HIV first appeared in the 1980’s largely in males practicing anal receptive sexual behavior. Although HIV had not yet been characterized, medical personnel noted that this population had stubborn infections, resistant to most medications. Human immunodeficiency virus (HIV) can result in profound viremia and low T-cell counts characterized as acquired immune deficiency syndrome (AIDS). Currently, it is theorized that both strains of HIV descend from simian immunodeficiency virus (SIV) a virus that infects non- human primates. (Sharp, 2005) While other factors may have contributed to the development of genetic immunity to HIV, some studies suggest that populations which are resistant to smallpox carry the CCR5 D32 mutation. Still others consider…show more content… Certainly, it is imperative to highlight the proposed age of the CCR5 D32 mutation. Hummel at al, examined DNA samples from 2,900-years-old Bronze Age skeletons and revealed that the frequency of the CCR5 D32 mutation (11.8%) was similar to those in modern German DNA samples (9.2%). Simply, the origin of the CCR5 D32 mutation is much older than we anticipated. Both, Yersinia pestis and smallpox lack genomic evidence linking either to the CCR5 D32 mutation and thus are null hypotheses. Hendrick at al, conducted research using a genetic map, and 32 single nucleotide polymorphisms (SNP) markers that were determined for D32 haplotypes, to estimate the deletion age more accurately. Subsequently, the age of the D32 mutation increased to approximately 5075 years (3150 – 7800; 95% confidence interval), which is consistent with the Bronze Age date discussed earlier. The high frequency of the deletion in the Bronze Age samples positively demonstrates that the deletion was present at least 3000 years ago, long before plague was an important human pathogen and, perhaps, even before smallpox was a widespread pathogen, suggesting that the initial potential selective agent was not the plague and perhaps not even…show more content… 1998). Siting that indeed, the homozygote carriers of the CCR5 D32 mutation could develop normally but only in a pathogen-free environment. Since a CCR5 D32 homozygote would exhibit reduced efficiency of bacterial clearance, thereby decreasing the overall fitness level. Subsequently, homozygotes carriers of the CCR5 D32 mutation exist at low frequencies in Caucasian populations, at about
