CCR5 and Protection from AIDS

James Howard jmhoward at sprynet.com
Mon Dec 7 12:24:33 EST 1998


Thank you for your response, Dr. Moné.  You made one very good point, i.e.,
I should have included citations to support the various points of my post.
I receive very few responses to my posts, so I tend to try to limit the
length of my posts as much as possible.  This is not an excuse, in fact, it
is a mistake as it fosters responses such as yours.  I am including, below
this response to you, a post, “Why HIV is so Prevalent in Africa,” which
contains an explanation of how increased testosterone may be involved in the
rampant rate of HIV infection in Africa, with supporting citations.  I
suggest this post “establish[es] a causal relationship between two
phenomen[a].”

The incidence of HIV infection in men and women is also directly connected
to levels of testosterone.  This is from my explanation of AIDS at my
website:  “November 24, 1995, the Associated Press reported the latest data
concerning HIV infection rates in people 27 to 39 years old in the U.S.  The
A.P. article included the following: women ‘are four times less likely to be
infected,’ and the infection rates are 1 in 139 in white males vs. 1 in
1,667 in white females: 1 in 33 black men are infected, while 1 in 98 black
women are infected.  The news release is based on the latest data from the
Centers for Disease Control and Prevention.’ (Science 1995; 270: 1372)”
Now, this series of least to most infected group, white females, black
females, white males, black males, directly parallels the levels of
testosterone in these groups.  So, Dr. Moné, no, “women are [not] at higher
risk for infection than men for contracting infection,” according to the
CDC.

Why 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; see my explanation of AIDS at
http://www.naples.net/~nfn03605. 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 white males, (J National Cancer
Institute 1986; 76: 45), and black females produce more testosterone than
white females, (J Clin Endocrin 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.”

"Jay Mone'" wrote in message <366BA7E6.7480 at marauder.millersv.edu>...
>OK, James Michael Howard.  You appear to have a single data point,
>namely a presumed statistical difference in testosterone levels and
>decreased incidence of AIDS.
>I'm not sure of your background in science in general, or biology in
>particular, but it takes a bit more to establish a causal relationship
>between two phenomenon.
>Where is the data which definitively links testosterone production to
>pathogenesis of HIV?  One could also look at where most new AIDS cases
>are appearing (Asia and sub-Saharan Africa, and one would notice that
>the majority of new cases in these regions are people with brown
>hair!!)  Does this establish a causal link?
>If one looks at the incidence of HIV infection after a sexual
>encounter with an HIV-infected individual, one sees that women are at
>higher risk for infection than men for contracting infection.  But
>women have lower testosterone levels than men.
>
>Jay Mone'





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