Relay-Version: version B 2.10 5/3/83; site utzoo.UUCP Posting-Version: version B 2.10.2 9/18/84; site ecsvax.UUCP Path: utzoo!watmath!clyde!burl!ulysses!mhuxr!mhuxt!houxm!whuxl!whuxlm!akgua!mcnc!ecsvax!emigh From: emigh@ecsvax.UUCP (Ted Emigh) Newsgroups: net.bio Subject: Re: Malaria and sickle cell Message-ID: <335@ecsvax.UUCP> Date: Wed, 31-Dec-69 18:59:59 EDT Article-I.D.: ecsvax.335 Posted: Wed Dec 31 18:59:59 1969 Date-Received: Sat, 31-Aug-85 03:42:55 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> Reply-To: emigh@ecsvax.UUCP (Ted Emigh) Organization: NC State University Lines: 22 Summary: In article <306@drutx.UUCP> jca@drutx.UUCP (ArnsonJC) writes: >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 are several polymorphisms thought to influence malaria resistance, including Sickle Cell Anemia (HbS), Beta Thalassemia, G6PD deficiency, as well as the Duffy trait. It is possible for many genes to contribute to disease resistance. For more information consult: Human Genetics, by Vogel and Motulsky. -- Ted H. Emigh Genetics and Statistics, North Carolina State U, Raleigh NC USENET: {akgua decvax duke ihnp4 unc}!mcnc!ecsvax!emigh ARPA: decvax!mcnc!ecsvax!emigh@BERKELEY BITNET: nemigh@TUCC