CCR5 and Protection from AIDS

James Howard jmhoward at
Sat Dec 5 10:22:52 EST 1998

CCR5 and Protection from AIDS

James Michael Howard
Fayetteville, Arkansas, U.S.A.

It is my hypothesis that vulnerability to HIV infection and AIDS results
from low dehydroepiandrosterone (DHEA).  Furthermore, it is my hypothesis
that testosterone interferes with the availability of DHEA.  Therefore, the
ratio of these two hormones is directly involved in HIV infection and AIDS.
(This is explained in detail at on the
internet.  My explanation of AIDS contains the citations supporting my
statements herein.)  Because chimps produce more DHEA and less testosterone
than humans, I have suggested this is why they are not easily infected by
the HIV.  Recently, research has produced the hypothesis that a mutation in
the gene that produces the cell surface receptor, CCR-5, confers resistance
to the HIV.  (CCR-5 receptors are one of the mechanisms whereby the HIV
enters target cells.  If the receptor is defective, the attachment of HIV is
reduced.)  People of European descent exhibit a higher incidence of this
mutation than other groups.  This has resulted in the hypothesis that this
difference in gene distribution accounts for reduced incidence of HIV
infection of individuals of European descent and the high incidence of HIV
infection and AIDS in other areas, especially Africa.

I have suggested for some time that the increased incidence of HIV infection
in black individuals, especially in Africa, results from the fact that black
men and women produce more testosterone than white men and women.  That is,
black individuals have a much higher ratio of testosterone to DHEA.  (Male
homosexuals are known, on average, to produce less DHEA than male
heterosexuals.)  If intact CCR-5 receptors increase HIV binding to cells,
then animals that carry this normal receptor should also exhibit increased
binding and, therefore, increased infection by the HIV.  It has been
determined that chimpanzees carry the normal CCR-5 gene sequence no chimps
were found to carry the mutated form of the gene (J Med Virol 1998
Jun;55(2):147-51).  Also, the receptor designated CXCR4 is also involved in
HIV attachment. AIDS Res Hum Retroviruses 1997 Dec 10;13(18):1583-7
indicates that chimpanzee CXCR4 and the CCR-5 are both capable of binding
HIV, yet infection of chimps by the HIV is very difficult. Therefore, I
suggest mutation of the CCR-5 recptor is only a minor genetic characteristic
that reduces HIV infection and AIDS in some humans, and that my hypothesis
that a proper amount of DHEA is involved in stopping HIV infection remains

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