Freethought & Rationalism Archive

Kevin Dorner · 08-20-2002, 06:35 PM

Found this article interesting, because it is a textbook case of a variation within a population that has no effect on survival until some environmental pressure (ie a disease) shows up that literally makes a life-and-death difference.

Quote:

The scientists compared genetic markers in rodents that died from those that did not, homing in on genes that control production of the enzyme oligoadenylate synthetase L1.

The mice that died after being infected with the virus carried a mutation on the oligoadenylate synthetase L1 gene, while the mice than survived infection had a normal copy of the gene. The severity of infection in the mice "is controlled by a major genetic determinant," concludes the team, noting the same could be true in humans.

<a href="http://www.nationalpost.com/utilities/story.html?id={AC5006FB-8700-4B74-9CF1-9381D6C65839}" target="_blank">Mutant gene may explain why some die of West Nile:
1 in 5 infected become ill</a>

Doubting Didymus · 08-20-2002, 07:06 PM

Why do you say that this is neccesarily a mutation that had no effect until the virus showed up? Isn't it more likely that the 'normal' gene is itself a mutant that was spread through the population after the virus became a selection pressure? Or am I missing something?

Kevin Dorner · 08-20-2002, 07:22 PM

From what I gather from the article: the hypothesis is that the same mutation present in the bred strain of mice for whom West Nile is fatal, is also evenly distributed in one-fifth of humans. This would indicate that it's been around far longer than West Nile. You may be correct that the "good" variation in four-fifths of humanity might be the newer mutation, akin to the mutation that causes lactose tolerance, but I can't determine that from the content of the article. However, as wild mice have only the "good" gene it would seem that the "bad" one is the mutant.

[ August 20, 2002: Message edited by: Kevin Dorner ]</p>

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08-20-2002, 07:06 PM	#2
Doubting Didymus Veteran Member Join Date: Jul 2002 Location: East Coast. Australia. Posts: 5,455	Why do you say that this is neccesarily a mutation that had no effect until the virus showed up? Isn't it more likely that the 'normal' gene is itself a mutant that was spread through the population after the virus became a selection pressure? Or am I missing something?

08-20-2002, 07:22 PM	#3
Kevin Dorner Senior Member Join Date: Dec 2001 Location: Toronto, Ontario, Canada Posts: 762	From what I gather from the article: the hypothesis is that the same mutation present in the bred strain of mice for whom West Nile is fatal, is also evenly distributed in one-fifth of humans. This would indicate that it's been around far longer than West Nile. You may be correct that the "good" variation in four-fifths of humanity might be the newer mutation, akin to the mutation that causes lactose tolerance, but I can't determine that from the content of the article. However, as wild mice have only the "good" gene it would seem that the "bad" one is the mutant. [ August 20, 2002: Message edited by: Kevin Dorner ]</p>

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