Nevirapine anti-viral drug, part of triple therapy for HIV/AIDS - Essay Example

CD4+ T-helper cells play an important role in antibody class switching of B-cells, activation and growth of T-cytotoxic cells, and synergizing the bactericidal activity of macrophages. Loss of these cells, seen in HIV infections and T-lymphocytpenia, causes loss of antibody class switching required to increase the affinity of antibodies, failure to produce B cells with IgA or IgG, loss of stimulation of T-cytotoxic cells, ultimately leading to loss of pathogen recognition by T cells culminating in opportunistic infections (3).

Life cycle of HIV and rationale for Anti-HIV drug design. In order to design an appropriate drug or to understand the pharmacology of the anti-HIV drugs it is quintessential to understand the molecular aspects of life cycle of HIV including the process of HIV infection, their assembly, gene structure and the products they encode. HIV-1 begins its life cycle (Figure 1) as an infectious particle binding to receptor CD4 and co-receptor (CCR5 or CXCR4). Targeting of HIV co-receptors forms an exciting frontier for antiretroviral therapeutics.

HIV entry inhibitors interacting with CXCR4 co-receptor (such as AMD3100; AMD3465; ALX40-4C; T22, T134 and T140), or which are antagonists to the CCR5 co-receptor (TAK-779, TAK-220, SCH-C, SCH-D, E913, AK-602 and NSC 651016) are either in preclinical or clinical trails (4). The next step in the life cycle of HIV1 is the process of fusion with the membrane and delivery of viral RNA genome into the cells. A new class of drugs that is based on inhibiting the process of fusion, such as T1249, is in clinical use (5).

Retroviruses possess enveloped RNA genome which replicates using a DNA intermediate by the catalytic activity of an enzyme called reverse transcriptase (RT) which also possesses RNaseH activity. HIV’s RT is a heterodimeric protein complex made of subunits p66 and p51. While p66 has the RT