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From: werner@aecom.UUCP (Craig Werner)
Newsgroups: net.bio,net.med
Subject: Re: Sickle-Cell Anemia population genetics
Message-ID: <1868@aecom.UUCP>
Date: Thu, 22-Aug-85 01:03:35 EDT
Article-I.D.: aecom.1868
Posted: Thu Aug 22 01:03:35 1985
Date-Received: Sun, 25-Aug-85 06:28:50 EDT
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Organization: Albert Einstein Coll. of Med., NY
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Xref: watmath net.bio:249 net.med:2181

> 
> 	What's a CBW?  I've been reading this group [.bio] and wondering.
> 	Also, is sickle-cell anemia really a defense against malaria?
> 	If so, how does it work?  Isn't the cure worse than the disease?
> 
	Hemoglobin(Sickle), or HbS, doesn't form the polymers that result
in sickling. When mixed with normal HbA, it prevents HbA from sickling too
by ruining the 'crystal' as it forms. That's how it works.
	HbS also lacks the site for the malarial parasite (its the same site.)

	It's not sickle cell that is selected for. That is fatal. It is the
carrier state - 1 sickle cell gene, 1 normal gene. Sickle cells carriers are
reasonably non-anemic.

	There are four genetic outcomes, 1 with HbA/HbA - these are more
prone to malaria (without malaria, these are the healthiest people), 1 with
HbS/HbS - these die young of sickle cell.  The other two are HbS/HbA - one
of each --> these people are resistant to both sickle cell and malaria.
They perpetuate the gene pool, and keep the Sickle gene around.

I have no idea what a CBW is, but I have doubts of the mental stability of
the original poster, so I don't consider it too important.
-- 
				Craig Werner
				!philabs!aecom!werner
		"The world is just a straight man for you sometimes"