Modulation of the immune system against the ccr5 Δ-32 variant in hiv infection

After the isolation of the HIV virus by the virologist Luc Montagnier, types I and II were characterized with some peculiarities of behavior and geography. AIDS is a disease that affects all races, social classes, sex, religion and sexual orientation. It is expressed as the viral load increases, depressing the immune system propitiating opportunistic pathogens. Responsible for entry of the viral genome into the cells, this genetic mutation was named CCR5Δ-32 for the loss of 32bp encoding the wild-type CCR5. This genetic variant results in the production of non-functional CCR5 coreceptors, the CCR5 / CCR5 allele is predominant in the population homozygous individuals who inherit both copies of the parent CCR5Δ32 mutant gene have an allelic formation (CCR5Δ32 / CCR5 Δ-32). These appear to be highly resistant to the HIV virus. Heterozygous individuals who inherit only one copy of the mutant gene CCR5Δ32, have an allelic formation (CCR5 / CCR5Δ32), however, they will be infected but the evolution to the disease is delayed in relation to people who have two copies of CCR5 gene. The objective of the projectis to discuss the interaction of the coreceptor with the HIV virus by reviewing theories that explain the possible appearance of the mutation, physiological aspects of the normal gene and the mutant gene. It can be concluded that the spotlight is on the CCR5 chemokine receptor, which is the main protagonist of the elevation of HIV / AIDS infection. Efforts to eliminate HIV / AIDS are succeeding, opening up prospects for curing and immunological protection in drug development, engineering and gene therapy, with the CCR5 Δ-32 polymorphism basilar.