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From: werner@aecom.UUCP (Craig Werner)
Newsgroups: net.bio,net.med
Subject: Re: Re: Malaria and sickle cell
Message-ID: <1879@aecom.UUCP>
Date: Thu, 29-Aug-85 00:17:08 EDT
Article-I.D.: aecom.1879
Posted: Thu Aug 29 00:17:08 1985
Date-Received: Sat, 31-Aug-85 08:20:57 EDT
References: <191@tekig5.UUCP> <314@kitty.UUCP> <678@cybvax0.UUCP> <1858@aecom.UUCP> <192@husky.uucp>, <1868@aeco<306@drutx.UUCP>
Organization: Albert Einstein Coll. of Med., NY
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Xref: watmath net.bio:256 net.med:2257

> It is not the HgbS that is responsible for malaria "immunity". It is
> due to lack of the Duffy Blood Group System genes, both a and b.
> [ie. Fya-, Fyb-].  It just happens that both the HgbS genes and
> Duffy {or should I say lack of} genes are both found in the same
> segment of the population. {Blacks}
> 				jill

	The Duffy Blood Groups antigens (the ones most different between whites
and Blacks) is the receptor for Vivax Malaria.
	The HbS/HbA mutation is for Plasmodium falcifurim malaria.  They are
two different diseases, but both called malaria.

Incidentally, I have been told that I switched one of my HbSs with an HbA. If
you saw an apparent contradiction, it was an unfortunate typo.  -- CW.
-- 
				Craig Werner
				!philabs!aecom!werner
		"The world is just a straight man for you sometimes"