Why HIV is so
Prevalent in
Copyright ã 1997 by James Michael Howard.
New Support: March, 2006: Testosterone and
Equine Encephalitis virus in macaques, November, 2006: Racial Disparities in
HIV infection, below
It is my hypothesis that increased
testosterone increases HIV infection rates and AIDS . This
will explain why AIDS is so high in
McCollum WH, et al.,
"Resistance of Castrated Male Horses to Attempted Establishment of the
"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 England 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
New Support:
|
Virol J. 2006 Mar 29;3(1):19 [Epub ahead of print] |
|
Testosterone correlates with Venezuelan
Equine Encephalitis virus infection in macaques.
Muehlenbein
MP, Cogswell
FB, James
MA, Koterski
J, Ludwig
GV.
ABSTRACT: Here we briefly report testosterone and cytokine responses to
Venezuelan Equine Encephalitis virus (VEEV) in macaques which were used as part
of a larger study conducted by the Department of Defense to better characterize
pathological responses to aerosolized VEEV in non-human primates. Serial
samples were collected and analyzed for testosterone and cytokines prior to and
during infection in 8 captive male macaques. Infected animals exhibited a
febrile response with few significant changes in cytokine levels. Baseline
testosterone levels were positively associated with viremia following exposure
and were significantly higher than levels obtained during infection. Such
findings suggest that disease-induced androgen suppression is a reasonable area
for future study. Decreased androgen levels during physiological perturbations
may function, in part, to prevent immunosuppression by high testosterone levels
and to prevent the use of energetic resources for metabolically-expensive
anabolic functions.
|
Am J
Public Health. 2006 Nov 30; [Epub ahead of print] |
|
Sexual and Drug Behavior Patterns and HIV/STD
Racial Disparities: The Need for New Directions.
Hallfors
DD, Iritani
BJ, Miller
WC, Bauer
DJ.
PIRE.
Objectives. We used nationally representative data to
examine whether individuals' sexual and drug behavior patterns account for
racial disparities in sexually transmitted disease (STD) and HIV prevalence. Methods. Data were derived from wave III of the National
Longitudinal Study of Adolescent Health. Participants were aged 18 to 26 years
old; analyses were limited to non-Hispanic Blacks and Whites. Theory and
cluster analyses yielded 16 unique behavior patterns. Bivariate analyses
compared STD/HIV prevalences for each behavior pattern, by race. Logistic
regression analyses examined within-pattern race effects before and after
control for covariates. Results. Unadjusted odds of
STD/HIV infection were significantly higher among Blacks than among Whites for
11 of the risk behavior patterns assessed. Across behavior patterns, covariates
had little effect on reducing race odds ratios. Conclusions.
White young adults in the