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From: urol@ecsvax.UUCP (Floyd A. Fried)
Newsgroups: net.bio
Subject: Re: Malaria and sickle cell
Message-ID: <372@ecsvax.UUCP>
Date: Wed, 31-Dec-69 18:59:59 EDT
Article-I.D.: ecsvax.372
Posted: Wed Dec 31 18:59:59 1969
Date-Received: Sun, 8-Sep-85 16:39:30 EDT
References: <191@tekig5.UUCP> <314@kitty.UUCP> <678@cybvax0.UUCP> <1858@aecom.UUCP> <192@husky.uucp>, <1868@aecoRe: Malaria and sickle cell <306@drutx.UUCP>
Organization: North Carolina Educational Computing Service
Lines: 20

> 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


There is an alternate hypothesis which can explain the selection
of the heterozygous Hg SA state.  This has to do with the fact
that if individuals with Hg SA have an increased resistance to 
malaria then males with Hg SA will not be exposed to the numerous
febrile episodes that characterize malaria.  The adverse effects
of high temperature on the seminiferous tubules of the testis is 
well known- therefore one could expect that the male with Hg SA
because he is relatively protected from malaria, his testes will
not be exposed to high body temperatures which will reduce the 
sperm count.  The net effect is that the male with Hg SA will have
a better sperm count and hence be more fertile than males with Hg AA.