Yes, I would say that politically it is a matter of "measured risk." Since the virus is still contained in Sutheast Asia and there is no "panic scare" amongst Americans, then there is no pressure on congress from the general public to react. Its not yet in the news headlines so the majority of Americans are unaware of the danger.one_raven said:
Avian flu pandemic?
- Thread starter The Mighty Billy
- Start date
Yes, and exactly as Invert_Nexus says, what vaccine should we give out? We don't know yet, but luckily we have a tremendous number of bio-immuniologist scientist out there that viligently try to quickly respond to trying to develop a responce to a quickly mutated strain.
This is a hot field of study that many students are trying to eagirly get into. The BIO 181 class at my university has over 130 students in just one class just trying to learn the fundamentals!
We can't know what to treat until the virus mutates into a virus transmittable betwen humans. Then we react.
This is a hot field of study that many students are trying to eagirly get into. The BIO 181 class at my university has over 130 students in just one class just trying to learn the fundamentals!
We can't know what to treat until the virus mutates into a virus transmittable betwen humans. Then we react.
So far there has not been any human to human transmission of this disease so until that happens there's nothing we can do except kill all the fowl that are in proximity of any fowl getting the disease.
Well, that's the plan, so it seems
Still doesn't help the migrating wild bird issue
On an unrelated note (from the same article)
Still doesn't help the migrating wild bird issue
http://news.bbc.co.uk/2/hi/europe/4324356.stm
On an unrelated note (from the same article)
I hate when officials say that.
I try to read CNN.com World news everyday and today they said the U.S. government has just poured in $100 million to start mass production of the vaccine "Tamiflu," but I'm pretty sure that this is the vaccine they said was no longer affective against the Bird Flu in Thailand because the flu has developed a resistance to it. Ten Asia countries have been hit by Avian Bird Flu: that's a pandemic.
One Raven,
I'm relatively sure this is the case. The flu vaccine is of the dead virus type. The main effects of the vaccine are to acquaint the body with the viral coat proteins (hemagglutinin and neuraminidase). As the vaccine has no active RNA in it, there is no danger of infection.
(Interestingly enough, Salk's original polio vaccine was of this 'dead virus' type but, due to contamination of some of the original batches of vaccine, several people contracted polio from the vaccine and this spooked the populace to vaccines. Sabin came out with his 'weakened virus' oral vaccine several years later and this became the most popular type of polio vaccine even though there is a risk of contracting polio from the live virus where there is no risk at all from Salk's vaccine despite the early contamination problem. Ironic.)
(And did you know that Salk tested his virus on himself and his family? This, in fact, has a long tradition, as Jenner (the creator of the smallpox vaccine using cowpox) originally tested his vaccine on an 8-year-old boy... (I don't think the boy was related to him though... Probably some street urchin.))
The only harm would be the resources diverted from creating a needed vaccine vs an unneeded one.
It doesn't learn the vaccine but it does learn the antigens in the vaccine. However, this learning process is futile in the flu and certain other viruses because of the rapid rate of mutation.
I'm not entirely certain how long, but I do believe that the vaccine does last. The body stores the memory of the antigens in specialized cells... I forget the specifics. It's been a while since I've studied directly into this... (T cells? A type of T cell? And the Thymus is where the antigen selection takes place? Damnit. I forget...)
Anyway. If the exact same strain were to break out later and you'd already either been infected by it or been vaccinated, then yes. You'd be safe from a reccurrence.
Valich,
Tamiflu isn't a vaccine. It's an antiviral drug. Apparently it is a neuraminidase inhibitor. Not entirely certain what that is, but I'd suspect that it prevents the virus from latching on to the cell membrane and being absorbed into the cell.
Back to the 1918 flu, an interesting aspect of this flu is that it is not dependent upon its host cell manufacturing trypsin (a protein that cleaves and activates the hemaggluttin). Instead the neuraminidase is able to do the job somehow. This means that this particular strain of virus is able to infect a larger amount of cells than an ordinary flu virus. Lung cells manufacture trypsin and this is apparently why the flu affects the lungs. The 1918 flu was able to infect more than the lungs. Quite interesting.
I hope that some of our resident epidemiologists or virologists find this thread and comment. The mechanisms of the influenza virus seem quite interesting and I'd definitely be interested in seeing an explicit treatment of its 8 genes and the functionings of its various proteins.
It really is amazing how such simple systems can cause such a muss and fuss.
I'm relatively sure this is the case. The flu vaccine is of the dead virus type. The main effects of the vaccine are to acquaint the body with the viral coat proteins (hemagglutinin and neuraminidase). As the vaccine has no active RNA in it, there is no danger of infection.
(Interestingly enough, Salk's original polio vaccine was of this 'dead virus' type but, due to contamination of some of the original batches of vaccine, several people contracted polio from the vaccine and this spooked the populace to vaccines. Sabin came out with his 'weakened virus' oral vaccine several years later and this became the most popular type of polio vaccine even though there is a risk of contracting polio from the live virus where there is no risk at all from Salk's vaccine despite the early contamination problem. Ironic.)
(And did you know that Salk tested his virus on himself and his family? This, in fact, has a long tradition, as Jenner (the creator of the smallpox vaccine using cowpox) originally tested his vaccine on an 8-year-old boy... (I don't think the boy was related to him though... Probably some street urchin.))
The only harm would be the resources diverted from creating a needed vaccine vs an unneeded one.
It doesn't learn the vaccine but it does learn the antigens in the vaccine. However, this learning process is futile in the flu and certain other viruses because of the rapid rate of mutation.
I'm not entirely certain how long, but I do believe that the vaccine does last. The body stores the memory of the antigens in specialized cells... I forget the specifics. It's been a while since I've studied directly into this... (T cells? A type of T cell? And the Thymus is where the antigen selection takes place? Damnit. I forget...)
Anyway. If the exact same strain were to break out later and you'd already either been infected by it or been vaccinated, then yes. You'd be safe from a reccurrence.
Valich,
Tamiflu isn't a vaccine. It's an antiviral drug. Apparently it is a neuraminidase inhibitor. Not entirely certain what that is, but I'd suspect that it prevents the virus from latching on to the cell membrane and being absorbed into the cell.
Back to the 1918 flu, an interesting aspect of this flu is that it is not dependent upon its host cell manufacturing trypsin (a protein that cleaves and activates the hemaggluttin). Instead the neuraminidase is able to do the job somehow. This means that this particular strain of virus is able to infect a larger amount of cells than an ordinary flu virus. Lung cells manufacture trypsin and this is apparently why the flu affects the lungs. The 1918 flu was able to infect more than the lungs. Quite interesting.
I hope that some of our resident epidemiologists or virologists find this thread and comment. The mechanisms of the influenza virus seem quite interesting and I'd definitely be interested in seeing an explicit treatment of its 8 genes and the functionings of its various proteins.
It really is amazing how such simple systems can cause such a muss and fuss.
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invert_nexus said:
Yeah! If only the "great, medical minds" of the world would spend just a few minutes at the sciforums, they'd know all they needed to know to cure the world's diseases, huh?
But, alas, they have to slave over a hot bunsen burner all day .....and don't have time.
Baron Max
Baron Max,
What, exactly, good troll, is your point?
Are you trying to say that because I called the flu virus a simple system that this somehow translates into an easy cure? If so, you've misinterpreted quite strongly.
The flu is a relatively simple virus. I made a bit of a mistake in my last post where I said 'eight genes'. The influenza virus actually has more than 8 genes, it has eight strands of RNA most of which code 1 gene each. But there are a few that code for more than one protein due to being read from different starting positions. Which is also interesting in that this is a form of data compression...
Anyway.
Shutup, troll. Or do you have something to say that makes sense?
The flu is a simple system in many ways. And it is a monument to the complexity that is capable of being manifested through simple systems.
If you want to look at a complex virus, take a look at the hiv virus.
Valich,
A vaccine is made of either pieces of a dead virus or weakened live viruses. The purpose of a vaccine is to produce antibodies that can repel a viral invasion without being either fully infected or infected at all depending on which type of vaccine you're dealing with.
An antiviral drug prevents infection through other means. As Tamiflu is a neuramidinase inhibitor, I think that its most likely effect is to block the neuramidine protein (one of the viral coat proteins, hemagluttin and neuraminidase) from attaching to the cell membrane of the host cell and thus blocks cell absorption of the virus.
So, a vaccine kicks in the body's immune system to repel viral invasion while an anti-viral drug takes advantage of some chemical property.
Now. Like I said, it's been awhile since I studied on this, but from the way that hemagglutin and neuraminidase are mentioned in the science article about the 1918 flu, I have this feeling that neuriminidase is the first step of the 'handshake'. Picture the flu virus rolling along. The N finds a receptor on the cell membrane and attaches. This stops the virus from rolling and allows the H to find its receptor which causes the cell to open up and absorb the virus inside.
Note: This is my conjecture. I've not gone out to study this all directly. It could be the opposite. Or it could be completely different. I conjecture this method because the hiv virus (which I have studied relatively recently) operates in such a fashion. A two part handshake. I'd enjoy someone who knows for sure to pop in and confirm or deny my guess. Or maybe I'll dig around in my biology texts and the net and see if I can't find something specific about the mechanics of the influenza virus.
What, exactly, good troll, is your point?
Are you trying to say that because I called the flu virus a simple system that this somehow translates into an easy cure? If so, you've misinterpreted quite strongly.
The flu is a relatively simple virus. I made a bit of a mistake in my last post where I said 'eight genes'. The influenza virus actually has more than 8 genes, it has eight strands of RNA most of which code 1 gene each. But there are a few that code for more than one protein due to being read from different starting positions. Which is also interesting in that this is a form of data compression...
Anyway.
Shutup, troll. Or do you have something to say that makes sense?
The flu is a simple system in many ways. And it is a monument to the complexity that is capable of being manifested through simple systems.
If you want to look at a complex virus, take a look at the hiv virus.
Valich,
A vaccine is made of either pieces of a dead virus or weakened live viruses. The purpose of a vaccine is to produce antibodies that can repel a viral invasion without being either fully infected or infected at all depending on which type of vaccine you're dealing with.
An antiviral drug prevents infection through other means. As Tamiflu is a neuramidinase inhibitor, I think that its most likely effect is to block the neuramidine protein (one of the viral coat proteins, hemagluttin and neuraminidase) from attaching to the cell membrane of the host cell and thus blocks cell absorption of the virus.
So, a vaccine kicks in the body's immune system to repel viral invasion while an anti-viral drug takes advantage of some chemical property.
Now. Like I said, it's been awhile since I studied on this, but from the way that hemagglutin and neuraminidase are mentioned in the science article about the 1918 flu, I have this feeling that neuriminidase is the first step of the 'handshake'. Picture the flu virus rolling along. The N finds a receptor on the cell membrane and attaches. This stops the virus from rolling and allows the H to find its receptor which causes the cell to open up and absorb the virus inside.
Note: This is my conjecture. I've not gone out to study this all directly. It could be the opposite. Or it could be completely different. I conjecture this method because the hiv virus (which I have studied relatively recently) operates in such a fashion. A two part handshake. I'd enjoy someone who knows for sure to pop in and confirm or deny my guess. Or maybe I'll dig around in my biology texts and the net and see if I can't find something specific about the mechanics of the influenza virus.
It's just a brand name.
It's real name is Oseltamivir.
As to the virus evolving in such a way as to render it ineffective, it's not surprising. The influenza virus mutates quite rapidly. I'm not familiar enough with the mechanics of the importance of neuraminidase or the method by which tamiflu inhibits it to comment much on it. It's said that there are only what... 7 varieties of neuraminidase? It seems to me that this part of the genome is relatively stable. But, perhaps there can be subtle changes in the protein that don't add a whole new protein to the list...
I really don't know. I wish Hercules would stop by. He's not a virologist, but he does know his molecular biology.
Well. Crap. I'm wrong on the function of the inhibitor.
From neuraminidase inhibitor.
"Neuraminidase inhibitors are a class of antiviral drugs, whose mode of action relies on blocking the function of viral neuraminidase protein, thus preventing the virus from budding from the host cell."
I would have thought this would have been more the function of an M1 or M2 inhibitor... shows what I know.
I would really love to see an indepth treatment of the mechanisms of influenza. I'm going to do some digging... enough guesswork.
It's real name is Oseltamivir.
As to the virus evolving in such a way as to render it ineffective, it's not surprising. The influenza virus mutates quite rapidly. I'm not familiar enough with the mechanics of the importance of neuraminidase or the method by which tamiflu inhibits it to comment much on it. It's said that there are only what... 7 varieties of neuraminidase? It seems to me that this part of the genome is relatively stable. But, perhaps there can be subtle changes in the protein that don't add a whole new protein to the list...
I really don't know. I wish Hercules would stop by. He's not a virologist, but he does know his molecular biology.
Well. Crap. I'm wrong on the function of the inhibitor.
From neuraminidase inhibitor.
"Neuraminidase inhibitors are a class of antiviral drugs, whose mode of action relies on blocking the function of viral neuraminidase protein, thus preventing the virus from budding from the host cell."
I would have thought this would have been more the function of an M1 or M2 inhibitor... shows what I know.
I would really love to see an indepth treatment of the mechanisms of influenza. I'm going to do some digging... enough guesswork.
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Ok. This is interesting.
Turns out that the neuraminidase is not active in absorption of the virus into the cell. The hemagglutin takes care of that entirely on its own.
The hemagglutin attaches to sialic-acid containing proteins. Then the protein trypsin comes into play and cleaves the HA protein which causes the cell to absorb the virus. Interesting that there is still a two-part handshake going on (sort of) but is done with only one initial protein... However, the mechanism is completely different from the hiv handshake, so the similarity is purely coincidental.
The cleaving of HA explains the NA mutation in the 1918 Spanish Flu. This particular virus cleaved itself and didn't need trypsin to be present on the cell membrane to gain entry. I wonder how much this had to play in the virulence of the virus? (Meaning, exactly how widespread was the infection seeing as how it could infect a wider variety of cells than your typical flu virus... Did it actually take advantage of that potential? What other limiting factors are present? How many cells have these sialic acid containing proteins which are the door knocker?)
What is odd is that it was still an H1N1 virus. Yet the NA was mutated in a pretty amazing fashion. This lends credence to the idea that the NA can mutate enough to stifle the effects of tamiflu while still remaining part of the 9 varieties.
Anyway. In a normal virus, the NA doesn't really come into play until budding. It cleaves the sialic acid proteins so that the same cell won't get infected again. Somehow, this cleaving also promotes the virus to bud.
I haven't found an explicit explanation of all the protein functions, but that's it in a nutshell. I'd love a link to something that goes into more depth of protein functioning... (especially neuraminidase functioning. How does it promote budding?)
Here's the best link that I found on my short search: http://www.bact.wisc.edu/Microtextb...s&file=index&req=viewarticle&artid=126&page=1
Edit:
Oh. And on the topic of vaccines:
"Some vaccines incorporate inactivated virus particles; others use the purified hemagglutinin. Both types incorporate antigens from the three major strains in circulation, currently:
* an A strain of the H1N1 subtype
* an A strain of the H3N2 subtype and
* a B strain."
http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/I/Influenza.html
That's kinda interesting. I never realized that it was so structured. Always one of each type. What about strains with other configurations? Are they not as virulent as these two listed? (The B strain is purely human and is very unlikely to become a pandemic as it is only affected by antigen drift (ordinary mutation) rather than antigen shift (when two viruses mix contents).
Turns out that the neuraminidase is not active in absorption of the virus into the cell. The hemagglutin takes care of that entirely on its own.
The hemagglutin attaches to sialic-acid containing proteins. Then the protein trypsin comes into play and cleaves the HA protein which causes the cell to absorb the virus. Interesting that there is still a two-part handshake going on (sort of) but is done with only one initial protein... However, the mechanism is completely different from the hiv handshake, so the similarity is purely coincidental.
The cleaving of HA explains the NA mutation in the 1918 Spanish Flu. This particular virus cleaved itself and didn't need trypsin to be present on the cell membrane to gain entry. I wonder how much this had to play in the virulence of the virus? (Meaning, exactly how widespread was the infection seeing as how it could infect a wider variety of cells than your typical flu virus... Did it actually take advantage of that potential? What other limiting factors are present? How many cells have these sialic acid containing proteins which are the door knocker?)
What is odd is that it was still an H1N1 virus. Yet the NA was mutated in a pretty amazing fashion. This lends credence to the idea that the NA can mutate enough to stifle the effects of tamiflu while still remaining part of the 9 varieties.
Anyway. In a normal virus, the NA doesn't really come into play until budding. It cleaves the sialic acid proteins so that the same cell won't get infected again. Somehow, this cleaving also promotes the virus to bud.
I haven't found an explicit explanation of all the protein functions, but that's it in a nutshell. I'd love a link to something that goes into more depth of protein functioning... (especially neuraminidase functioning. How does it promote budding?)
Here's the best link that I found on my short search: http://www.bact.wisc.edu/Microtextb...s&file=index&req=viewarticle&artid=126&page=1
Edit:
Oh. And on the topic of vaccines:
"Some vaccines incorporate inactivated virus particles; others use the purified hemagglutinin. Both types incorporate antigens from the three major strains in circulation, currently:
* an A strain of the H1N1 subtype
* an A strain of the H3N2 subtype and
* a B strain."
http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/I/Influenza.html
That's kinda interesting. I never realized that it was so structured. Always one of each type. What about strains with other configurations? Are they not as virulent as these two listed? (The B strain is purely human and is very unlikely to become a pandemic as it is only affected by antigen drift (ordinary mutation) rather than antigen shift (when two viruses mix contents).
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The link you provided (Oct. 10, 2005) states that a nasal vaccine under development is proving to be 93% effective. I think that is the one they were saying is effective against the Avian Flu, while tamiflu is not always, even though tamiflu is the one we're producing. I recall the article I said that the alternative vaccine was a nasal spray but that it takes too long to be absorbed, where time is critical in these cases. They were hoping that an injectable type of that nasal spray could be developed that would be effective within a matter of hours (4 hrs.)
That latest outbreak in Romania is in the Danube delta, Europe's largest wetlands, and is a major migratory stopover for birds coming from Russia, Scandinavia, Poland and Germany flying to warmer areas in North Africa for the winter. Romania is part of Europe so now the pandemic has spread from the 10 affected Asian countries to Europe.
That latest outbreak in Romania is in the Danube delta, Europe's largest wetlands, and is a major migratory stopover for birds coming from Russia, Scandinavia, Poland and Germany flying to warmer areas in North Africa for the winter. Romania is part of Europe so now the pandemic has spread from the 10 affected Asian countries to Europe.
Just as a sidenote, neuraminidases are also often apathogenicity factor found at bacteria. They hydrolyze the terminal, non-reducing, sialic acid linkage in glycoproteins, glycolipids, gangliosides, polysaccharides.
As such they inhibit the transport of the bacteria (or virus) by mucoid cells (if infecting the respiration tract) and specifically for viruses they are often important for the release from infected cells (by cleaving the receptor which are attached to the said cells).
The neuraminidase blockers are sialic acid analoga.
Regarding the risks of vaccinations, I am no expert in it, but I am pretty sure that one potential risk is allergic reactions (if suscepticle) to some vaccines (or rather the proteins).
As such they inhibit the transport of the bacteria (or virus) by mucoid cells (if infecting the respiration tract) and specifically for viruses they are often important for the release from infected cells (by cleaving the receptor which are attached to the said cells).
The neuraminidase blockers are sialic acid analoga.
Regarding the risks of vaccinations, I am no expert in it, but I am pretty sure that one potential risk is allergic reactions (if suscepticle) to some vaccines (or rather the proteins).
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invert_nexus said:
I'm trying to catch up and follow you on this but there's a lot I don't know yet. The following may be of interest to you although you probably already know it:
"MedImmune plans to develop at least one vaccine for each of the 16 variations of a surface protein — known as hemagglutinin — found on the avian flu virus, including the one for the H5N1 virus that is spreading throughout Asia, Kazakhstan and Russia.
Influenza A he viruses mutate from year to year, making it necessary to update flu vaccines annually. Less frequently, but with deadly results, the virus goes through a major change called an antigenic shift that creates new strains to which humans have no immunity. This happens when two distinct flu strains exchange genes and is especially deadly when the exchange occurs between human and bird flu."
There is one vaccine "FluMist produced by MedImmune," and two anti-viral drugs - Tamiflu (oseltamivir) and Relenza (zanamivir) - but Thailand has found Relenza to be ineffective. FluMist contains 3 live flu strains but the current one approved to be produced must be different, according to what I posted that they are saying above?
NO! I AM WRONG, TAMIFLU IS NOT EFECTIVE. And that means that the U.S. Government is wrong for allocating $100 million to produce an anti-virul drug that is showing to be not effective. I better just post the whole article from CNN.com:
"Bird flu 'resistant to main drug'
Friday, September 30, 2005; Posted: 7:33 a.m. EDT (11:33 GMT)
HONG KONG, China (Reuters) -- A strain of the H5N1 bird flu virus that may unleash the next global flu pandemic is showing resistance to Tamiflu, the antiviral drug that countries around the world are now stockpiling to fend off the looming threat.
Experts in Hong Kong said on Friday that the human H5N1 strain which surfaced in northern Vietnam this year had proved to be resistant to Tamiflu, a powerful antiviral drug which goes by the generic name, oseltamivir. They urged drug manufacturers to make more effective versions of Relenza, another antiviral that is also known to be effective in battling the much feared H5N1. Relenza is inhaled.
"There are now resistant H5N1 strains appearing, and we can't totally rely on one drug (Tamiflu)," William Chui, honorary associate professor with the department of pharmacology at the Queen Mary Hospital in Hong Kong, told Reuters. Chui was referring to the Tamiflu-resistant strain of H5N1 in Vietnam. Chui also said general viral resistance to Tamiflu was growing in Japan, where doctors habitually prescribe the drug to fight the common influenza. "Manufacturers should think about producing an injectable form of Relenza because resistance to Tamiflu has been seen in Japan and Vietnam. Also with injections, high doses can be given where necessary and onset time is a lot faster," Chui said.
Two reports in The Lancet medical journal this month said that resistance to anti-flu drugs was growing worldwide. In places such as China, drug resistance exceeded 70 percent, suggesting that drugs like amantadine and rimantadine will probably no longer be effective for treatment or as a preventive in a pandemic outbreak of flu, the reports said."
"Bird flu 'resistant to main drug'
Friday, September 30, 2005; Posted: 7:33 a.m. EDT (11:33 GMT)
HONG KONG, China (Reuters) -- A strain of the H5N1 bird flu virus that may unleash the next global flu pandemic is showing resistance to Tamiflu, the antiviral drug that countries around the world are now stockpiling to fend off the looming threat.
Experts in Hong Kong said on Friday that the human H5N1 strain which surfaced in northern Vietnam this year had proved to be resistant to Tamiflu, a powerful antiviral drug which goes by the generic name, oseltamivir. They urged drug manufacturers to make more effective versions of Relenza, another antiviral that is also known to be effective in battling the much feared H5N1. Relenza is inhaled.
"There are now resistant H5N1 strains appearing, and we can't totally rely on one drug (Tamiflu)," William Chui, honorary associate professor with the department of pharmacology at the Queen Mary Hospital in Hong Kong, told Reuters. Chui was referring to the Tamiflu-resistant strain of H5N1 in Vietnam. Chui also said general viral resistance to Tamiflu was growing in Japan, where doctors habitually prescribe the drug to fight the common influenza. "Manufacturers should think about producing an injectable form of Relenza because resistance to Tamiflu has been seen in Japan and Vietnam. Also with injections, high doses can be given where necessary and onset time is a lot faster," Chui said.
Two reports in The Lancet medical journal this month said that resistance to anti-flu drugs was growing worldwide. In places such as China, drug resistance exceeded 70 percent, suggesting that drugs like amantadine and rimantadine will probably no longer be effective for treatment or as a preventive in a pandemic outbreak of flu, the reports said."
invert_nexus said:
Okay, I'm at the point where this is the part that I do not understand. The virus enters the host cell by attaching its HA protein to sialic-acid containing proteins on the host cell and then enters by "receptor-mediated endocytosis," not "cleavage." What do you mean by cleavage? And what is the "two-part handshake"?
The whole world seems to still think that increased production and distribution of the anti-virul Tamiful is the answer. Read my above post about how Tamiful has been found to be ineffective in Vietnam. This doesn't make any sense. Why don't they concentrate on producing Relenza instead?