Abstract

<p><span>Studying the replication pattern of Human immunodeficiency virus (HIV) is essential to understand modalities that could halt its survival <em>in-vivo</em>. The CC chemokine receptor 5 (CCR5) is exploited by HIV to gain entry into CD4+ cells. There are several polymorphisms in CCR5; the major coreceptor of HIV that has major influence on HIV transmission and progression to acquired immunodeficiency syndrome (AIDS). CCR5 genes that code for the CCR5 differ in humans, some individuals acquire mutant form of this genes with 32 base pair deletion through mendelian inheritance pattern. Individuals who are homozygous for this gene are completely resistant to HIV infection while heterozygous individuals had extended life span while being infected for an average of 2 to 3 years. CCR5delta32 allele is young in evolutionary time, yet it has reached relatively high frequencies in Caucasians but very low among native Africans. These properties indicate that the mutation has been under intense pressure selection. Surprisingly, there has not been any categorical explanation for this genetic selection. The absence or rare occurrence of CCR5delta32 allele among native Africans may be an explanation for the high HIV transmission rate and disease burden in this race. There are very limited CCR5delta32 studies from Africa thus, justifies the need for researchers to embark on more CCR5delta32 projects in order to establish full range of mutant CCR5 genes that may exist in our societies.</span></p>

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