As little as the CDC knew about HIV/AIDS in 1983. The same year, Francoise Barr-Sinoussi & Luc Montagnier of the Pasteur institute in France claimed to have discovered the first HIV strain which they called lymphadenopathy-associated virus (LAV) (HIV-1) (Cantwell, 2005). The LAV (HIV-1) or virus mutation frequency is common than the human genomic mutation occurrence in an attempt for adaptive mechanism against the infection.  It takes years or centuries or thousands of years for an adaptive genomic mutation to occur in response to extrinsic risk factors.

Evolutionarily, humans and other life forms live under the selective pressure of the environment (extrinsic factors), which select better suited traits for that environment. For this fact, HIV may have been re-introduced in the population in the 80’s. It takes several years to induce micro-evolution (genetic mutations in the human genome population) to confer a phenotype. For instance, repeated exposure to plasmodium pathogen, which causes malaria fever, induced a recessive genetic mutation called “sickle cell anemia”.

In mid-1990’s, scientists discovered that possession of the CCR5-∆32 homozygous allele confers complete resistance to HIV-1 (LAV) infection and AIDS (Cohen, & Weaver, 2006). This allele show strong geographical traits among European descendant and are thus far, not found among Africans, Amerindians and East Asians. Among certain European population, the mutation prevalence can go up to 18%. How could a population who has never at one time or several times in the past centuries exposed to HIV-1 (LAV) show a resistance allele to the virus. This is not a coincidence this virus may have caused an epidemic or pandemic before. Recently, using skeletal remains of northern European as early as 2900 years ago scientist showed that CCR5-∆32 mutation is about 5075 years and cannot be attributed to any recent disease outbreak (Cohen, & Weaver, 2006). In addition, they also found that a correlation of long term estimate of lactose tolerance (LCT) in Europe corresponds to the emergence of CCR5-∆32.

Those that carry a homozygous CCR5-∆32 allele are resistance to HIV-1 (LAV), and they do not develop AIDS. Heterozygous carriers may develop AIDS but very slowly. There is a lot that the scientific community did not know.  Hypothesis in this field is a learning curve as we move towards finding a cure for this epidemic.

Reference

Cantwell, A. (2005). Debunking the out of Africa origin of HIV and AIDS the greatest    conspiracy story. Retrieved from http://rense.com/general61/outof.htm.

Cohen, S., & Weaver, L. (2006). The Black Death and AIDS. CCR5-DEL32 in genetics and        history. Retrieved from http://qjmed.oxfordjournals.org/content/99/8/497.full