Stoddard County, Missouri has detected low pathogenic H5N1 in Northern Shovetel ducks. Additional testing will attempt to confirm and expand on these findings, but don’t hold your breath that any detailed test results or genetic sequence information will be made public.
For those that need to verify such lovely news, please note the following:
I have asked sources repeatedly what the definitive difference is between High Path and Low Path H5N1, and was told it is primarily symptomatic…low path doesn’t make chickens sick, high path does. But there has been no real proof that sick chickens are the only way humans contract H5N1…as a matter of fact there are many cases in which no sick chickens were around when humans came down with it. I guess we’ll have to wait and see whether lo path H5N1 in migratory waterfowl ends up causing problems in human health or not, but I for one am not particularly comforted by the “lo path” tag.
I too am not convinced that low path means no worry. I am under the impression that low path can mutate to high path. Also, I thought the ducks didn’t die from H5N1, they were carriers, so does that make the H5N1 in ducks low path or high path that doesn’t kill them.
Mary in Hawaii – at 21:30
I’m with you Mary. I have yet to understand why the USDA continully states that low pathogenic H5N1 should not be a concern to these hunters that are bringing down these sick birds. Unless the USDA can “show me” (no, I’m not from Missouri) a human with low path H5N1 sera, I will remain caustious.
By the USDA definition of High Path, they base a lot on the HA cleavage site of the virus and whether there is polybasic amino acids that show up there. Well, the 1918 H1N1 pandemic virus did not have this characteristic and it killed 50 million people world wide. So, again, I have no idea what they base there opinions on since they have no case histories of what this low path virus will do if humans become infected.
Ruth – at 21:46
I do not know if there is scientific evidence of just how long it takes H5N1 to go from low to high path once it infects a domestic flock of chickens, but I bet every time that there is a new detection of this virus in America, Tyson executives are excercising their options and selling stock.
When H5N2 went high path in Pennsylvania in 1983, it was only a matter of months, basically low in April, and then high in October. Then it spread into other states and within two years millions of chickens had to be culled and destroyed.
I just came back from the humor thread. I think I’ll stay there, much safer, since I live in the midwest.
This occured in Stoddard County, Missouri, southeast MO, refered to as the “boothill” of MO, and 128 miles South of St. Louis. Thanks for posting this. I am in Southwest Mo so this was of particular interest. This is the primary route for us to Memphis. It’s a beautiful area. Full of rivers and creeks, great canoeing in the Spring.
If you assume that the only way to switch from low to hi path is random mutation, then you will wait a long time, because you not only have to change bases, but you have to insert new bases in a peculiar pattern. The Qinghai sequence is RERRKRR, for example, and the low-path is just R. A quicker way to change from low-path to hi-path is to have a dual infection with a different strain that already has the polybasic cleavage site. This can be done in a single infection. Now note that changing from low- to high-path seems to happen overnight, and you don’t find evidence for all the intermediatee steps from R to RERRKRR. So what are we to think? That this is a gradual, almost accidental change? Or that a dual infection can change everything in an instant.
You decide.
disgruntled – at 22:09
The gain of amino acids at the HA cleavage site is usually associated with a similar loss of amino acids in the NA segment, and sometimes in other segments as well. So, at least at first blush it does not appear to be associated with random mutations as much as a chemical change in the proteins and some type of movement of genetic material between segments that only seems to happen in domestic fowl.
Some research has shown that if you pass a low path virus several times through replication in host cells, you begin to see this change in HA, but how fast it actually occurs in nature is still unclear. However, to rest on the assumption that such changes are random and accidental is in my opinion imprudent at this stage of understanding.
The definition of HPAI is based on the degree to which it is pathogenic to chickens. There are various standards but a common one is that the disease kills 75% of 4–8 week old poultry.
Whereas previous definitions were based more on virulence, in recent years, because of the improved understanding that H5 and H7 are probably the only subtypes that can cause HPAI, and that LPAI can change into HPAI after moving from wild birds to domesticated chickens or turkey, and that such changes can happen at any time and randomly, the World Organisation for Animal Health (OIE) has made LPAI from H5 and H7 subtypes notifiable, in recognition of that.
A good explanation of issues involved, including trade and economic ones, can be found here.
Well, I didn’t read some of the later debate on this thread before i posted. So let me clarify before everyone starts responding. In this sentence, “that such changes can happen at any time and randomly,” I used the word ‘randomly’ randomly :-), ie with no intention of signifying any interpretation of the molecular process, but as events on a macro and not micro level.
So if H5N1 is found in ducks, which are carriers, and they go near chickens it could or could not be high path for the chickens?
Besides chickens, how about all of the turkeys that are getting readied for market(in less than desirable accomodations, I’m sure!).
Mamabird – at 22:20 to disgruntled – at 22:09
So the conclusion of this is that low path H5N1 which is now being found in many parts of the US is something we need to watch carefully and not just dismiss as nothing. Right?
Ruth – at 07:44 So the conclusion of this is that low path H5N1 which is now being found in many parts of the US is something we need to watch carefully and not just dismiss as nothing. Right?
Yes, however, the chance of it turning into HP on US soil is not that high. And the chance of that turning into a pandemic strain may not be high either. This is becauset so far all the HP H5N1 strains have only come out of southern China. We don’t know why exactly, it could be some ecological condition, since farming practices are not that different in other parts of China or indeed in many parts of the world.
all the new HP H5N1 strains
Thanks for the information. It’s appreciated.
NS1 – at 00:58
“The 20aa deletion in the NA stalk (res49–68) has nothing to do with the HA gain of multiple basic aminos. No exchange typically occurs between those gene segments.”
I respectively ask that you read the following research abstract and see if you would agree that there may be other possibilities.
Authors J. Banks, E. S. Speidel, E. Moore, L. Plowright, A. Piccirillo, I. Capua, P. Cordioli, A. Fioretti, D. J. Alexander
Abstract Summary. Outbreaks of avian influenza due to an H7N1 virus of low pathogenicity occurred in domestic poultry in northern Italy from March 1999 until December 1999 when a highly pathogenic avian influenza (HPAI) virus emerged. Nucleotide sequences were determined for the HA1 and the stalk region of the neuraminidase (NA) for viruses from the outbreaks. The HPAI viruses have an unusual multibasic haemagglutinin (HA) cleavage site motif, PEIPKGSRVR RGLF. Phylogenetic analysis showed that the HPAI viruses arose from low pathogenicity viruses and that they are most closely related to a wild bird isolate, A/teal/ Taiwan/98. Additional glycosylation sites were present at amino acid position 149 of the HA for two separate lineages, and at position 123 for all HPAI and some low pathogenicity viruses. Other viruses had no additional glycosylation sites. All viruses examined from the Italian outbreaks had a 22 amino acid deletion in the NA stalk that is not present in the N1 genes of the wild bird viruses examined. We conclude that the Italian HPAI viruses arose from low pathogenicity strains, and that a deletion in the NA stalk followed by the acquisition of additional glycosylation near the receptor binding site of HA1 may be an adaptation of H7 viruses to a new host species i.e. domestic poultry.
There just seems to be quite a bit of research describing the importance of coordination between the HA and NA segments of the Type A viruses. So, while there may not be a trade of exact genetic material from one segment to another as in non-homologous recombinations, the chemical affects may be similar with changes or mutations to compensate for either the loss or gain of amino acids in the HA and NA. For example:
Functional balance between haemagglutinin and neuraminidase in influenza virus infections
Ralf Wagner 1, Mikhail Matrosovich 1 2, Hans-Dieter Klenk 1 * 1Institut für Virologie, Philipps-Universität, 35011 Marburg, Germany 2M.P. Chumakov Institute of Poliomyelitis and Viral Encephalitides, Russian Academy of Medical Sciences, 142782 Moscow, Russia
Abstract Influenza A and B viruses carry two surface glycoproteins, the haemagglutinin (HA) and the neuraminidase (NA). Both proteins have been found to recognise the same host cell molecule, sialic acid. HA binds to sialic acid-containing receptors on target cells to initiate virus infection, whereas NA cleaves sialic acids from cellular receptors and extracellular inhibitors to facilitate progeny virus release and to promote the spread of the infection to neighbouring cells. Numerous studies performed recently have revealed that an optimal interplay between these receptor-binding and receptor-destroying activities of the surface glycoproteins is required for efficient virus replication. An existing balance between the antagonistic HA and NA functions of individual viruses can be disturbed by various events, such as reassortment, virus transmission to a new host, or therapeutic inhibition of neuraminidase. The resulting decrease in the viral replicative fitness is usually overcome by restoration of the functional balance due to compensatory mutations in HA, NA or both proteins.