"Laboratory tests from 70 patients are examined, of which eight patients have died. Total is the mutation found in five of the patients. Two of them are dead, while the other three have been hospitalized with serious illness in intensive care units.

The new mutated virus thrives further down the respiratory system than the original. It shuts down the lungs of patients, which means more severe disease than the original virus, which first affects the throat and upper respiratory tract.

Since the new virus in the lungs and is only detected in patients who have been admitted to hospital, experts expect that it is less contagious than has affected most who are infected so far."
Source: http://www.recombinomics.com/News/11200902/Norway_225.html

Quote above (translated from Norwegian) has Geir Stene-Larsen from the NIPH reporting on the two flu deaths, part of a worrying mini-epidemic of the H1N1/09 Mexican Swine Flu in Norway.

The Norwegians have found, as now acknowledged by the World Health Organization, that both patients were infected with a mutated variant of H1N1/09 known as D225G. It is a H1N1 version first reported in the Ukraine, with low contagion but extreme virulence, if this bug hits you, you’ve got yourself one hell of a whopper!



Distinctive features of H1N1/D225G Ukrainian Swine Flu:


- The virus directly attacks the lungs, causing swelling and hemorrhage. Observed symptoms include progressive over 38C temperatures, breathing difficulty, a dry cough producing blood, with X-ray showing destruction of lung tissue starting in the lower lungs. Time from onset of symptoms to death was 4-7 days.


- Post mortems showed lungs were blackened, as if burnt, perhaps related to lung hemorrhage.


- Both the D225G marker, a socalled ‘domain changing receptor’, and the symptoms listed above seem to link the Ukrainian variant to the Spanish Flu Pandemic of 1918.



Cases of H1N1/D225G have been reported in Brazil, China, Japan, Mexico, Ukraine, and the United States. As to mechanism for spread, spontaneous recombination of the H1N1 virus is suggested, that is, if you contract H1N1/09 it could itself acquire the D225G marker, and like totally ruin your day. A far worse possibility is that the Ukrainian flu has been spreading across large distances using human to animal to human, or even human-human transmission. (That’s a secondary pandemic, folks.)
Sources:
http://www.physorg.com/news177945959.html
http://thebirdflupandemic.com/archives/con...train-spreading



My position on the H1N1/D225G news, is that we are at risk from a secondary pandemic, by a highly virulent mutation of H1N1/09 (=mexican swine flu). It will be vital imo to determine if the available vaccines are effective against the new Ukrainian variant. And to find out how it spreads.



Debate questions:


Do you think the fatalities in Norway by H1N1/D225G predict a risk of a secondary swine flu pandemic?


Are you convinced by the linkage to the 1918 Spanish Influenza. Please explain why.


Using facts available to you: Make a prediction for H1N1/09 vaccin effectivess against the mutated Ukrainian flu strain.



Nighthunter

Do you think the fatalities in Norway by H1N1/D225G predict a risk of a secondary swine flu pandemic?

There isn't enough evidence yet to answer. But the fact that this has been detected "only in patients who have been admitted to the hospital" and "experts expect that it is less contagious" and has only effected those "who are infected already" so far, would indicate (to me) that this is an opportunistic infection for individuals already immunocompromised. Immunocompromised people contract all sorts of illnesses, to include cryptococcus neoformans. This black mold can migrate to the brain and has all kinds of awful implications, way beyond the symptoms mentioned in the article above. It's spread by pigeon guano, and is pretty much everywhere you see pigeons (I suppose the WHO should offer a warning to visitors of Venice, perhaps traveler restrictions are warranted?).

There's likely no way for anyone here to make any knowledgeable hypothesis as to whether or not the H1N1 vaccine will have any level of cross-effectiveness for this "less contagious" disease. I do believe that some day there will be a vastly deadly influenza strand that spreads with efficacy and leaves many many dead. When that happens, we won't have to rely on obscure events reported from some portion of the Ukraine.

From my perspective, I don't believe in superfluous vaccinations any more than I believe in superfluous antibiotics. Marginally effective antibiotics are now generally discouraged (unless warranted necessary), and I'm not sure why marginally effective vaccinations aren't discouraged (unless warranted as necessary), for the same reasons. But that's just my opinion.

Do you think the fatalities in Norway by H1N1/D225G predict a risk of a secondary swine flu pandemic?
The scientific knowledge needed to predict such risk (and that would include virology, infectious disease, pulmonology, and community health) based on the report cited in the original post is way over my head. I'd like to know the credentials of anyone here making such predictions.


Are you convinced by the linkage to the 1918 Spanish Influenza. Please explain why.
The only relevant evidence I can find in the cited material from the original post is this description in an unattributed article on the "Bird Flu Pandemic" site (which seems to be a site devoted to scaring people enough to buy all the vitamins, herbal supplements, essential oils, emergency food supplies, and face masks they sell):

One doctor in Western Ukraine was quoted as saying the following about what the lungs of people who have died from this flu look like....

"We have carried out post mortems on two victims and found their lungs are as black as charcoal. They look like they have been burned. It’s terrifying."

This frightening thing is that these reports sound chillingly similar to descriptions of how people died from the Spanish flu back in 1918. That horrific flu outbreak killed somewhere between 50 and 100 million people worldwide, and it is regarded as the worst flu pandemic in modern times.

One unnamed author on a decidedly non-scientific site quotes one unnamed physician in Ukraine and thinks it's "chillingly similar," all the while trying to sell you stuff that would make sense to buy only if you agreed that it's chillingly similar ...

So, no. I'm not convinced.



Using facts available to you: Make a prediction for H1N1/09 vaccin effectivess against the mutated Ukrainian flu strain.
According to the sources provided (see the second link in the original post), this mutation was found in "Brazil, China, Japan, Mexico, Ukraine, and the United States, as early as April." That tells me it's a variant that was already out there when the vaccine was produced, not a mutation that has taken place since.

I see no evidence in the OP, and I have no other facts at all, to help me predict whether the vaccine will be effective against this strain. I encourage anyone having facts relevant to this question to go ahead and post them.


edited to add:

From a link found on the first page linked to in the OP:

All H and N sequences [from the Ukraine strain] are typical for H1N1, as indicated in early WHO announcements. There are no large changes. Additional gene segments have been deposited from a subset of these isolates (but not analyzed below). There are silent changes that are in all or most Ukraine sequences, but the only HA polymorphism was the receptor binding domain change, D225G. This polymorphism was in the three lung, as well as the one throat sample. It was not in the nasopharyngeal washes or the isolate grown in MDCK cells suggesting the D225G may have a tissue tropism component and may allow for high levels of virus in the lung.

http://www.recombinomics.com/News/11180903/Ukraine_D225G_Lung.html

Anyone able to briefly explain in layman's terms the significance of "silent changes," "HA polymorphism," "receptor binding domains," "tissue tropism," and "MDCK cells"??






There are significant differences in the modes of action of vaccines vs. antibiotics. These differences answer your question.

Antibiotics (which are much more akin to antivirals like Tamiflu and Zovirax than they are to vaccines) only work for the period of time you are taking them. Vaccines are given once, and create a very long-lasting effect mediated by the body’s own immune system. Also, vaccines are very specific, whereas many antibiotics are broad-spectrum, affecting not only the target but many other bacteria as well.

Thus, antibiotics are prone to misuse (people who take them only until they feel better, instead of taking the full course), and overuse (in cases where infection is possible or suspected, instead of only in cases of confirmed and identified bacterial infection), while vaccines are not.

Misuse, as described above, leads to many surviving bacteria (the bacteria that were least susceptible to the antibiotic), and therefore to drug resistance. Vaccines are not susceptible to this kind of misuse.

Overuse of antibiotics has the potential effect of creating drug resistance in all affected bacteria in the body, even where no susceptible infection existed in the first place. Vaccines can’t be overused in this way because they are so specific. That is to say, if you get vaccinated needlessly (you never come into contact with the targeted virus), no other viruses are affected in any way.

Although I agree with the above regarding antibiotics, I still don't understand why marginally effective vaccinations (speaking of the flu vaccine specifically, really) wouldn't effect influenzae viruses in a similar manner. They are "broad spectrum". Not in the way that antibiotics can be broad spectrum, but each vaccination targets different froms of influenza viruse. Every year, the recipe changes to try to adapt to a new variation of strand. The viruses mutate so fast, the vaccines cannot keep up and sometimes they are marginally effective other times not at all. Sometimes the recipe is very good and it fits the target precisely. but either way, it's a 'broad spectrum' formula with marginal effectiveness on a target that is designed by nature to change itself on a dime, again and again in order to adapt to its host and escape the defenses. So the claim of 'specificity' above is false for influenza vaccines. That's why we're discussing issues of 'cross-effectiveness' here and hoping the H1N1 vaccine might cover the new strand as well as the old.

Thought I'd add, I really found the site you linked to above interesting!
I've heard of some of the above and looked up the rest (didn't know what HA was, or couldn't recall, if I had known once upon a time). MDCK cells are a medium for culturing viruses (there are many types they use for mediums to grow: mouse, sheep, dog). Silent changes refer to changes in the amino acid sequence that don't change the protein it makes (it codes for the same thing, IOW). Tissue tropism is an affinity for certain tissue...sounds as though the virus can grow only in lung tissue, not in the cell medium they use in the lab, and it doesn't show up in nasal swabs for H1N1 either. HA is the binding site where the influenza (stands for hemagglutinine, or somesuch) hooks on to the cell it invades (in order to multiply), so I think the above means that there was a change in the code where the receptor hooks on that makes it 'take' to lung tissue, more than other sites typical for influenza infection.

Reading further on that site, it sounds as though the above altered strand would show false negatives for H1N1 in routine screening, and can only be assessed from a lung biopsy at this time.

Yes. As vaccinations make certain strains of the influenza virus less successful, other strains come to the fore ... but not because these other strains are resistant to vaccination, per se. These other strains have merely escaped immediate detection by our immune systems by virtue of not having been vaccinated against. Our immune systems have unlimited capacity for recognition and destruction of viruses which have been presented. As new ones crop up, all we have to do is create a new vaccine. (Which is exactly what happens every year with the seasonal influenza vaccine.)

In the case of antibiotics, bacteria develop resistance to the very mechanism of action of the drug, then we have to look for whole new ways to disrupt the bacteria's activity and reproduction.



Cool. Thanks.

What does this tell us in terms of the effectiveness of the H1N1 vaccine against the D225G mutation?

I don't think the above tells us much if anything about the level of cross-effectiveness (HA is the primary site for immune response, so a change might be problematic, and apparently this form is difficult to culture in the lab). But I just found a more recent article on the same site that indicates the vaccine probably does cover the new varient.

H1 is the identified for the outside of the virus while N1 is the material from the inside of the influenza virus. Once exposed to the H1 outside an individual should have protection against other H1 influenza.

Vaccinations do have disadvantages. Vaccines are made to stimulate the immune system. The immune system is stimulated to increase response to specific antigens. When the immune system has been stimulated it is less likely to respond to new stimulus for a period of time. In the case of vaccinations this is usually around two weeks. Vaccinations leaves a person more susceptible to infection for this period of time. Give two different vaccines at the same time and the body will respond to both vaccines. Give the exact two a week apart and the second vaccine will generate a diminished response. In the face of a disease outbreak, vaccinations may provide better protection for some while at the same time increasing the numbers who become infected due the suppressed immune systems.

Multiple vaccinations may have another deleterious effect which is more of a theory than a known truth. There is a concern than too many vaccinations overstimulates the immune system to make an individual more likely to have metabolic problems such as autoimmune disease or inflammatory disease. There may be other problems which are more likely to occur: Alzheimer's, autism, etc.. There is a genetic factor, a predilection towards stronger inflammatory reactions involved. Even cancer may be more likely to occur in those individuals with an 'overstimulated' immune system due to vaccinations. I put overstimulated in quotes as it may not be so much the stimulation as a diversion of the immune system to respond to some insults to the detriment of the ability to respond to other insults.

It is not just vaccines which stimulate the immune system. The timing and exposure to various proteins entering our bodies does alter how and what is developed as we grow.

Though the specifics of stimulating the immune system are not understood the current observations should be enough to give one pause before using vaccines when the benefit is marginal.

.

Yes and information from the 1918 Pandemic indicates that people who got what is believed to be a milder version of the H1N1 earlier that year did not get nearly as sick (or die) from the deadly strain.




Well some of this is theory at best. Our immune systems are designed to fight infection, parasites and viruses constantly. Most kids in grade school (and their parents) get sick a lot.

Daycare is even worse. We had two kids in daycare and my wife and I were sick for what seemed like half the time.

Most vaccinations are given at least 2 weeks apart and if you are sick you have to come back later.

Clearly the risk of the disease (H1N1) is far higher than any other possible side effect.

"There is a concern ..."

Who is expressing this concern?




Same question: Who is indicating "There may be other problems ..."?




Same question: Who says cancer "may be more likely to occur in those individuals with an 'overstimulated' immune system due to vaccinations"?



Same question: Who is indicating "the specifics of stimulating the immune system are not understood the current observations should be enough to give one pause before using vaccines when the benefit is marginal"?

My most recent exposure to this was an immunologist from the University of Wisconsin, Madison WI. I do not recall his name. He was presenting for a few hours at a meeting in Kentucky.

What was the date of this presentation, where exactly was the meeting, and who sponsored the event? I'll look him up.

Thanks for all your responses, I'm reading through them them with interest right now. But Maybe Maybe Not's query makes a lot of sense (I'm a layperson too when it comes to viral genetics) so I'll address this one first.

The next explanations are open to further correction or refining.



SILENT CHANGES

Term refers to gene mutations that sofar generally are seen to have no influence on how proteins are created. Also known as 'Synonymous Mutations' and 'Silent Mutations' they should not affect changes in a organism (/virus). One effect of silent changes recently has been discovered: they can affect the amount of proteins produced.
Source: http://www.sciencedaily.com/releases/2009/...90409142258.htm



RECEPTOR BINDING DOMAINS

It's a part of a proteine enabling it to replicate (=copy) or recombine (new version). In the case of a virus it may signal changes in how it will 'express', that is the way in which a human/animal host gets sick.
Source: http://en.wikipedia.org/wiki/DNA-binding_domain



POLYMORPHISM

Term meaning more versions of organisms of the same species (of the H1N1/09 Mexican Swine Flu virus, in this topic) exist.
Source: http://www.thefreedictionary.com/polymorphism



TISSUE TROPISM

Term refers to specific tissues/cells of a host targeted by a virus, plus how these tissues are affected. In our case, the new Ukrainian H1N1/D225G strain under investigation is reported to attack the lungs, starting a destructive process in the lower lungs. The reported changes in lung tissue include hemorrhaging, swelling and (at post mortem) blackening of the lungs.
Source: http://en.wikipedia.org/wiki/Tissue_tropism



MDCK CELLS

Stands for Madin-Darby Canine Kidney cell. In 1958 researchers S. H. Madin and N. B. Darby reconstructed the 1918 Spanish Flu virus from the kidney tissue of an adult female cocker spaniel infected during the 1918 epidemic. The dog's tissue sample was taken 18 hours after infection. MDCK cells have been studied to explain the deadly characteristics of the Spanish Flu.
Source: http://en.wikipedia.org/wiki/File:Reconstr...h_Flu_Virus.jpg


That's as fast as I can Google for now...






Good points, Mrs. Pigpen. I'd like to add for additional focus on the H1N1/D225G spread, that seeing this marker only in (very sick) patients, already given intensive care in hospitals, is consistent with low contagion. Simply, it maybe hard to catch this one bug at this point in time.





Maybe Maybe Not,

This goes to the severity/virulence of the Ukrainian epidemic, involving Acute Respiratory Illness: WHO related links

- http://www.who.int/csr/don/2009_11_01/en/index.html
- http://www.recombinomics.com/News/11030902...aine_Hemor.html

Nighthunter,

While I appreciate your definitions of the terms silent changes, HA polymorphism, receptor binding domains, tissue tropism, and MDCK cells, I still don't have enough scientific knowledge to apply them meaningfully to the situation with the D225G mutation or provide any legitimate speculation on the effectiveness of vaccination.




... thus confirming the WHO's (and every other reputable scientific and medical organization's) recommendations regarding mass vaccination.