The huge, alleged AIDS epidemic in Africa is based on several factors which have no scientific basis: 1) WHO's faulty estimates, 2) the nonspecific clinical case definition of AIDS, and 3) grossly inaccurate HIV antibody tests which are not applicable in Africa.

While AIDS authorities proclaim that 25.3 million Africans are doomed to die, in reality, no one knows if a single one of them is infected with HIV.

Johnson is an independent free-lance journalist who lives in the Los Angeles area and can be reached at

When might these epidemics have happened? Patterns of allele frequencies among different ethnic groups help to answer this question. As noted, CCR2-64I is found in all groups, while CCR5-delta32 is restricted to Caucasians and, rarely, African Americans. SDF1-3'A has an intermediate distribution. Caucasians are thought to have diverged from an African ancestry some 150,000 to 200,000 years ago, with Asians diverging subsequently from Caucasians (Figure 7). If so, CCR2-64I, occurring in all ethnic groups, would be the oldest of the mutations, whereas CCR5-delta32 occurring almost exclusively in Caucasians, would be the newest. (Its occurrence in African Americans would reflect gene flow from Caucasians during the last 500 to 600 years.) SDF1-3'A would have an intermediate age.

...the result is 27.5 generations, or only 688 years, with a 95% confidence interval of 11 to 75 generations, or 275 to 1,875 years. This places the age of the CCR5-delta32-bearing haplotype--or rather, a sweep of selective mortality favoring the survival of persons with the mutation--in a span of years centered in the early 14th Century, a timing intriguingly close to history's worst epidemic among Caucasians, the Black Death, which killed as much as a third of all Europeans in the years 1346 to 1352. Three-fourths of all infected persons died. As it happens, the bubonic plague pathogen, Yersinia pestis, carries a 70-kilobase plasmid, which in turn encodes a protein, Yop 1, that enters and kills macrophages. One wonders whether the pathogen targets CCR5, and whether a mutation like CCR5-delta32 protected its carriers against plague, as it protects today against AIDS. Work is now underway to determine whether cells with differing CCR5 genotype react differently to plague. There is also the question of how the genotype affects Shigella, Salmonella, and Mycobacterium tuberculosis --all of which attack host macro-phages. Thus, the findings in AIDS suggest a new context in which to explore how pathogens prey on host cells. Our laboratory is now applying approaches learned in AIDS to a search for host resistance genes against hepatitis B and C.

"a sweep of selective mortality favoring the survival of persons with the mutation"

Thats a re-statement of my point: "It seems more likely to me that people from the 1300's randomly carrying  the genotype resulting in the misfolded proteins survived at a higher rate, increasing the frequency of the genes."


yale