Sally Furniss
Well-known member
Re: PB2/627 temperature theory issues
Thank you Anne but the credit belongs to AlaskaDenise
Thank you Anne but the credit belongs to AlaskaDenise
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PB2/627 temperature theory issues
- Thread starter Sally Furniss
- Start date
AlaskaDenise
In Memoriam
Re: PB2/627 temperature theory issues
Anne:
Perhaps we can fight H5N1 by altering its environment. Even if temperature is only one factor in a combination therapy, it may help.
My childhood physician would advise against taking fever-relieving medications until our temperature was over 102F. He said germs couldn't thrive in a hostile (too hot) environment. It does, however damage growing tooth enamel.
.
Anne:
Perhaps we can fight H5N1 by altering its environment. Even if temperature is only one factor in a combination therapy, it may help.
My childhood physician would advise against taking fever-relieving medications until our temperature was over 102F. He said germs couldn't thrive in a hostile (too hot) environment. It does, however damage growing tooth enamel.
.
Re: PB2/627 temperature theory issues
"...advise against taking fever-relieving medications until our temperature was over 102F ..."
Denise, unfortunately like we all knows, ordinary seasonal flu induced very high body temperature itself.
If somebody have a such robust body to resist an pandemic flu temperature vithout medicaments, with an respiratory failure, than maybe ("an terminator" body is needed...)
"...advise against taking fever-relieving medications until our temperature was over 102F ..."
Denise, unfortunately like we all knows, ordinary seasonal flu induced very high body temperature itself.
If somebody have a such robust body to resist an pandemic flu temperature vithout medicaments, with an respiratory failure, than maybe ("an terminator" body is needed...)
Shannon Bennett
Well-known member
Re: PB2/627 temperature theory issues
I suspect in the case of bf infection the damage is already done prior to the increased temperatures in humans. Replication is already going 'off the charts' when the body suddenly recognizes the dangerous invader. Taubenbergers experiments with the Spanish flu indicated rapid and massive numbers of virus prior to host recognition of peril. Still, keeping the temp below dangerous levels but above normal could help later replication it would appear.
I suspect in the case of bf infection the damage is already done prior to the increased temperatures in humans. Replication is already going 'off the charts' when the body suddenly recognizes the dangerous invader. Taubenbergers experiments with the Spanish flu indicated rapid and massive numbers of virus prior to host recognition of peril. Still, keeping the temp below dangerous levels but above normal could help later replication it would appear.
Re: PB2/627 temperature theory issues
Somewhere (I apolgoise - no time to search) there is reference to the fact that 1918 victims who were left outside on stretchers, or in very cold unheated corridors has higher survival rates than those who were kept warm.
Simple metabolic laws that apply to living systems would suggest that viral replication will slow at lower temps (the host cell's metabolic rate will definately slow in these circumstances) - so perhaps symptom onset in 1918 was as a result of massive viral load buidling up prior demonstrating illness, producing high temperatures - but once at that stage, keeping the body cool as possible may inhibit or slow the rate of viral replication thereafter? This might have give a survival edge. Covered in the famous book on the period (a name beginning with 'b'!)
In haste
Somewhere (I apolgoise - no time to search) there is reference to the fact that 1918 victims who were left outside on stretchers, or in very cold unheated corridors has higher survival rates than those who were kept warm.
Simple metabolic laws that apply to living systems would suggest that viral replication will slow at lower temps (the host cell's metabolic rate will definately slow in these circumstances) - so perhaps symptom onset in 1918 was as a result of massive viral load buidling up prior demonstrating illness, producing high temperatures - but once at that stage, keeping the body cool as possible may inhibit or slow the rate of viral replication thereafter? This might have give a survival edge. Covered in the famous book on the period (a name beginning with 'b'!)
In haste
Shannon Bennett
Well-known member
Re: PB2/627 temperature theory issues
Don't know about the cold reference but those in New York who were treated in tents outside the hospital had a lower CFR than did those inside the building. I seem to recall that the time of year was September. I will check it out.
Don't know about the cold reference but those in New York who were treated in tents outside the hospital had a lower CFR than did those inside the building. I seem to recall that the time of year was September. I will check it out.
AlaskaDenise
In Memoriam
Re: PB2/627 temperature theory issues
I usually shake off illnesses very quickly, after my body temp plunges - sometimes into the hypothermic range.
Lower CFR fin a September tent environment - would there be other factors in addition to temperature?
Early TB sanitariums had high windows with "cross ventilation" & lots of time spent outdoors (warm weather). People who were treated that way have said it was to reduce the germ load in the air. ????
.
I usually shake off illnesses very quickly, after my body temp plunges - sometimes into the hypothermic range.
Lower CFR fin a September tent environment - would there be other factors in addition to temperature?
Early TB sanitariums had high windows with "cross ventilation" & lots of time spent outdoors (warm weather). People who were treated that way have said it was to reduce the germ load in the air. ????
.
Shannon Bennett
Well-known member
Re: PB2/627 temperature theory issues
Denise, I have hypothesized the reason was based more on vitamin D and a reduced viral load do to UV. I am fairly certain the temps in New York don't plummet in September. But perhaps that year they did dip into the 40's at night. I don't know. Cross ventilization might also have reduced viral load.
Denise, I have hypothesized the reason was based more on vitamin D and a reduced viral load do to UV. I am fairly certain the temps in New York don't plummet in September. But perhaps that year they did dip into the 40's at night. I don't know. Cross ventilization might also have reduced viral load.
Sally Furniss
Well-known member
Re: PB2/627 temperature theory issues
Co-infection is required for recombination. Maybe the co-infection last for a long time at low levels. The bird becomes stressed and then one infection becomes more dominant and kills the bird.
Dual infection?
That would mean when the large number of Qinghai bird deaths tested positive for E627K (lower human-temperature setting), that large population were all dually infected with both strains. Does that seem reasonable? Would not BOTH strains have been found by the tests?
Would it follow that the surviving birds, flying elsewhere, were those infected by only one strain - the one adapted to lower temperature replication? But when those birds arrived on the shores of the Crimean Penn., remember how many died - going in circles with bent necks? Wouldn't that require the higher temperature setting?
My brain is getting whip lash from this issue.
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Co-infection is required for recombination. Maybe the co-infection last for a long time at low levels. The bird becomes stressed and then one infection becomes more dominant and kills the bird.