HIV strains that efficiently infect T cells are referred to as T-cell tropic and preferentially utilize the chemokine receptor CXCR4 as the co receptor. Other strains of HIV, which efficiently infect cells of the monocyte/macrophage lineage, are referred to as macrophage tropic and preferentially utilize the chemokine receptor CCR5 as the co receptor. Binding to the co receptor induces additional conformational changes within gp120, which exposes the fusogenic gp41 domain. This results in fusion of the viral envelope with the target cell membrane. The gp120-chemokine receptor-binding event is an essential part of the infection process. This is exemplified by a small group of people who remain uninfected despite multiple exposures to HIV. These individuals possess a homozygous mutation of the CCR5 gene, which prevents the CCR5 receptor from being presented at the cell surface. This mutation renders these individuals virtually resistant to infection by macrophage tropic strains of HIV (Website 1).
Once the viral envelope has fused with the target cell membrane, the contents of the virion enter the host cell and infection is achieved. The reverse transcriptase enzyme then copies the viral genomic RNA into DNA. Next, the DNA copy of the viral genome is readily transported to the nucleus and subsequently integrated into the host cell genomic DNA by the integrase enzyme. Once integration is completed, viral genes can be transcribed by host cell polymerizes into viral mRNA, and consequently translated into viral proteins. The next step is virion assembly, followed by processing of the Capsid proteins by the viral protease. At this point, the nascent virions are able to bud from the host cell in search of new target cells to infect (Long et al., 2000).
Epidemiology.
Acquired Immune Deficiency Syndrome (AIDS) is the leading cause of death in persons aged 25-44. It is characterized by a progressive decline in immune function over a period of 8-15 years, which is paralleled by an increase in susceptibility to a wide range of opportunistic infections.