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Avian Influenza and Wetlands: Complex Interactions
Henry, those were CLINICAL signs, historically used to determine HPAI in poultry and in occasional wild bird outbreaks. I know **** well that LABORATORY confirmation includes serology and molecular diagnostics.
How about tthe word 'susceptible'? You seem to be working under a major misconception that HPAI is silent and nonlethal in wild birds.
When the conditions are right, HPAI infected birds die in large numbers MANY SPECIES in the SAME LOCATION, as they did on the Tibetan Plateau.
The pathogenicity index is determined in the LAB and is based on symptoms in EXPERIMENTAL CHICKENS. It has nothing to do with wild birds or any other host.
HPAI usually does NOT kill waterfowl. At Erhel lake in 2005, less than 100 birds died from H5N1 clade 2.2.
Re: Avian Influenza and Wetlands: Complex Interactions
Perhaps one key to the spread of HP H5N1 is cited in the article which started this interesting thread:
"After an HPAI virus has arisen in poultry, it has the potential both to re-infect wild birds and to cause disease in other non-avian taxa..."
There are lots of historical examples of H7 and H5N2 LP viruses in wild birds and poultry, and then suddenly they turn highly pathogenic in the chickens, i.e. they quickly devestate the domestic flocks. Upon careful examination of the virus, they are found to have the multi-basic amino acids at the HA cleavage site. However, H5N1 appears to be unique in that once it turned HP, it began to be spread by migratory birds, as well as imported birds and material. Ducks in particular were found to be asymptomatic with HP H5N1.
One theory for the Qinghai strain becoming so widespread is that the E627K mutation in PB2 allowed for wild bird respiratory tracks to be infected, as opposed to the lower intestinal track. In the bird respiratory track, the virus may not replicate as quickly, allowing the wild migratory bird to carry the pathogene long distances with only mild symptoms.This particular virus is likely to be around a very long time causing mischief.
Perhaps one key to the spread of HP H5N1 is cited in the article which started this interesting thread:
"After an HPAI virus has arisen in poultry, it has the potential both to re-infect wild birds and to cause disease in other non-avian taxa..."
There are lots of historical examples of H7 and H5N2 LP viruses in wild birds and poultry, and then suddenly they turn highly pathogenic in the chickens, i.e. they quickly devastated the domestic flocks. Upon careful examination of the virus, they are found to have the multi-basic amino acids at the HA cleavage site. However, H5N1 appears to be unique in that once it turned HP, it began to be spread by migratory birds, as well as imported birds and material. Ducks in particular were found to be asymptomatic with HP H5N1.
One theory for the Qinghai strain becoming so widespread is that the E627K mutation in PB2 allowed for wild bird respiratory tracks to be infected, as opposed to the lower intestinal track. In the bird respiratory track, the virus may not replicate as quickly, allowing the wild migratory bird to carry the pathogene long distances with only mild symptoms.This particular virus is likely to be around a very long time causing mischief.
The problem with the examples of LPAI converting to HPAI is the fact that such a conversion has NOTHING to do with the H5N1 that emerged from teh Gunagdong goose in 1996.
This is a ploy by the conservation groups to make a VERY simlpe story "complex", which is the cornerstone of their propaganda campaign.
HPAI is defines by the HA cleavage site, and the RERRRKKR cleavge site of H5N1 in Asia is clearly HPAI and has been circulating in poultry, wild birds, and humans for over a decade (no poultry farms, or conversion of LPAI to HPAI required).
Most waterfowl infected with HPAI H5N1 are asymptomatic. There are exceptions, like Qinghai Lake in 2005 or Uvs Lake in 2006, where the waterfowl die off is massive, but the fatal cases (like the swannery in England this year) are relatively small (in the swannery it was 11 dead confirmed birds over a period of a few months).
The OIE Mission Report (on H5N1 in Russia in the summer of 2005) described more than 2 dozen species that were hunter killed (i.e. healthy before being shot), but H5N1 positive (Qinghai strain).
The issue of H5N1 and long range migratory birds was resolved in the summer of 2005, which is when the propaganda campaign shifted into high gear (including swamping of message boards with wild bird / H5N1 nonsense). The posts were quite obvious, as was the e-mail campaign, and the posts on ProMED.
In 2005, some of this was misinformation, but now, 3 years after the fact, the information has moved well into the disinformation category, and the use of LPAI to spread confusion is rather obvious.
Re: Avian Influenza and Wetlands: Complex Interactions
I speculate :
In wild birds LP is evolutionary more fit and thus prevalent.
Then wild birds introduce it to poultry and it often mutates
to HP in poultry (while apparantly it never mutates back to LP).
Then the HP usually dies or is wiped out.
That didn't work so well with H5N1 which persists in wild birds and poultry.
We don't know whether H5N1 was already HP when it emerged in poultry
in 1996, but no LP H5N1 was observed. However no HP H5N1 was observed in birds
in China before 1996 either. The H5 is similar to LP-H5 from Hongkong,Japan,Italy
but not H5N1.
That particular combination/reassortment of segments which first formed
H5N1 in China, was presumably LP. But the new combination was a dramatic change
which might have caused the HP-mutation as well as many subsequent
reassortments with all sorts of serotypes. Then that virus went to the goose-farm in 1996.
Or...
Some LP-H5Nx was already present on some Guangdong poultry farm.
Then some wild bird brought a new virus with N1, H5N1-LP was formed
by reassortment, and after some time it mutated to HP
Re: Avian Influenza and Wetlands: Complex Interactions
Right on gsgs. Most of the literature would support this view.
More precisely, an H5 virus apparently reassorted with H9N2 and H6N1 as they mixed in live bird markets in Hong Kong, producing an H5N1 variant. That virus likely turned highly pathogenic in poultry as many of the H7 and H5 viruses are prone to do, and it has been HP ever since 1996 spreading rapidly on the wings of migratory birds that cannot be controlled.
In wild birds LP is evolutionary more fit and thus prevalent.
Then wild birds introduce it to poultry and it often mutates
to HP in poultry (while apparantly it never mutates back to LP).
Then the HP usually dies or is wiped out.
That didn't work so well with H5N1 which persists in wild birds and poultry.
We don't know whether H5N1 was already HP when it emerged in poultry
in 1996, but no LP H5N1 was observed. However no HP H5N1 was observed in birds
in China before 1996 either. The H5 is similar to LP-H5 from Hongkong,Japan,Italy
but not H5N1.
That particular combination/reassortment of segments which first formed
H5N1 in China, was presumably LP. But the new combination was a dramatic change
which might have caused the HP-mutation as well as many subsequent
reassortments with all sorts of serotypes. Then that virus went to the goose-farm in 1996.
Or...
Some LP-H5Nx was already present on some Guangdong poultry farm.
Then some wild bird brought a new virus with N1, H5N1-LP was formed
by reassortment, and after some time it mutated to HP
What does any of the above have to do with H5N1 in Asia since 1996 (or any H5N1 positive country west of China since 2005)?
Right on gsgs. Most of the literature would support this view.
More precisely, an H5 virus apparently reassorted with H9N2 and H6N1 as they mixed in live bird markets in Hong Kong, producing an H5N1 variant. That virus likely turned highly pathogenic in poultry as many of the H7 and H5 viruses are prone to do, and it has been HP ever since 1996 spreading rapidly on the wings of migratory birds that cannot be controlled.
The H5N1 in Hong Kong in 1997 was quite distinct from the H5N1 currently in circulation. It had wild bird (H9N2 and H6N1) internal genes but that constellation is not widespread (limited to a few more recent isolates from eggs in Vietnam).
The HPAI H5N1 in circulation now has been divided into something like 10 clades. Of these, clade 1 and 2 have been reported to cause human disease and were actually more closely linked to early isoaltes from NORTHERN China than the Hong Kong isolates.
Moreover, the first post on this thread is a propaganda piece focused on wild birds as victims, which has NOTHING to do with the current version of H5N1 in circulation (other than a possible role a decade ago).
.....Moreover, the first post on this thread is a propaganda piece focused on wild birds as victims, which has NOTHING to do with the current version of H5N1 in circulation (other than a possible role a decade ago).
Did you even read this article?
The message I took away was that people, poultry, wild birds, etc could all end up being victims of Avian Influenza if more appropriate steps in its prevention weren't taken in the future. I truly don't see an argument with that.
The salvage of human life ought to be placed above barter and exchange ~ Louis Harris, 1918
The message I took away was that people, poultry, wild birds, etc could all end up being victims of Avian Influenza if more appropriate steps in its prevention weren't taken in the future. I truly don't see an argument with that.
The LPAI data had NOTHING to do with pandemic H5N1. The article was a snow job.
not so attractive to read long articles without abstract or summary.
wetlands = mainly the large west sibirian wetlands ?
> HP was rare before H5N1 came along
HK'97 was different, but in HA it was not so different,
we can see the evolution of H5N1-HA separately.
When there are dramatic changes, then reassortment
tries to compensate for occurring problems.
New strains need some time to find their stable points
The polybasic cleavage site has been around (and in MANY H5N1 clades and sub0clades) since 1996. No poultry required to go from LPAI to HPAI since 1996 in Asia (and now clade 2.2 in Europe, the Middle East, and Africa).
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