The United States' secret 1971 Special 'AIDS' Virus Flow Chart
U. S. Secret Virus Program
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