Studies Spot Obstacle to Human Transmission of Bird Flu

WEDNESDAY, March 22 (HealthDay News) -- Two new studies help explain why human-to-human transmission of the bird flu virus has so far not happened -- and might not happen in the future.

Both reports found the H5N1 virus prefers to settle in cells deep within the lungs, rather than in the upper respiratory tract, as happens with human flu strains.

That's important because "most of the coughing and sneezing that transmits flu is going to be from the upper respiratory tract, and not way down in the lower respiratory tract," explained Dr. Arnold S. Monto, a professor of epidemiology at the University of Michigan School of Public Health. "So, unless you have relatively close contact, you're not going to have much virus get out."

more....

http://www.forbes.com/lifestyle/health/feeds/hscout/2006/03/22/hscout531699.html

As we speak someone is probably somewhere injecting more chickens with the dreaded virus...and a few cats.

to harm us. I've no doubt that labs are cooking up super virus...just to check this out you know.

Of course, it might mutate it's surface in such a way that it binds better to the upper respiratory tract. But then, if that happens maybe it will become much less lethal. Assuming it's current lethality has something to do with it's preference for "deep" lung tissues.

The hack job Seigal who acts like he knows something about virology states
"The finding also helps explain another phenomenon: The fact that many people have tested positive for exposure to H5N1, but have never developed actual infection or illness.

"They didn't have bird flu, but they made antibodies to it," explained Dr. Marc Siegel, a clinical associate professor of medicine at New York University School of Medicine and author of Bird Flu: Everything You Need to Know About the Next Pandemic.

According to Siegel, it appears that these people may have encountered H5N1, but because the virus failed to reach the lower lung, it never gained a "foothold" for infection."

See http://www.fluwikie.com/index.php?n=Science.Seroprevalence for a debunking of this statement



From the cnn article on the same subject
http://www.cnn.com/2006/HEALTH/conditions/03/22/us.birdflu.ap/index.html
But the virus could change that behavior by genetic mutation, taking a step toward unleashing a worldwide outbreak of lethal flu.
snip
Robert M. Krug of the University of Texas at Austin called Kawaoka's work an important observation, and said that if H5N1 begins to use the human virus docking site "we've got a lot to worry about." It's not clear whether that would be enough to produce a pandemic germ, he said.

James Paulson of the Scripps Research Institute in La Jolla, California, stressed that other viral factors may be important in human-to-human transmission. But he said that once the virus has a foothold in a person, regardless of where it is in the respiratory tract, it may mutate to gain the abilities it needs to start spreading among people.

why it was more lethal on the young than on older people who get the bird flu. They claim the difference is due because of the different hygiene habits between the two, but I think it may have to do with the fact that people over 40 may have been exposed to something very similar at one time and have antibodies for it.

Some speculate that previous exposure to the N1 portion of the strain may provide some immunity.



http://www.summitdaily.com/article/20051120/NEWS/111200017

have the immunity are disposable? Gee, and here I thought they were the ones that were suppose to pay for our wild expenditures.

No it was not Siegel, if you read the snip, and go to the link it was Dr. Edwin Kilbourne who has been a flu researcher since the 50's...

ANd I don't see any value judgement in the statement. He is just making an observation.

"I am less concerned about all this business than others because I think the N1 immunity that everyone in this population has now ... may well mitigate the effects," he said. Emphasis mine.

I did make one major conclusion which may well be a stretch. That the N1 immunity is what is keeping the over 40's mortality rate low. I'm assuming that is why they are faring better than the under 40s. And if they are connected, N1 immunity and low mortality then it's evident that not everyone in the population has it.

Again, this is assuming that it's the immunity which is making the difference and not behavior patterns.

is if it is due to cytokine storm which affects those with the most robust immune systems which would be the young and would be just like the 1918 flu did. I hope it IS that we have some immunity though. That would be awesome and the best scenario.

And if efficient spread among humans requires infection higher up in the respiratory tract, wouldn't it also lead to the conclusion that it would necessarily be less deadly in that case? Wouldn't that also bolster the case that the virulence of the 1918 virus was due to the immobility of sick soldiers crammed together in trenches and hospitals, where they were repeatedly exposed to the virus, affording more of a chance for severe infection?

Also, if it is that difficult to get sufficient virus deep into the lungs, wouldn't it make sense that young people are disproportionitley(sp) likely to get it, as they would be more likely to be doing the work around fowl that would lead to that.

Sorry my spelling is getting worse as I get older

It has been many years since I was a nurse.If it affected mostly the upper resp tract at first it could easily move into the lungs if it was virulent enough.We get plenty of pneumonias from seasonal flu as it is. God knows I have suctioned mucous out of a gazillion people in my time with terrible pneumonias.

Having it in the upper resp tract would make it easier to spread. There is a temp difference where the deep lung is closer to a chickens body temp. I think that is why it likes the deep lung tissue now. Plus so many of the afflicted right now are young children and they have not developed their resp system fully. I don't know if that is a factor.

Cytokine storm is being seen in the cases now.. affecting multiple organs, and I have read literature that speaks of thrombocytopenia, DIC, and of whacked out white blood counts in people who are getting it now. The literature from the 1918 flu seems to back up the claim that cytokine storm was what caused it to be so deadly if you go by the symptoms that people had in the books that cover the era so it would fit. I don't see why it could not keep it's virulence and still mutate to be comfortable in the upper resp tract and be more easily spread. It does not seem to only affect the resp tract.

Until we see some good reports on the medical aspects of the people who have come down with it now it is hard to say. What little I have read is pretty awful re sxmptoms.I am not sure if having it in the upper resp tract has any correlation to the virulence of it but would definately make it easier to spread. I am really tired so I am sorry if this does not make much sense.

There is a lack of published data. And the data cited about a lack of antibodies among health care workers, cullers etc is not conclusive. These are the people who would be taking the most precautions. No comprehensive seroprevalence studies have been done. Looking at this chart it looks as though there have been under 200 tested from the population that has been most affected so far. Rural families with backyard poultry. Also, this chart does not show no asymptomatic cases. If I am reading this right 10% of the poultry workers tested in Hong Kong in 1997 showed asymptomatic exposure to the illness. That is significantly more than those that became sick.

Please provide credible evidence that Dr. Siegel is a "hack."

And, the reason this is news today because of two published studies. While this was generally expected to be the case I am not aware of any study of the magnitude being published before. And that does not alter the conclusion that the virus will have to make a significant mutation to go H2H.

The fact that these kind of studies are being done is a good thing. It will speed up detection of any mutation, and may calm some of the unwarranted panic being generated by the alarmist press.

There was also a study that came out on cambodia today which said the same thing. I can dig up the link if you want.Still waiting for the studies done in turkey though. I think those will give some good info. Seigal is a hack. He is selling his book.
Effect measure had a good rant about him recently.
http://effectmeasure.blogspot.com/
Scroll down to
The Siegel has (crash) landed
exerpt
"Siegel, like Orent, has made a career out of being a contrarian. Not always a bad thing, but, like his criticism of Webster (who knows more about flu than Siegel will ever know), it should have some basis. Siegel says Webster knows about test tube virology but not about how the virus will behave in the real world. I don't know what the basis for this claim is, but I can tell you Siegel is no epidemiologist. I knew him many years ago and he is a dilettante who now hawks his books describing how everyone else is wrong. The pot calling the kettle, etc."

I have been reading what Seigal writes for a good while now I cringe whenever I see his words.

It seems to me Webster is making the unsubstantiated comments...giving odds on a random process...anyone who puts specific odds on a viral mutation is practicing bad science.

I have seen Revere's comments before...he seems to be a debunker debunker...I am very skeptical about someone who needs to keep his identity secret. It calls his credentials into question.

As to Siegel, he does not deny the potential of the virus to mutate, but simply takes the position that a mutation is not inevitable, nor can one ascribe a specific timeline of when it will mutate or if it will happen. He is a strong advocate for development of new vaccination production techniques, which in any pandemic is what is going to be needed.

As to the study, do you dispute the Hong Kong results ?

The virus has mutated all over the place since then and I don't know if that makes any difference. Until the recent studies are published there is no way to say one way or another, but from the site I posted it does not look good. Do you deny the info there? What do you make of it?

I also have to wonder if the WHO has these results and they show a high asymptomatic rate, why they are not putting the info out there? It sure would be reassuring to hear that instead of statements like today
where they were almost begging countries to get ready. I sure hope you are right but I have not seen much evidence lately that would give me reassurance.

Re the Revere's :
"The Editors of Effect Measure are senior public health scientists and practitioners. Their names would be immediately recognizable to many in the public health community. They prefer to keep their online and public lives separate to allow maximum freedom of expression. Paul Revere was a member of the first local Board of Health in the United States (Boston, 1799). The Editors sign their posts "Revere" to recognize the public service of a professional forerunner better known for other things.


I have found their info to be progressive and informative in analyzing public health issues. They definately have a background set in science. I need to go to bed. I have my first root canal tomorrow and I am terrified!

I've had 2 now and they really do not hurt. First, the nerve is dead which is why they have to do it. And the novocaine really kills any pain. I found it no worse than getting a cavity filled except it took longer. The only pain I had was my jaw was sore from holding my mouth open for so long.

I don't think WHO has any data, which is the problem I think. They have been derelict in conducting these studies if you ask me. I don't deny the statistics in the studies on the website...but they are so small that I'm not sure any conclusion can be drawn. ANd I don't see any done of rural farmers.

Good luck tomorrow...it will be way easier than you think!!!

It did hurt after the novocaine wore off but not too bad.
I found this from pro med and thought you might be interested.


"I looked up the articles that were cited as implying that approximately 35
million Chinese citizens have antibodies to H5N1 influenza.

The article referenced in the RFI is Palese, P. 2004. Influenza: old and
new threats. Nature Medicine 10(12): S82-S87. This article states that:
"...seroepidemiological studies conducted among the rural population in
China suggest that millions of people have been infected with influenza
viruses of the H4-to-H15 subtypes. Specifically, seroprevalence levels of
2-7 percent for H5 viruses alone have been reported...".

The reference given for this claim is Shortridge, K.F. 1992. Pandemic
influenza: a zoonosis? Seminars in Respiratory Infections 7(1):11-25. This
paper reports seroprevalence ("presumptive antibody detected by single
radial hemolysis using antigenic material from avian virus only") of 13 HA
subtypes (H1 to H13) in 4 human populations. H5 antibodies were detected in
2 percent of samples from the Pearl River Delta (n=400), 7 percent of
samples from Jiangsu Province (n=300), 2 percent of samples from Taichung,
Taiwan (n=150), and 0 percent of samples from Urban Hong Kong
(n=100). There are no corresponding data reported for N subtypes, so a
conclusion that these antibodies indicate prior presence of H5N1 in the
human population is unfounded, and there is no support for an estimate of
35 million Chinese citizens with H5N1 antibodies.

This same paper reports the results of a study of ducks (8737), geese
(1353), and chickens (1708) originating from southern China and Hong Kong
over a 5-year period (Nov 1975-Oct 1980) at a poultry-dressing plant in
Hong Kong. Of 586 viral isolates obtained from this survey, 23 had HA
subtype H5: 22 of these isolates were H5N3 (one from a goose, and 21 from
ducks), and one isolate was H5N2 (from a duck). No H5N1 virus was found."

--
Juliet Pulliam
Dept. of Ecology & Evolutionary Biology
Princeton University
Princeton, New Jersey 08544
<pulliam@Princeton.EDU>

This is something I hadn't ever heard...35 mil. It's hard to tell but it looks like these studies were done well prior to the 1997 outbreak.

Glad you got through the root canal. Personally, I am pretty dentophobic...so I can sympathize!

It's not a human pandemic virus yet (and might never be one) precisely because of its particular combination of transmissibility parameters-- but it's those same parameters that will change if it does enter a human pandemic stage, e.g. perhaps an acquired ability to use human upper respiratory cell flu docking receptors. This is a silly news report-- it misses the point entirely.

by the presence of tuna and powdered milk under one's bed.

I saw his toothy smiling face on the t.v. yesterday and with "bird flu" flashing on the screen and I thought to myself, what the hell is Forbes doing giving advice on bird flu?

we are learning an enormous amt about viruses or is it viri? because of this and that is a good thing.

will come out and slam this report.

Chicken of the Sea stock has plummeted.

Now, this is good news, but I wouldn't expect it to get too much airplay since "news" these days is meant to scare us and sell product more than anything else.

Mercury exposure AND bird flu.

That's the exact reason why if H5N1 were to combine with normal flu that it could spread so fast. In other words a repeat of 1918.

the people WHO DIED of it.

Avian flu: Influenza virus receptors in the human airway

Avian and human flu viruses seem to target different regions of a patient's respiratory tract.

Although more than 100 people have been infected by H5N1 influenza A viruses, human-to-human transmission is rare. What are the molecular barriers limiting human-to-human transmission? Here we demonstrate an anatomical difference in the distribution in the human airway of the different binding molecules preferred by the avian and human influenza viruses. The respective molecules are sialic acid linked to galactose by an alpha-2,3 linkage (SAalpha2,3Gal) and by an alpha-2,6 linkage (SAalpha2,6Gal). Our findings may provide a rational explanation for why H5N1 viruses at present rarely infect and spread between humans although they can replicate efficiently in the lungs.

...