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Author Topic: how do "we" know what strain of flu to vaccinate for?  (Read 4823 times)

paul.fr

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sorry to pose another flu related question.

Now my understanding is that the flu jabs some of us may be getting this winter, are different to those we may have got last winter. something sciency about the strain changing or something...

but how do we know what the next strain will look like...are they just guessing? And why do they use chicken eggs to incubate the virus?


 

Offline iko

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how do "we" know what strain of flu to vaccinate for?
« Reply #1 on: 24/10/2007 18:03:31 »
This is a virology issue, specific for Prof. Chris.

I may give my contribution here by citing
an old discussion about influenza epidemics
and Dr. Edgar Hope-Simpson's 'seasonal stimulus'...
But this really is another story!
 
ikod   [^]


Talking of 'revisiting' and looking backwards,
allow me a cut&paste from Complementary Medicine
(Cod Liver Oil topic) and final comment from the
discussion in "Epidemic influenza and vitamin D"
J.J. Cannell et al. 2006.

Quote
Revisiting Vitamin D in humans.
just a few clever minds got this point
first, several years ago...



A hypothesis concerning deficiency of sunlight,
cold temperature, and influenza epidemics associated with
the onset of acute lymphoblastic leukemia in northern Finland.


Timonen TT.

University of Oulu, Department of Internal Medicine, Kajaanintie 50, FIN-90220 Oulu, Finland.

Research to detect new factors contributing to the etiology of acute leukemia (AL) is urgently needed. Located between latitudes 65 degrees and 70 degrees north, the population in northern Finland is exposed to extreme seasonal alterations of ultraviolet-B light and temperature. There is also a seasonal variation of both the 25(OH)- and 1,25(OH)2-D3 vitamin serum concentrations. In the present work, the frequencies of different types and age-groups at diagnosis of AL were compared during the dark and light months of the year, to uncover seasonality. Between January 1972 and December 1986, 300 consecutive patients aged >/=16 years and diagnosed as having AL were enrolled. The observed mean monthly global solar radiation, temperature measurements, and influenza epidemics were compared with the monthly occurrence of AL. Both acute lymphoblastic leukemia (ALL) (p=0.006) and total AL (p=0.015) were diagnosed excessively in the dark and cold compared with light and warm period of the year. There was a tendency for de novo leukemia to increase also in the dark and cold, but for acute myeloid leukemia (AML) patients the excess was not significant. Age >/=65 was strongly associated with the dark and cold season (p=0.003). Significantly more ALL (p=0.005) and de novo leukemias (p=0.029) were observed during influenza epidemics than during nonepidemic periods. However, a seasonality, i. e., the fluctuation of numbers of AL cases, was not determined, either monthly or during different photo- and temperature periods or influenza epidemics; this might be due to the small numbers of patients studied. Nevertheless, it is hypothesized that sunlight deprivation in the arctic winter can lead to a deficiency of the 1, 25(OH)2D3 vitamin, which might stimulate leukemic cell proliferation and block cell differentiation through dysregulation of growth factors in the bone marrow stromal cells, causing one mutation and an overt ALL in progenitor cells damaged during the current or the previous winter by influenza virus, the other mutation.

Ann Hematol. 1999 Sep;78(9):408-14
.




Epidemic influenza and vitamin D.

Cannell JJ, Vieth R, Umhau JC, Holick MF, Grant WB, Madronich S, Garland CF, Giovannucci E.
Atascadero State Hospital, 10333 El Camino Real, Atascadero, CA 93422, USA. jcannell@dmhash.state.ca.us

In 1981, R. Edgar Hope-Simpson proposed that a 'seasonal stimulus' intimately associated with solar radiation explained the remarkable seasonality of epidemic influenza. Solar radiation triggers robust seasonal vitamin D production in the skin; vitamin D deficiency is common in the winter, and activated vitamin D, 1,25(OH)2D, a steroid hormone, has profound effects on human immunity. 1,25(OH)2D acts as an immune system modulator, preventing excessive expression of inflammatory cytokines and increasing the 'oxidative burst' potential of macrophages. Perhaps most importantly, it dramatically stimulates the expression of potent anti-microbial peptides, which exist in neutrophils, monocytes, natural killer cells, and in epithelial cells lining the respiratory tract where they play a major role in protecting the lung from infection. Volunteers inoculated with live attenuated influenza virus are more likely to develop fever and serological evidence of an immune response in the winter. Vitamin D deficiency predisposes children to respiratory infections. Ultraviolet radiation (either from artificial sources or from sunlight) reduces the incidence of viral respiratory infections, as does cod liver oil (which contains vitamin D). An interventional study showed that vitamin D reduces the incidence of respiratory infections in children. We conclude that vitamin D, or lack of it, may be Hope-Simpson's 'seasonal stimulus'.

Epidemiol Infect. 2006 Dec;134(6):1129-40. Epub 2006 Sep 7.




...from the final conclusion in the full-text:

  Today, in a rush from multiplex reverse transcriptase-polymerase chain reactions that rapidly subtype influenza viruses to complex mathematical formulas that explain infectivity, many of us have forgotten Hope-Simpson's simple 'seasonal stimulus' theory for the lethal crop of influenza that sprouts around the winter solstice.   The faith and humility that characterized his life and his writings insulated him from despairing that his 'seasonal stimulus' would not be sought.  Among his last published words was the suggestion that 'it might be rewarding if persons, who are in a position to do so, will look more closely at the operative mechanisms that are causing such seasonal behaviour' [3,p.241].



A Gloucestershire GP carefully recorded the incidence of influenza in his practice over a period of nearly 30 years. Dr Hope-Simpson obtained a picture of the timing and intensity of these cases from 1946 to 1974.
Is it possible to compare Kilbourne’s chronological model of the spread of influenza with this data?
Such a comparison indicates that there should be evidence of the following factors influencing the final picture:
- A distinct seasonal pattern, with the highest incidence in winter.
- A series of decreases in the size of epidemic waves as the population becomes immune to one particular strain of the virus.
- The appearance of a new strain with changed antigens, meaning that the body’s defence mechanism does not recognise it. The whole process of infection should then begin again.
- The presence of more than one strain of influenza in the population at any one time.
- Newly introduced strains from other parts of the world, which can be especially virulent.

for more reading click here:  http://www.makingthemodernworld.org.uk/learning_modules/geography/05.TU.01/?section=6





« Last Edit: 24/10/2007 18:10:42 by iko »
 

Offline SquarishTriangle

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how do "we" know what strain of flu to vaccinate for?
« Reply #2 on: 11/11/2007 03:23:54 »
Not really sure how it works in the UK. But here in the southern hemisphere (since the majority of the world's population resides in the north...and that seems to be where our influenza strains come across from) we basically vaccinate according to the strain that occured in the northern hemisphere the previous winter.
 

Offline chris

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how do "we" know what strain of flu to vaccinate for?
« Reply #3 on: 12/11/2007 09:05:43 »
SquarishTriangle is absolutely right. Influenza undertakes an annual world tour, with activity peaking during the winter in each hemisphere.

During the 'flu season in any country, doctors such as GPs (known as spotter practices) and diagnostic laboratories, like mine, collect potential flu "isolates" from symptomatic patients. Isolates in which influenza infection is confirmed are sent to an international reference laboratory (at the WHO), which compares how effective antibodies produced by the current vaccine are at neutralising the present strains of the virus being detected in the population.

If the virus is showing signs of genetic drift (a subtle viral "face-lift", which makes it harder for the immune system to recognise it) and the vaccine is in danger of losing its effectiveness, then the decision may be taken to update the vaccine so that it is more representative of what is circulating in the community.

But production of flu vaccines is a slow process; the virus is grown in eggs, and each egg yields sufficient material to vaccinate about three people. Consequently it takes about 6 months to prepare sufficient vaccine stocks to protect on a population level.

To get around this problem we look at the strains of virus circulating in the opposite hemisphere, where it is winter during our summer. We assume that the viruses infecting people at this time will be the ones that make their way around to us in the opposite hemisphere when winter arrives six months later.

This "lead time" gives vaccine manufacturers sufficient time and advanced warning to prepare an altered vaccine, if required.



 

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how do "we" know what strain of flu to vaccinate for?
« Reply #3 on: 12/11/2007 09:05:43 »

 

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