Key Points

• Infection with HIV proceeds in a series of steps, the first step being virion binding to the host cell and releasing the viral RNA. Fusion inhibitors can interrupt this step.

• In step 2, HIV uses reverse transcriptase to convert viral RNA to DNA. RT inhibitors can prevent this step.

• The HIV DNA is then incorporated into the host genome to form the provirus, facilitated by integrase. The virus may remain latent until the CD4+ cell is immune activated, making viral proteins. Integrase Inhibitors interfere with this step.

• Transcription of DNA to RNA occurs in the nucleus. During translation, mRNA takes over the protein-making mechanism to form viral proteins as well as viral RNA. The products are then divided into functional units using viral protease. Protease inhibitors interrupt this step.

• The final step consists of assembly, budding, and pinching off of the viral proteins, RNA, and enzymes inside the host membrane to form the complete virion.

Human immunodeficiency virus gains access to CD4+ cells in stages (Berger et al., 1999; Smith and Daniel, 2006; Zheng et al., 2005). CD4+ cells are the main mediators of cellular immune response, helping T lymphocytes and B lymphocytes to perform their functions. The 800 to 1200 cells/mm3 of blood in healthy people are usually decimated by HIV. Minor infections, such as herpes simplex virus, thrush, and vaginal candidiasis may occur as the CD4+ count falls below 500, when 50% of the immune reserve is depleted. With a worsening disease process and decreasing CD4+ count (<200), risk of life-threatening opportunistic infections and cancer increases. Research has focused on medications that can interrupt the life cycle and slow the infection of cells.

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