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H5N1


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Back to the bird flu - as it is, it is not much of a threat. It can cross to people and if it then becomes contagious there will be a big heap of dead people. Last time that happened with a bird flu strain there were 50 million dead bodies.

 

Stocks of anti-virals held by various nations has been rising quite significantly in the last couple of years since this thing first started to show itself.

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Stocks of anti-virals held by various nations has been rising quite significantly in the last couple of years since this thing first started to show itself.

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Not in the US they haven't. The WHO suggested years ago that nations stockpile enough anti-virals to administer them to at least 25% of their populations. While many European nations have already met that goal, the US has barely enough for 2% of the population.

 

CIDRAP: Center for Infectious Disease Research & Policy

A recent report in the British magazine Nature said that Britain has ordered enough oseltamivir for about 25% of its population and Canada has stockpiled enough to cover about 5% of Canadians. The current US stockpile would cover less than 1% of the population.

 

Vaccine Status

 

The vaccine, while being tested, has some hurdles associated with it. One is the size of the dose needed to produce an adequate immune response.

 

The problems with a high-dose H5 vaccine are twofold:

First, since people have never been exposed to H5 viruses, a "primer" vaccination would have to be given, then a month later another dose would be required. Because of this two-dose regimen, immunity wouldn't take hold for about six weeks, giving the virus a bigger window to infect even immunized individuals, Treanor said.

Second, the higher dose would place a strain on manufacturers' ability to produce enough vaccine, he said.

It's also not known if the vaccine being tested now would protect against an H5 virus strain that might trigger a flu pandemic.

 

Have a nice day.

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Well I was unaware of the exact stats on US Vaccine provision, I guess we are going to be a tad better prepared if this goes poor.

 

As for the effective nature of the vaccine - well who knows? It might prove EXTREMELY effective, if it is not effective at all then a lot of bodies are going to need to be buried. Better to be prepared as much as possible, though, rather than ignore the problem.

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Well I was unaware of the exact stats on US Vaccine provision, I guess we are going to be a tad better prepared if this goes poor.

 

As for the effective nature of the vaccine - well who knows? It might prove EXTREMELY effective, if it is not effective at all then a lot of bodies are going to need to be buried. Better to be prepared as much as possible, though, rather than ignore the problem.

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Coli works in biotech. He's got a better idea than most of us on the nature of the vaccine.

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Coli works in biotech.  He's got a better idea than most of us on the nature of the vaccine.

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To be completely fair, I am a bacteriologist, not a virologist. However, the basic hurdles for getting something safely into humans are roughly the same for antibiotics or vaccines. As far as safety is concerned, you just can’t mass-manufacture something overnight and start injecting it into humans, no matter how “fast-tracked” that something is. Unlike antibiotics or some antivirals which act directly on the organism/virus, a vaccine is designed to produce an immune response and recognition mechanism so that the second time an individual “sees” this object again it can eliminate it before it can do considerable damage. That can compound the safety/effectiveness issue for a vaccine.

 

The hurdles are how much should be administered to get the appropriate primary response, yet also achieve immunologic memory, ie the ability to quickly recognize the foreign object. A memory response can take several days for the body to ramp up its mechanisms to combat an infection. In the case of the influenza virus, it has such a rapid incubation period that symptoms are already apparent before the body can muster a defense. Therefore, you need to have the primary response already in place, via an adequate number (serum level or titer) of antibodies.

 

A second problem is the viral surface variability. The vaccine could ultimately be useless if the primary immune response and immunologic memory are generated for the H5N1 (the components of the viral envelope) surface, but a mutation changes the makeup of the envelop proteins. You will probably hear the words “antigenic shift” in the news. All this means is that a mutation occurred and the proteins of the viral envelope that the body recognizes have changed, causing problems with the recognition aspect of the immune response.

 

Clearly there are people infinitely more qualified than me in the virology field who could probably do a better job of relaying this information. But I will do my best to explain in simpler terms any information that I come across on this subject…dude. :blink:

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I have worked on influenza vaccine in the past, your garden variety A/H3N2, A/H1N1 and B strains though, not H5N1. JC's synopsis is a very good one.

 

 

To be completely fair, I am a bacteriologist, not a virologist.  However, the basic hurdles for getting something safely into humans are roughly the same for antibiotics or vaccines.  As far as safety is concerned, you just can’t mass-manufacture something overnight and start injecting it into humans, no matter how “fast-tracked” that something is.  Unlike antibiotics or some antivirals which act directly on the organism/virus, a vaccine is designed to produce an immune response and recognition mechanism so that the second time an individual “sees” this object again it can eliminate it before it can do considerable damage.  That can compound the safety/effectiveness issue for a vaccine.

 

The hurdles are how much should be administered to get the appropriate primary response, yet also achieve immunologic memory, ie the ability to quickly recognize the foreign object.  A memory response can take several days for the body to ramp up its mechanisms to combat an infection.  In the case of the influenza virus, it has such a rapid incubation period that symptoms are already apparent before the body can muster a defense.  Therefore, you need to have the primary response already in place, via an adequate number (serum level or titer) of antibodies.

 

A second problem is the viral surface variability.  The vaccine could ultimately be useless if the primary immune response and immunologic memory are generated for the H5N1 (the components of the viral envelope) surface, but a mutation changes the makeup of the envelop proteins.  You will probably hear the words “antigenic shift” in the news.  All this means is that a mutation occurred and the proteins of the viral envelope that the body recognizes have changed, causing problems with the recognition aspect of the immune response. 

 

Clearly there are people infinitely more qualified than me in the virology field who could probably do a better job of relaying this information.  But I will do my best to explain in simpler terms any information that I come across on this subject…dude.  :blink:

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As far as safety is concerned, you just can’t mass-manufacture something overnight and start injecting it into humans, no matter how “fast-tracked” that something is.

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You mean, things don't happen immediately, no matter how much you want them to? :D I thought if the response to a crisis wasn't immediate, it was because Bush !@#$ed up. Ray Nagin told me so. :blink:

 

Your synopsis looked good to me...but then, I'm no virologist either. Just well-read. :blink:

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I have worked on influenza vaccine in the past, your garden variety A/H3N2, A/H1N1 and B strains though, not H5N1.  JC's synopsis is a very good one.

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I have some antigenic drift/shift questions wrt influenza vaccine development, if you don't mind.

 

How much change in the individual envelope components is necessary for an evasion of recognition? Basically, do minor changes in the protein secondary structure result in major problems for antigen recognition?

 

How predictive are the models as far as measuring the rate of antigenic drift? Is there a known frequency for the point mutations that lead to antigenic drift in influenza, and are there biases towards certain envelope component combinations?

 

Lastly, :blink: , how much of the above is taken into account when designing the vaccine, if any?

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I'm probably not much better qualified than you are to answer those questions, my invlovement in the influenza vaccine project revolved around finding adjuvants that would enhance the immune response in the elderly when added to the existing vaccine. However, it is my understanding that antigenic shift is the bigger problem in influenza. Antigenic shift essentially creates new heamagluttinin or neuraminidase proteins with epitopes that are unrecognizable to existing circulating serum antibodies. I do remember using a H3N2 from 2001 in an ELISA that would give me a signal when using serum from mice immunized with a 1999 H3N2 strain, any differences there would be the result of antigenic drift.

 

I have some antigenic drift/shift questions wrt influenza vaccine development, if you don't mind.

 

How much change in the individual envelope components is necessary for an evasion of recognition?  Basically, do minor changes in the protein secondary structure result in major problems for antigen recognition?

 

How predictive are the models as far as measuring the rate of antigenic drift?  Is there a known frequency for the point mutations that lead to antigenic drift in influenza, and are there biases towards certain envelope component combinations? 

 

Lastly,  :D , how much of the above is taken into account when designing the vaccine, if any?

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I'm probably not much better qualified than you are to answer those questions, my invlovement in the influenza vaccine project revolved around finding adjuvants that would enhance the immune response in the elderly when added to the existing vaccine.  However, it is my understanding that antigenic shift is the bigger problem in influenza.  Antigenic shift essentially creates new heamagluttinin or neuraminidase proteins with epitopes that are unrecognizable to existing circulating serum antibodies.  I do remember using a H3N2 from 2001 in an ELISA that would give me a signal when using serum from mice immunized with a 1999 H3N2 strain, any differences there would be the result of antigenic drift.

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I was going to say that. :D Pretty much exactly that, except for the word "epitopes".

 

In support of that, though...there is epidemiological evidence that the reason the over-40 demographic didn't suffer over-much in 1918-1919 was that they were partially immunized by a previous H1N1 strain some three decades back or so. The epidemiology supports the idea that antigenic drift is not sufficient, and antigenic shift is required to cause evasion of recognition.

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I was going to say that.  :(  Pretty much exactly that, except for the word "epitopes".

 

In support of that, though...there is epidemiological evidence that the reason the over-40 demographic didn't suffer over-much in 1918-1919 was that they were partially immunized by a previous H1N1 strain some three decades back or so.  The epidemiology supports the idea that antigenic drift is not sufficient, and antigenic shift is required to cause evasion of recognition.

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More importantly, can I still eat turkey?

 

The answer lies within

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More importantly, can I still eat turkey?

 

The answer lies within

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Considering that precisely zero turkeys have been infected in this country so far... :(

 

The article in National Geographic made an interesting point, though: the powers-that-be don't necessarily know how it's being spread from bird to human as of the writing (which I assume was about four months ago). The necessary investigation hadn't been done at the time; it could have been inhaled droplets, inhaled dust from bird droppings, ingested, etc.

 

And the CDC's answer to the question was just waffling enough to make me believe that the epidemiology still hasn't been done in that regard.

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