About
About Flu Wiki
How To Navigate
New? Start Here!
Search FW Forum
Forum Rules
Simple HTML I
Simple HTML II
Forum Shorthand
Recent Active Diaries
RSS Feed

Search




Advanced Search


Flu Wiki Forum
Welcome to the conversation Forum of Flu Wiki

This is an international website intended to remain accessible to as many people as possible. The opinions expressed here are those of the individual posters who remain solely responsible for the content of their messages.
The use of good judgement during the discussion of controversial issues would be greatly appreciated.

Non-pharmaceutical Interventions - Lessons from 1918

by: SusanC

Wed Apr 18, 2007 at 21:21:12 PM EDT


( - promoted by Bronco Bill)

What do we have today that we didn't have in 1918?  Hindsight!

Exploring 2 studies on efficacy of NPI in 1918
SusanC :: Non-pharmaceutical Interventions - Lessons from 1918
One unique feature of the pandemic of 1918 in the US was that mortality figures in different cities showed tremendous variations (up to 4-fold).  This now-famous chart shows the difference between Philadelphia and St Louis. 

2 recent studies published in PNAS analyzed the data from 23 cities in detail to determine if social distancing measures accounted for such differences, if so by how much, and what lessons we might draw for today.

The first one, Public health interventions and epidemic intensity during the 1918 influenza pandemic Hatchett, Mecher, and Lipsitch, compared the timing, number and type of interventions in 17 cities in relation to their peak and overall excess mortality rates.  In all, 19 different types of interventions were studied during the fall wave of 1918. 

First, a couple of (slightly) technical terms to explain: since we do not have actual data on how many people died as a result of the pandemic virus, one way to estimate the death rate in the population would be to use the excess deaths due to pneumonia and influenza (excess P&I deaths) compared to what the normal death rates would be during that time of the year.  ie we assume excess PID = mortality rate due to pandemic

Then, as the pandemic progressed, we can also measure the total no of deaths up to a specific time, ie cumulative deaths.  Thus, the CEPID (cumulative excess P&I deaths) becomes a measure of the total number of people who had died as a result of the epidemic up to that point. 
If we assume that the CFR remained the same, then CEPID is also a reflection of the AR (attack rate or no of people infected) up to whatever point we are referring to.

Finally, if we assume the epidemic unfolds initially in similar ways in different cities, we can also compare CEPID between different cities, and assume that the same CEPID would represent the same phase of an unmitigated epidemic wave. ie use the same CEPID as a measure of timing eg CEPID at 20/100,000 population would reflect the same point of an epidemic wave in different cities, and would be earlier in time than 30/100,000 population in whatever city you are considering.

OK, that's all the technical stuff you need to know.  Now onto the paper.

  1. In comparing the various parameters, the study showed that the strongest correlation was between the timing when interventions were introduced and lowered peak mortality.  (Now, that was painless, wasn't it?)  ie the earlier the set of interventions were implemented, the lower the peak death rate.

  2. Secondly, there was a correlation between the number of interventions and reduction in peak deaths. 

  3. These two in combination give the following result: cities with 4 or more interventions before CEPID reached 20/100,000, compared to those with 3 or less, had death rates of 65 as opposed to 146/100,000.

  4. A weaker correlation was obtained for total deaths, at 405 vs 551/100,000.

  5. Some interventions were effective, some were not.  Cities that closed school, theaters, and churches (often announced together) before CEPID reached 30/100,000  had peak deaths at 65-68 vs 127-146 /100,000 for those that didn't.

  6. Interventions that did not show significant correlations: closure of dance halls, other closures, isolation of cases, bans on public funerals, and making influenza notifiable.

  7. Some cities experienced second waves.  This gave some very significant insights. Cities that had the most effective interventions ie most reduction in peak, in the first wave were most likely to have bigger second waves.  They also tended to have them sooner than those that did not have very effective NPIs.  Most crucially, no city experienced a second wave while NPIs were in force.

What do these results tell us?

Multiple NPIs applied early, with the emphasis on early, were correlated with reduced peak mortality and flattening of the epidemic curve.

The benefits only applied while the NPIs were in force.  The epidemic came back when NPIs were lifted, and slowed down again if the NPIs were re-applied.

There was a smaller effect on reduction of total mortality.

Now, we shouldn't take researchers on faith.  So we should ask this question, how do we know that the differences in death rates were due to NPIs and not due to other factors such as differences in virulence either between cities or over time?

There are several indications:

  1. they removed any variations in death rates by dividing the peak deaths by the median death rates over the epidemic of that particular city, so that cities that might have had an exceptionally high or low death rates would have that effect canceled out in this `normalized' peak death rate, which, after the adjustments, still showed the same degree of correlation.

  2. Not all interventions resulted in reductions in death rates.

  3. The correlation between the stage of the epidemic ie CEPID was stronger than with the actual calendar date of the onset, showing the effects were not due to attenuation of the virus over time, even though some attenuation did happen by January 1919.

  4. The presence of second waves only in those cities with effective NPIs shows that the reduction in the first peak were due to reduction in transmission and no of cases, and not due to a milder virus.  Indeed, the most significant effect is that no second waves were observed in any city when NPIs were in force, which tells us that the second waves were caused by insufficient number of people having immunity in the city.

-------------------------------------------------
Onto the second paper, The effect of public health measures on the 1918 influenza pandemic in U.S. cities by Bootsma & Ferguson.  This one is rather more esoteric, but when de-constructed, is still fairly easy to understand and similarly fascinating.

The first thing is, they analyzed the data and came to more-or-less the same conclusion as Hatchett et al, that multiple `imperfect transient interventions' when applied early was correlated with reductions in peak deaths, and the strongest correlation was with the timing of intervention, ie earlier interventions gave bigger reduction in peak deaths.  There was also a weaker correlation with total deaths ie total epidemic size.

Having gotten an idea of what NPI's might do, the next thing they did was to take the historical data of how the epidemic unfolded in 1918 in the various cities, and use models of disease transmission and effects of interventions to try and predict what the outcome might have been, comparing the two to see how well the results fitted what actually happened.

The answer?  There was very good fit!  Showing that the correlations that we hypothesize as possible cause and effect were reproducible in a theoretical model, as the following example for St Louis shows.

The 1918 data is shown as purple crosses, the red curve is the predicted outcome from modeling, which in most cases fit the actual outcome pretty closely.  The dark green curve is what it would have been if there were no interventions, the horizontal light green lines show the timing of intervention, with the height of the line showing their effectiveness.  You can see when the interventions were started by looking at the beginning of the horizontal green line in relation to the epidemic curve.  Notice how for Philadelphia the actual outcome was worse than the model predictions and very close to the worst case scenario, ie no mitigation at all. 

In addition, the paper also explored some very important concepts.  In order for an epidemic to be over, there needs to be enough immunity in the population, ie herd immunity.  In theory, herd immunity is achieved when the proportion of people infected (ie AR) = 1-1/R0.  The 1918 fall wave in the US was estimated to have an R0 of 2, which in theory would have meant that the epidemic would stop when 50% of people were infected.  But, in reality, due to the time needed for those infected to acquire immunity, uncontrolled epidemics tend to overshoot, so that completely unmitigated epidemic would result in AR of 80%! 

Now, transient NPI's, as we said, result only in transient reduction of transmission.  When NPI's are very effective, the no of infections are so low that when the NPI's are lifted, there is still a large proportion of people without immunity, and the epidemic takes off again in an uncontrolled manner ie with overshoot, resulting paradoxically in an AR of say 65% (see chart above). 

In principle, the most you can hope for, in the absence of vaccines, is to achieve the baseline AR of 50%, and the way to do that is to maintain NPI's just sufficiently to have some ongoing transmissions that would build immunity, and maintain NPI's for long enough until 50% immunity is achieved, which could take a fairly lengthy period of interventions. 

Finally, using the models, the study estimated that in 1918, for those cities with the most successful NPIs eg St Louis or San Francisco, if they had been able to maintain their NPIs for however long it took to achieve herd immunity, they would have resulted in close to 40% reduction in total mortality, instead of the 10% (St Louis) or 25% (San Francisco). 

Translated to the 21st century, the question is not just whether we should use NPI's for mitigation, as they are so undeniably effective, but how long you can feasibly maintain them to obtain the optimum result.  One answer, if we cannot maintain NPIs for say 6 months, would have to lie in the much earlier availability of vaccines.

UPDATE

Part of the lesson for me is that if, in 1918, with none of this knowledge, and the NPI's were not implemented in a very systematic way nor for long enough, they could still reduce peak mortality by 50%, and overall mortality by 10-30%, how much total reduction can we achieve today with targeted approaches applied early and in an organized manner?  I would suggest that a reduction from say 50% AR to 10% AR over a 12-week school closure period is certainly feasible.  Which would buy us the time to ensure health services can cope, the infrastructure will hold up, and vaccines can be made as quickly as possible.

Tags: , , , , , (All Tags)
Print Friendly View Send As Email

Tradeoffs.
I have not had time to read these yet, so I am probably asking the 'instructor' for an answer I could find in the book - so apologies up front.

The CEPID (cumulative excess P&I deaths) is a measure of the total number of people who had died as a result of the epidemic up to that point.  So when you say

cities with 4 or more interventions before CEPID reached 20/100,000, compared to those with 3 or less, had death rates of 65 as opposed to 146/100,000

this is the death rate at the peak, or cummulative deaths per 100,000 through that peak point, correct?

And when you say

weaker correlation was obtained for total deaths, at 405 vs 551/100,000

this is the cummulative death rate through the end of the pandemic, correct?

It seems that one of the points that comes out of the last study in particular is that in order to build a fire-break in the form of 'herd immunity' we will need to allow the fire to burn while containing it to some 'acceptable level'. 

If the severity of the pandemic virus was not the differnce, then lives were saved because the systems could reach a higher percentage of the sick. By keeping the death rate lower during the peak of each pandemic wave, we hopefully would give our societal systems enough breathing space to reduce the total number of people that die. 

A 20% reduction in total mortality is still huge, and gets more important as the CFR goes up higher than the 1918 experience that was used in the model - anywhere near what H5N1 has today.  But another factor to consider is that our 'systems' are much more effective at keeping people alive than they were in 1918.  So the greater portion of our sick that can get acces to those systems, the higher impact we will see.

In other words, in 1918 given their limited resources and knowledge, getting into a hospital might only save you half the time, where now it might save you 75% of the time. 

As you point out, the cost paid for this reduction in total mortaliy is keeping the fire going longer.  It seems like St Louis was at around 30/100,000 to 55/100,000 deaths for about 50 to 100% longer than Philidelphia had for that wave.

But the long-term resilience question you pose can be addressed only if we can hazard a guess at the performance of the subsequent waves. 

The recovery after each wave will get tougher and tougher, with more time needed and less time available. The lower stress on systems will begin to have negative effect if left in place for extended periods. 

Do we know what was the cummulative pandemic (multi-wave) duration  for these two cities - adding up the total number of days during which the pandemic was active in the city above an identifiable level.  Not start to finish, but cutting out the days between waves.  I would be surprised if each wave looked like the one shown at the top for both cities. 

Based on what the reports said, I also wonder whether the NPI could result in less time between 'waves' as loosening the NPI would lend fresh air to the banked fire.

Interesting studies.  Interesting questions they raise.

ITW(Joel J)
Courage is resistance to fear, mastery of fear - not absence of fear.
- Mark Twain
 


First, your 2 questions
1.  65 vs 146 was peak weekly deaths per 100,000 population, not cumulative

2. 405 vs 551 was cumulative or total deaths per 100,000 population during the study period of September to Dec 1918, not the whole pandemic.

Let me clarify some terminology here.  These 2 studies were focused on the period from September to Dec 1918, ie what we would normally call the 'second wave' of the pandemic, the first being in spring of 1918, and the third being spring of 1919. 

In these studies, within this 'second wave', there were 2 peaks for some cities.  So the discussion of first and second wave within these 2 studies refer to the first and second PEAK of the second pandemic wave.

It seems that one of the points that comes out of the last study in particular is that in order to build a fire-break in the form of 'herd immunity' we will need to allow the fire to burn while containing it to some 'acceptable level'.

Yes, the lesson here is that pandemics are ugly realities, and we can't expect to stop them from happening.  Which also means that total SIP can only really be 'reserved' for the most vulnerable.  If a large segment of society goes total SIP, and there is overall 'too much' social distancing, then once you stop you would get the return of the uncontrolled epidemic with overshoot, and the result may not be optimum, as is shown by the second study (chart with 65%AR)

If the severity of the pandemic virus was not the differnce, then lives were saved because the systems could reach a higher percentage of the sick. By keeping the death rate lower during the peak of each pandemic wave, we hopefully would give our societal systems enough breathing space to reduce the total number of people that die.

Yes and no.  To be absolutely accurate, if we assume there was no difference in severity at all, that would have to include no difference in outcome due to better care.  However, intuitively one would like to think that better care resulted in better survival, but we don't know that from the data. 

BUT, we haven't factored in any deaths from secondary consequences yet, and these would most likely be more significant in the interconnected world today compared to 1918.  In other words, even if we cannot affect the CFR directly by NPI, we can still reduce the secondary deaths and the systemic stresses if we lower the peak.

A 20% reduction in total mortality is still huge, and gets more important as the CFR goes up higher than the 1918 experience that was used in the model - anywhere near what H5N1 has today. 

Yes, a 20% reduction is huge.  I would buy a 10% reduction in overall deaths any day!

As you point out, the cost paid for this reduction in total mortaliy is keeping the fire going longer.  It seems like St Louis was at around 30/100,000 to 55/100,000 deaths for about 50 to 100% longer than Philidelphia had for that wave.

I don't know that we can quantitatively compare in that way, but the bottom line is that the speed of accumulation of new cases, ie the epidemic slope, in an of itself is a stressor to the system.

But the long-term resilience question you pose can be addressed only if we can hazard a guess at the performance of the subsequent waves.

These studies and this current discussion are really strictly speaking only focused on discovering whether NPIs reduced transmission.  Again, reducing transmission is always better than uncontrolled outbreaks (see Ferguson above on 50% vs 80% AR), but the overall outcome would depend on the sum total of what you are measuring: total deaths due to the virus?  plus secondary deaths?  plus economic and social consequences?  These are tougher questions to quantify, but generally, still if the effect of an epidemic is to cause all these negative consequences, then slowing down the outbreak up to a certain point again intuitively should give you better results in all the parameters.

Do we know what was the cummulative pandemic (multi-wave) duration  for these two cities - adding up the total number of days during which the pandemic was active in the city above an identifiable level.

Well, I suppose one could count that, I don't think this was done in and of itself here.

Based on what the reports said, I also wonder whether the NPI could result in less time between 'waves' as loosening the NPI would lend fresh air to the banked fire.

Referring to the first part of my comment here, this was less time between 'peaks' of the same September to December 'wave'.  ;-)



All 'safety concerns' are hypothetical.  If not, they'd be called side effects...


[ Parent ]
asymptomatic infection
almost everyone was exposed(=infected , including asymptomatic)
in 1918/19, I read.

There was already considerable flu in 1920 and following years,
how did St.Louis vs. Philadelphia handle these ? The charts chould
be longer than a few months.

So the trick was to be infected in the first wave.
Or to be infected late in the 2nd wave, when the CFR had fallen.

Or to be infected asymptomatically.
How does asymptomatic infection happen ?
Too small initial load ?
So would it help to expose yourself several times
to small amounts of viruses - thus building immunity
while not becoming symptomatic ?

would it had been a good strategy to restart the first-wave-virus
infection deliberately in Oct.1918 to gain immunity against
wave 2 ?

ask experts for their subjective
panflu death expectation values
and report the replies


I think you are assuming ;-)
that we have more ability to control the specifics of who gets infected than the reality would be!  Plus, there is no guarantee which way the CFR would go.  Later waves could be milder, or they may not be. 

In Oct 1918, I don't think there was any need to 're-start' the virus infections.  All you need was to lift interventions and infection rate would go up!



All 'safety concerns' are hypothetical.  If not, they'd be called side effects...


[ Parent ]
but gs has a point,
if we detect a much milder version of the pandemic virus then we might all go to that place and breath deeply! ;-)

You arm yourself to the teeth just in case.  You don't leave the gun near the baby's hand.

[ Parent ]
the problem is, how would you define mild?
until you know the CFR, which you probably won't know for some time. 

During SARS, they didn't know the CFR till the outbreak was almost over, and this was at a time with no other systemic crisis.  I suspect we won't know the CFR till the first wave is over, cos you might get new infection data from primary care sources, but death data from hospitals and mortuaries, and there would be missing cases or double counting, and so on, so the data would not be representative of the whole outbreak until you have a fairly thorough accounting!



All 'safety concerns' are hypothetical.  If not, they'd be called side effects...


[ Parent ]
same concept as what went on with 9/11 in a way
Initial estimates were upwards of 25,000 dead when the dust was still settling.

Later, after several unusual factors were taken into account, and after people have been able to report in and official numbers were put together, it was found that the total deaths were closer to 3,000.

I'm certainly not belittling the survival of nearly 20,000 people ... but it wasn't until the official numbers started coming in that people could really get ahold of what happened.

In the event of a pandemic, the situation could go in the opposite direction.  Fewer deaths are initially confirmed so people don't think it is as bad as it could be.  They get sloppy with their mitigation procedures and then the stinky stuff really hits the fan.

[shrug]

Not the best example I'm sure, but the stages of belief and knowledge are probably going to prove similar.

Never doubt that a small group of thoughtful, committed citizens can change the world, indeed it is the only thing that ever has. -- Margaret Mead


[ Parent ]
yes, it's likely to swing
from too high to too low, depending on what captures the headlines, I think.



All 'safety concerns' are hypothetical.  If not, they'd be called side effects...


[ Parent ]
"much milder" meaning "no calculations needed" :-)


You arm yourself to the teeth just in case.  You don't leave the gun near the baby's hand.

[ Parent ]
The mind boggles.
As the free market system would scramble to meet the 'demand'.

Pandemic Express Tours

The Pandemic Inn (You can checkout any time you like)

Pandemic Oxygen Bars

But then, it could have already mutated by then to a more pathogenic variation and oooops there goes my loafer.

ITW(Joel J)
Courage is resistance to fear, mastery of fear - not absence of fear.
- Mark Twain
 


[ Parent ]
Deeper mind twisting -
ITW,

  Hope my HMO does not plan to save money by having us pass "the communal cup" with a mildly sick person.

Kobie
"Hmo director dies and goes to the pearly gates. 
  St. Peter welcomes him saying: "I have good news and bad news."
  Whats the good news?
  You have been approved for the full treatment.
  What's the bad news?
  You can only stay three (3) days."


[ Parent ]
that's funny, ITW! lol n/t




All 'safety concerns' are hypothetical.  If not, they'd be called side effects...


[ Parent ]
1st wave
not the 2nd wave dangerous virus, of course, but the mild
1st, spring wave virus.

In theory, could they have infected the soldiers in the camps
with the 1st wave virus in Sept.1918 to protect them
from 2nd wave ARDS ?

ask experts for their subjective
panflu death expectation values
and report the replies


[ Parent ]
How would they have known the 2nd wave would be worse? n/t


ITW(Joel J)
Courage is resistance to fear, mastery of fear - not absence of fear.
- Mark Twain
 


[ Parent ]
timing
they knew it in Sept, early Oct 1918.

Maybe not too late to start a counterpandemic in distant regions
like SF,LA while trying to delay the spread of the real one.

Suppose panflu erupts badly in Indonesia,
should you catch normal flu in USA deliberately,
maybe treat it with Tamiflu, so to gain immunity ?

ask experts for their subjective
panflu death expectation values
and report the replies


[ Parent ]
normal flu should do
in a severe H5N1 pandemic you might consider to catch
normal flu (H3N2 or H1N1) immediately.
Maybe they can design particularly mild flu for that purpose,
H9N2 or such. It needn't be so much transmissable, when people
catch it deliberately.

The real disease probably provides better immunization
than some vaccine.
It's not H5, but should provide T-cell immunity.

Hmm, those who caught the 1st wave

ask experts for their subjective
panflu death expectation values
and report the replies


[ Parent ]
it's not always the second wave
that is most severe.  In 1957 the first wave was more lethal.


from Arnold Monto's presentation, CDC Dec 06 http://www.newfluwik...



All 'safety concerns' are hypothetical.  If not, they'd be called side effects...


[ Parent ]
that chart shows higher number of cases - was there higher CFR too?


You arm yourself to the teeth just in case.  You don't leave the gun near the baby's hand.

[ Parent ]
sorry you are right
that slide does not show CFR, but that comment from Arnold Monto was in my notes, with special emphasis on "Don't count on the first wave being milder!"



All 'safety concerns' are hypothetical.  If not, they'd be called side effects...


[ Parent ]
interesting picture
looks like wave 2 and 3 in 1918/19

is it for USA ?
It's "incidence", not mortality.

I'd like to have such graphics extended over centuries
(estimates) digitalized for computer readability


ask experts for their subjective
panflu death expectation values
and report the replies


[ Parent ]
Hmmm, 6,000 cases per 100,000 people. 6% of the population sick. n/t


[ Parent ]
and if you catch H1N1
or H3N2 or whatever, you still do not have immunity to H5N1, or any virus where the HA has changed.



All 'safety concerns' are hypothetical.  If not, they'd be called side effects...


[ Parent ]
cross-immunity
you probably have some T-cell  cross immunity,
which works for all genes, not only HA,NA.
But it's short expiring  3-9 months.

1918 immunity was also short range, no immunity 1st --> 3rd wave

This sort of immunity is supposed to be responsible
why a pandemic almost wipes out previous strains.
(paper by Ferguson AFAIR, which I could search for,
if there's interest)

ask experts for their subjective
panflu death expectation values
and report the replies


[ Parent ]
if there is enough cross immunity
there would not be a pandemic.  Or at least it would be really mild one, like 1968, but that only happens if the pandemic is caused by reassortment with circulating human flu, not if it was a pure avian virus.

The HA is the main determinant of immunity, the NA plays a lesser role.  So any change in HA will produce a pandemic.

The severity of illness also depends to a large degree on the internal genes.

1957 was milder than 1918 because 5 of the internal genes from the circulating human seasonal flu was retained.

1968 was milder than 1957 because 6 genes, 5 of the internal gens and the N2 stayed the same.

But in this discussion, we are not talking about a 1968-like event.  We are talking about a virus where none of the genes are human adapted. 



All 'safety concerns' are hypothetical.  If not, they'd be called side effects...


[ Parent ]
virulence
you have to distinguish B-cell immunity and T-cell immunity.
Although they are somehow connected and intertwined.

A change in HA not necessarily produces a pandemic,
but has done so several times already.

I'm not so sure whether/why a reassorted pandemic should be milder.
H5N1 has reassorted lots of times, getting genes from H6N1,H9N2
but it didn't decrease in virulence, all those variants are particularly
dangerous for humans.

It could be different when it reassorts with H3N2,H1N1 because we should have
some immunity to their inner genes. But these inner genes are pretty much similar
to the inner genes of other flu, including H5N1 already.
So this is not clear IMO.

Why 1918 was so virulent - that's unsolved AFAIK.
Just saying because it wasn't reassorted as the 1957,1968
that's too simple. The sample is rather small with only
3 pandemics. Where 1918 came from - we don't know.

Virulence seems to be rather independent of the other
"features" of a flu-strain like transmissability, phylogenetic neighborhood
to previous strains or avian strains

ask experts for their subjective
panflu death expectation values
and report the replies


[ Parent ]
I said reassortment with human flu
not avian flu.  The key is to what degree is the virus human adapted. 



All 'safety concerns' are hypothetical.  If not, they'd be called side effects...


[ Parent ]
human vs. avian flu
OK, current human flu has some decades of history of almost independant development
from avian strains. So it should be somehow different
even in the internal genes.
Suppose such a human adapted virus reassorts with H5N1.
They tried it in the laboratory last year and failed, but that needn't
mean too much. They only tested some specific strains and some
combinations out of many.

Now, assume the new strain keeps its H5 and acquires some new genes
from H3N2 or H1N1.
Would it reduce its virulence ?
I would still think no, but that's unclear.

ask experts for their subjective
panflu death expectation values
and report the replies


[ Parent ]
I would think so
if the current seasonal virus reassorts with H5N1, and only 1 or 2 of the avian genes are acquired, the virulence could be a lot less than what we are seeing now. 

Even the 1997 H5N1, which had internal genes from H9N2, an avian virus that from time to time causes mild human infections, showed a lower mortality (1 in 3) than the current H5N1.  OTOH, the more human adapted viruses are much more likely to cause a pandemic, of course!



All 'safety concerns' are hypothetical.  If not, they'd be called side effects...


[ Parent ]
...
my understanding is that folks have yet to succeed in producing a pandemic strain in the lab via reassortment - if that is correct, then their failure isn't really significant, is it - other than to say that efforts failed again?  also... if it's the story i'm thinking of, it wasn't last year that the work was done - it was closer to 4 years ago..  the story was hyped again last year, but it wasn't recent lab work.

[ Parent ]
...
and the hype was that they can't do it in the lab, so there's nothing to worry about...  not surprising in that instance that the reporters that ran the story didn't investigate it even enough to get the timeline correct on when the work was done -- hardly an indicator of a source to be trusted for reliable information..  apologies for straying off topic - didn't want to let it slip by, if it's what i'm thinking it was.

[ Parent ]
except for the media
the scientific community certainly did not conclude that reassortment is not likely, based on one study. 



All 'safety concerns' are hypothetical.  If not, they'd be called side effects...


[ Parent ]
...
:-)  i was concerned that frequently the media are the conduit to the public, and when the media take it out of context...  and folks refer to it..  it seems useful to keep it in context - not for the scientific community, but for the public that only heard the media's version.

[ Parent ]
reference
I'd like to see a reference where experts discuss this :
whether H5N1 would become less virulent when it picks
up genes from human flu.
What's the argument ? Are human flu-genes intrinsically
less virulent than avian ones ? Why ? Where ?

H5N1 picked up lots of different avian genes already and mixed
them but no variant had small CFR for humans.

ask experts for their subjective
panflu death expectation values
and report the replies


[ Parent ]
WHO document
Influenza research at the human and animal interface

page 15

One especially important question that was discussed is whether the H5N1 virus is likely to retain its present high lethality should it acquire an ability to spread easily from person to person, and thus start a pandemic.  Should the virus improve its transmissibility by acquiring, through a reassortment event, internal human genes, then the lethality of the virus would most likely be reduced. However, should the virus improve its transmissibility through adaptation as a wholly avian virus, then the present high lethality could be maintained during a pandemic.




All 'safety concerns' are hypothetical.  If not, they'd be called side effects...


[ Parent ]
the argument is based on
virus evolution and adaptation.  A virus can only jump into a new species AND establish itself if it has significant competitive advantage over circulating human strains.  The more virulent avian polymerase complex, according to Taubenberger, eg in Characterization of the 1918 influenza virus polymerase genes, appears to give it competitive advantage as long as it is capable of h2h transmission, wiping out circulating human strains and becomes established in a pandemic, and as the ancestor of subsequent human viruses.

(See also Marc Lipsitch on Virulence and transmissibility of pathogens: what is the relationship?

But once it starts circulating in humans, the polymerase genes especially PB1 comes under severe selection pressure from host immune responses, and adapts quite quickly over time, causing a reduction in virulence.  In essence, a more avian-like polymerase is associated with higher virulence, a more human-adapted polymerase is associated with diminished virulence.  A pandemic virus caused by the reassortment of H5N1 with human flu viruses (ie a surface H5 and varying numbers of internal human genes get combined) would have a lower virulence than a pure H5N1 without reassortment, because of existing host immune response to these internal proteins.



All 'safety concerns' are hypothetical.  If not, they'd be called side effects...


[ Parent ]
reassorted pandemic
thanks. I'll have to think about it and check...

also the magnitude, a reassorted H5N1 with polymerase
from H3N2, what CFR would it have when H5N1 has 60% ? 30% ?

in 1918's 2nd wave it went down from 2% to 1% in USA in 3 months
approximately.

So is it 30% immediately or after 3 months of adaption ?

host immunity targets PB1 ? when we have immunity, the wave is over...

still lots of questions

ask experts for their subjective
panflu death expectation values
and report the replies


[ Parent ]
why don't you start another diary
with your questions and thoughts?  Might be useful to others, instead of being hidden in this NPI one.  ;-)



All 'safety concerns' are hypothetical.  If not, they'd be called side effects...


[ Parent ]
later
maybe later, dealing with the new Russian paper and sequences today.

Maybe I can find a online paper about CFR-reassorted panflu.
You references were not freely available - I only read
the abstracts so far.

also, not much feedback/interest expected here except from you maybe ?!?
maybe another forum is better ? which ?
are there forums, mailing lists where the experts meet ?

let's merge the birdflu forums.

ask experts for their subjective
panflu death expectation values
and report the replies


[ Parent ]
gs, good provocation as usual - could there be "forum watch"?
I'm thinking something with RSS feeds and linking the titles of conversations on different forums, just so that we're all alerted to conversations we feel are more important than others, or more "to be shared widely" than others (a family's own preps are a different level of concern compared to worldwide policy).  Could that be explored in a diary of its own?

You arm yourself to the teeth just in case.  You don't leave the gun near the baby's hand.

[ Parent ]
UPDATE
added to top diary:

Part of the lesson for me is that if, in 1918, with none of this knowledge, and the NPI's were not implemented in a very systematic way nor for long enough, they could still reduce peak mortality by 50%, and overall mortality by 10-30%, how much total reduction can we achieve today with targeted approaches applied early and in an organized manner?  I would suggest that a reduction from say 50% AR to 10% AR over a 12-week school closure period is certainly feasible.  Which would buy us the time to ensure health services can cope, the infrastructure will hold up, and vaccines can be made as quickly as possible.




All 'safety concerns' are hypothetical.  If not, they'd be called side effects...


What Else do we have today that we didn't have in 1918? Years of warning!
Might officals try a bit harder to tell the public the (first nine) 'things the WHO thought people needed to know about pandemic influenza back in Oct 2005', and, the similarities in ages and surge problems between 1918 and H5N1, and, why we're worse off now, so we can all be on the same page about why the populace needs to be preparing to be able to do NPIs on very short notice? We've had years of warning and they could be being used better. Politicians and bureaucrats are still too short-sighted.

History has got us by the ugly end now, and it is going to get worse before it gets better.

Hindsight! Warning! Foresight! Action! They don't even have workable plans for all the bodies in an unmitigated pandemic, so, start telling the public everything, have communities make Pandemic Preparation, let go the reams of plans that look like the Emperor's New Clothes and start thinking how to solve local problems with fully-informed public's contributions to policy and implementation now.

"completely unmitigated epidemic would result in AR of 80%!"

Since there is no way to make the cfr drop, (wishing won't make it so) we'd better get going on mitigation, and that requires a prepared public, and the 1918 public didn't rely on life-or-death imports and power grid the way we do now.

  ..."if they had been able to maintain their NPIs for however long it took to achieve herd immunity, they would have resulted in close to 40% reduction in total mortality"...

Given that right now H5N1 looks like it could be fatal untreated (and under pandemic conditions I don't see treatment being possible after the first fortnight) regions that don't want their attack rate to kill swaths of their populace might find a 40% reduction in total mortality might save them enough skilled productive-age people to have a post-panflu-year Recovery.  Also, there are many possibly non-panflu deaths; if the public knew a time was coming they would be On Their Own; fire prevention and suppression, basic nursing and first aid, better plans for the vulnerable, the right translations distributed now; many different things would help. (Like figuring out what is really "essential", on a family, community, economic/ecological level.)
We could do NPI's for 6 months, if the public knew what will happen if they don't. (Look how much the US presidential candidates are raising for an election campaign for pity's sake; millions and millions! It is not lack of money, but lack of awareness and poor priority choices; even US people living below the poverty line can prep, I know, they just have to give up some things for a while until they get themselves more secure. But, they have to have some understanding what went on in 1918 and what has been going on right now with the H5N1 taking lives and livestock. Not only hearing about drills to hand out vaccine when that will not be how pandemic response starts, if it happens this year.
No place is "ready" because they had a vaccine drill, if the public isn't ready for months of NPIs, and there isn't effective PPE for HCW and first responders. The media needs to stop writing those articles that are meant to only reassure the public. We need true readiness.

At least as much in our pantries as homes in 1918 had. At least as much willingness and know-how to look after ourselves.


Menu

Make a New Account

Username:

Password:



Forget your username or password?



Active Users
Currently 0 user(s) logged on.

Contact
  DemFromCT
  pogge (In Memorium)
  Bronco Bill
  SusanC (emeritus)
  Melanie (In Memoriam)

  Flu Wiki (active wiki resource)
  How To Add To Flu Wiki
  Get Pandemic Ready (How To Start Prepping)
  Citizen's Guide v 2.0
  Effect Measure
  Dude's FTP

Home
Powered by: SoapBlox