Why the HIV is so Prevalent in Africa

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

It is my hypothesis that increased testosterone increases HIV infection rates and AIDS. This will explain why AIDS is so high in Africa. Blacks produce more testosterone than whites, and the infection rate of blacks far exceeds the rate in whites. (Blacks males produce significantly more testosterone than while males, (J Natl Cancer Inst 1986; 76: 45), and black females produce more testosterone than white females, (J Clin Endocin Metab 1996; 81: 1108). In the following quotations regarding establishment of a virus, equine arteritis virus (EAV) in horses, it is demonstrated that testosterone is directly involved in infection and maintenance of the EAV. It has been determined that: "The findings confirm that persistent EAV infection is unlikely to occur in geldings and support the results of previous studies, which demonstrated that testosterone plays an essential role in the establishment and maintenance of the carrier state." (J Comp Pathol 1994; 111: 383), first quotation below). Also: "These findings confirm that the virus can replicate in the reproductive tract of a significant proportion of colts for a variable period of time after clinical recovery in the absence of circulating concentrations of testosterone equivalent to those found in sexually mature stallions." ( J Comp Pathol 1993; 109: 29), second quotation below). I suggest the same influence of testosterone is occurring in the infection rate of HIV, and resultant AIDS, in high testosterone people, that is, blacks.

McCollum WH, et al., "Resistance of Castrated Male Horses to Attempted Establishment of the Carrier State with Equine Arteritis Virus," (J Comp Pathol 1994; 111: 383)

"Twelve geldings all became infected when inoculated intranasally with the KY-84 strain of equine arteritis virus (EAV), a strain previously shown to be capable of establishing the carrier state in the stallion. With the exception of one animal that showed no effects other than pyrexia, all of the geldings developed clinical signs characteristic of equine viral arteritis (EAV). The geldings were febrile for varying periods within the range of 2-10 days after inoculation. Viraemia occurred from day 2 onwards, for periods varying from 9 to at least 19 days. Nasal shedding of virus began 2-4 days after inoculation and persisted for periods ranging from 7-14 days. All geldings "seroconverted" to EAV by day 11, with serum neutralization titres ranging from 8 to 64. The titres ranged from 8 to 32 after 4 weeks. Low concentrations of EAV were detected in the kidney and blood of one gelding killed 30 days after inoculation and in the blood of another killed after 57 days. Virus was not isolated from any tissue or fluid collected from the remaining 10 geldings, all of which were killed between days 30 and 148. The findings confirm that persistent EAV infection is unlikely to occur in geldings and support the results of previous studies, which demonstrated that testosterone plays an essential role in the establishment and maintenance of the carrier state."

Holyoak GR, et al., "Relationship between Onset of Puberty and Establishment of Persistent Infection with Equine Arteritis Virus in the Experimentally Infected Colt," (J Comp Pathol 1993; 109: 29)

"The relationship between stage of reproductive tract maturity and susceptibility to the experimental establishment of persistent infection with equine arteritis virus (EAV) was investigated in 21 prepubertal and 15 peripubertal colts. Five of six peripubertal colts inoculated intranasally remained infected in the reproductive tract from post-challenge day 28 to 93 and two of six from post-challenge day 120 to 180. No virus was detected in five of these animals killed on post-challenge day 210. Each of two peripubertal colts remained infected in the reproductive tract at post-challenge day 60 and one of nine was found to be persistently infected with EAV 15 months after challenge. These findings confirm that the virus can replicate in the reproductive tract of a significant proportion of colts for a variable period of time after clinical recovery in the absence of circulating concentrations of testosterone equivalent to those found in sexually mature stallions. Long-term persistent infection with EAV does not appear to occur in colts exposed to the virus before the onset of peripubertal development. We suggest that colts should be vaccinated at approximately 6 months of age, before peripubertal development but after the disappearance of maternally acquired antibodies."

There are a number of investigations that support my contention that testosterone adversely affects the immune system vis-à-vis the HIV. One contains this generality: "...sexually mature male vertebrates are often more susceptible to infection and carry higher parasite burdens in the field." (Int J Parasitol 1996; 26: 1009). Another investigation determined the following:

"CONCLUSIONS: Castration before soft-tissue trauma and hemorrhagic shock maintains normal immune function in male mice, but sham-castrated male mice show significant immunodepression. The maintenance of immune function by androgen deficiency does not seem to be related to changes in the release of corticosterone. We conclude that male sex steroids are involved in the immunodepression observed after trauma-hemorrhage. Thus, the use of testosterone-blocking agents following trauma-hemorrhage should prevent the depression of immune functions and decrease the susceptibility to sepsis under those conditions." (Arch Surg 1996; 131: 1186).

For sake of brevity, I have not gone in to detail regarding my explanation of how I think testosterone reduces the immune response. The next citation supports the negative effect of testosterone on the immune system, regarding malaria, and continues to say that the testosterone effect is not due to the classical explanation. My explanation does not rely on the "classical AR response."

"Our data suggest that testosterone suppresses the development of protective immunity against P. chabaudi malaria, and that this immunosuppressive effect of testosterone is not primarily mediated by the classical AR response." (J Endocrinol 1992; 135: 407).

Another investigation examined a specific phase of the immune response and found the same anti-immune function of testosterone. "These results suggest that the male sex hormone, testosterone, but not the female sex hormone has a role in the down-regulation of the systemic eosinophil responses of C57BL/6 mice to infection with B. pahangi." (Immunopharmacol 1992; 23: 75). You may know that tuberculosis, Mycobacterium tuberculosis, is more prevalent in blacks than whites, in a socioeconomically controlled study (New Eng J Med 1990; 322: 422). I explained this, then in 1990, as an example that testosterone adversely affects the immune system in humans, especially in blacks. In a study of mice exposed to Mycobacterium marinum, testosterone was found to increase susceptibility in males and females. This study carefully controlled for the presence of testosterone. "Although this ordering corresponded to the susceptibilities of both male and female mice to the organisms, much greater strain dependency was seen in males than in females. Castration caused an increase in the host resistance of males, but this effect was substantially reversed by continuous testosterone treatment. Testosterone also increased the susceptibility of female mice to this infection. These findings imply that the male sex hormone is involved in the lowered anti-M. marinum resistance of males." (Infect Immun 1991; 59: 4089).

Now, the data in the paragraph above, and citations regarding testosterone and the EAV in horses, all support negative effects of testosterone on differing types of infection in different mammals. Bearing in mind that I cited solid evidence that black males produce significantly more testosterone than white males and black females produce more testosterone than white females, it is my hypothesis that increased testosterone in blacks is why the HIV infects blacks more readily in the U.S.A. and much more so in Africa. For the very same reason, it also explains why blacks exhibit more tuberculosis, and other infections, than whites.