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. (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, and, in the first quotation, below, no chimps were found to carry the mutated form of the gene. Also, the receptor designated CXCR4 is also involved in HIV attachment. The second quotation, below, 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 receptor 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 intact.

"A survey for 32 nucleotide deletion in the CCR-5 chemokine receptor gene (deltaccr-5) conferring resistance to human immunodeficiency virus type 1 in different ethnic groups and in chimpanzees" Voevodin A, Samilchuk E, Dashti S J. Med. Virol. 1998; 55: 147-151

"The 32 nucleotide deletion in the CCR-5 chemokine receptor gene referred to as deltaccr-5 has been shown to confer resistance to HIV-1. Using PCR, 1,105 human subjects and 33 common chimpanzees were genotyped attributing them to one of the three possible genotypes: wild-type homozygote (w/w); deltaccr-5 homozygote (deltaccr-5/deltaccr-5) and deltaccr-5/wild-type heterozygotes (deltaccr-5/w). The ethnic groups investigated included different Middle Eastern nationalities (mainly Arab) and Russians. Carriers of the deltaccr-5 mutation were found among Arabs, Iranians and Russians. The highest frequency of the mutation was seen in Russians (24.4% of the deltaccr-5 heterozygotes, allele frequency-0.1221). Surprisingly, the only deltaccr-5 homozygote identified in our study was an Egyptian. The origin of the deltaccr-5 mutation in the Middle Eastern populations, both Arab and non-Arab, is most probably due to a gene flow from the Europeans. The frequency of the deltaccr-5 mutation in Russians is one of the highest known. It might be one of the factors contributing to a relatively slow pace of increase in the incidence of sexually acquired HIV infection in Russia. None of the chimpanzees tested was positive for deltaccr-5. Interestingly, the DNA sequence of the chimpanzee CCR-5 gene in the region including the site of the deltaccr-5 mutation, and flanking areas, was virtually identical to the homologous human sequence, only two mismatches (silent substitutions) were found."

"Chimpanzee CXCR4 and CCR5 act as coreceptors for HIV type 1" Pretet JL, Zerbib AC, Girard M, Guillet JG, Butor C AIDS Res. Hum. Retroviruses 1997; 13: 1583-7

"Chemokine receptors are molecules involved in the fusion of immunodeficiency viruses after their attachment. As chimpanzees are the animal model for infection by HIV-1, we cloned and sequenced chimpanzee CXCR4 and CCR5 from PBMCs. Chimpanzee CXCR4 was found to be identical to human CXCR4, which provides an explanation for the sensitivity of chimpanzees to lymphotropic isolates of HIV-1. Chimpanzee CCR5 showed two substitutions with respect to human CCR5. However, we show that the macrophage-tropic isolate HIV-1-Ba-L can use chimpanzee CCR5 as a fusion receptor. Therefore, the resistance of chimpanzee PBMCs to infection by macrophage-tropic isolates of HIV-1 is unlikely to be due to substitutions in CCR5."