difficult, if not impossible, to assess the mathematical probability for adverse reassortment in nature. However, information is available to judge the possibility of a reassortment event. Basic calculation may be based on the requirement that cold-adapted influenza virus and virulent wild virus infect and replicate at the same time and at the same level in the same human host. For simplification of calculation, one can say that the NA gene is of no real significance and to consider it along with the low virulence genes of influenza viruses. For calculation of a reassortment event of two paired influenza virus genes from cold-adapted influenza virus and wild virus the phenomenon can be illustrated as follows: cold-adapted influenza virus has eight genes (1◦, 2◦, 3◦, 4◦, 5◦, 6◦, 7◦, 8◦) corresponding to eight genes of the wild virus (1, 2, 3, 4, 5, 6, 7, 8). From the pool of 16 genes, the chance for reassembling a virus with a 1, 2, 3, 4, 5, 6, 7, 8◦ combination would be 1 in 256. Assuming a thousand new particles were released from an infected cell, then the number of reassortant particles per double-infected cell would be four. It is unknown how many cells of an individual will be double-infected following vaccination and concurrent wild virus infection or during co-infection of a human cell with a human and a zoonotic influenza virus, but one may anticipate that the final number of reassortants must be very high. The mathematical principle explained above will be the same when live attenuated influenza vaccines are routinely used in a significant proportion of the population. One might speculate that the probability of a co-infection event in man is increased due to fact that many more individuals will carry live influenza virus at the same time.
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