Posted on 03/10/2005 3:11:16 PM PST by Pyro7480
"...computer modeling..."
...automatically raises a flag of suspicion with me ever since the global warming computer modeling fiasco.
"...example of scientific ignorance from Reuters..."
What is the obvious example of scientific ignorance from Reuters in this?
Why should we consider that resistance to the virus that causes the plague a mutation? As to environmental pressures, I don't see that from what I read in the article. It looks like the resistance became more prevalent because those without the resistance succumbed to the plague...survival of the fittest.
The suggestion inferred from the "forced up the rate of mutation" statement, is that the genetic code was responding to the presence of the disease by mutating. This is not how it works. Mutations exist and may give selective advantage to those who contain those traits. When such an advantage exists, over time, the inheritors of the favored trait will tend to be more successful in reproducing. Short of increasing radiation near the gonads (as suggested in post 17), mutations--either to their nature or rate--occur randomly.
I agree with you regarding the resistance surviving and reproducing itself. Is this trait a mutation? Is the lack of resistance a mutation? Is a genetic weakness in the immune system a mutation, or vis-a-versa?
We each have the genetics to reproduce with various traits. We may have the genetics to reproduce either with this plague resistance or without it. That does not mean that my DNA is undergoing change in this process.
One of my favorite short stories addresses this topic--it talks about how the first geneticists to come up with this kind of gene-target viruses use it to spread genetic mutations that end racism by spreading white and black and Asian racial characteristics to everyone.
It's an interesting story. I just wish I remembered the title...must be the Alzheimers' virus.
From the comments of the others on this point, I see that there is an ambiguity that revolves around the meaning of the word "frequency." The origninal statement, as I read it, meant "the number of mutations per capita." However, one could read it as meaning "nuber of mutations per unit time," which would not be what the author meant.
In demographics and epidemiology, "frequency" almost always means "number of cases divided by the total population."
bttt
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Our knowledge of the medieval plagues in Europe compared to other areas of the old world is probably more related to documentation than to prevalence.I agree. Also, any epidemic prior to about WWI is either still with us, somewhere, or is extinct. Some tissue samples from those who succumbed from the "Spanish Lady" flu epidemic that hit in full force (apparently there were a few bad years in sequence prior to it) at the end of WWI still exist. The rest of the "data" appears to be speculation, at best.
I am skeptical. Plague continued to be endemic and intermittently epidemic in China and India for most of the 20th century. Why would Europeans have developed the highest degree of resistance?The gene was already there (according to this speculation), but (according to this speculation) those with it had more children than those who didn't.
"That which does not kill you, only makes you stronger"
amazing stuff, those genes.
The problem came when many West Africans (virtually all slaves who came to the US were from the western part of Africa, which also has the highest incidents of sickle cell) came to the US. Here sickle cell had virtually no benefit. After all, the risk of malaria went to what can be statistically called nil, but the drawbacks of sickle cell were still there 100%. Without malaria to make it 'worth it,' sickle cell just became a hindrance (and every now and then a lethal hindrance).
Sickle cell was a blessing when the malaria scourge was ubiquitous, but without the risk of malaria sickle cell became a true detriment.
It is really interesting how bad things can be good things, and what was a good thing can become a bad thing.
But researchers at the University of Liverpool in England said computer modeling, based on the changing demographics of Europe from 1000 to 1800 AD, showed how hemorrhagic fever forced up the frequency of this mutation from 1 in 20,000 at the time of the Black Death to values today of 1 in 10.
Fascinating stuff. At first glance, I took 'changing demographics' to mean that individuals without the gene mutation were weeded out by disease. Thinking about it, there's more to it--changing demographics also led to increased opportunity for exposure to the plague....that is, the growth of villages into cities (in Europe) started around the year 1000. IOW, a population center was a target area & the larger the population, the larger the target. So, large population centers would have functioned to accelerate the natural selection process.
My comment was not with regards to whether resistance can develop in a population. Of course it can.
It was with regards to whether it would develop to a greater extent in Europe than in the Middle East, India and the Far East, areas where the population was exposed to repeated epidemics of plague for a much longer period than in Europe.
......until a rock fell on them.
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