Role of the CCR5 delta 32
allele in resistance to HIV-1 infection in West Africa
The National Library of
Medicine
determined the frequency of the mutant CCR5 delta 32 allele in high-risk
HIV-seronegative Africans as compared with the general African population,
and assessed its in vitro protective efficacy against HIV-1 infection. In
the homozygous form, the CCR5 delta 32-allele confers resistance to
macrophage-tropic (M-tropic) strains of HIV-1. Assuming that genetic
characteristics favoring HIV resistance would prevail in a high-risk HIV-seronegative
population, they examined the CCR5 genotypes of female commercial sex
workers (CSWs) from Dakar,
Senegal, who have remained uninfected for an elongated period.
The following Methods
were used: The CCR5 genetic profile of study participants was determined by
polymerase chain reaction (PCR) amplification of genomic DNA followed by
sequencing. Peripheral blood mononuclear cells (PBMCs) were infected with
different strains of HIV-1 and monitored by p24 enzyme-linked immunosorbent
assay (ELISA).
The
Results Follow: They confirmed the presence of two CCR5wt/delta 32
genotypes among 139 individuals (1.44%). PBMCs from these 2 heterozygous
individuals were also found to be less susceptible to in vitro infection by
an M-tropic HIV-1 primary isolate. The following were conclusions: Evidence
was found of an increased prevalence of the CCR5wt/delta 32 genotype in a
high-risk HIV-seronegative cohort in West Africa. Furthermore, reduced
susceptibility to HIV-1 infection among heterozygous individuals supports a
role for 32-bp CCR5 deletion in HIV-1 resistance.
Comment
from the Stormfront White Nationalist Community:
In the mid 1990's, an exciting
new example of intense selection against one of the homozygotes for a trait
came to light. This stemmed from the discovery that some people do not get
AIDS even if they are repeatedly exposed to the virus ( HIV ) that is
responsible for this usually fatal disease. The people who are immune have
inherited two copies of a rare mutant gene known as CCR5-delta 32 --they are
homozygous. Those who are heterozygous apparently have a partial
immunity or at least a delay in the onset of AID's. Approximately 10% of
Europeans now have the CCR5-delta 32 gene variant, but it is extremely rare
or absent in other populations of the world. There is a surprising
connection in this story. The CCR5-delta 32 gene also provides immunity to a
deadly disease of bacterial origin, bubonic plague. People who are
homozygous for the OCR5-delta 32 gene variant are completely immune, while
heterozygotes have partial immunity. It is very likely that this life-saving
allele occurs as a random mutation and that it was selected for by the
devastating black plague epidemics that swept over Europe beginning in the
14th century. During the first wave of plague, between 1347 and 1350, one
fourth to one third of all Europeans died from this disease. Natural
selection favored those who by chance had inherited the CCR5-delta 32 gene
variant. Repeated waves of plague over the next three centuries resulted in
an increase in the frequency of CCR5-delta 32 in the European population.
The Proof for the Development of AIDS
|
U.S. Public Law 91-213
signed March 16, 1970, by Richard Nixon states: "In the United States’
effort to 'stabilize the population of Sub-Saharan Africa' and thus,
increase the national security of future United States, Nixon proclaims
there would be 'explosive events' (relative to John D. Rockefeller, III’s oversight on the problem of African overpopulation). To date
nary a single U.S. official will address the ‘peculiar’ public law
that authorizes the United States to kill its own citizens and others
in the name of the national security of future (White) Americas. If
the United States is above board, then the President should take
immediate corrective action to fully disclose this secret
(Manhattan-style) program. |
|
J. Craig Venter, Jr., holds
the patent to the gene called the "African American HIV/AIDS Entryway." This is the same gene
that early U.S. science used on African children in the late 50’s
(CCR5 Delta 32 positive). |