Molecular strategies to inhibit HIV-1 replication

Abstract

The human immunodeficiency virus type 1 (HIV-1) is the primary cause of the acquired immunodeficiency syndrome (AIDS), which is a slow, progressive and degenerative disease of the human immune system. The pathogenesis of HIV-1 is complex and characterized by the interplay of both viral and host factors. An intense global research effort into understanding the individual steps of the viral replication cycle and the dynamics during an infection has inspired researchers in the development of a wide spectrum of antiviral strategies. Practically every stage in the viral life cycle and every viral gene product is a potential target. In addition, several strategies are targeting host proteins that play an essential role in the viral life cycle. This review summarizes the main genetic approaches taken in such antiviral strategies.

Figure 1

Summarization of the HIV-1 life cycle and the inhibiting strategies targeting the different steps in the viral life cycle.

Figure 2

Schematic representation of the HIV-1 provirus and the different RNA species. Gag; group specific antigen, Gag-Pol; group specific antigen-polymerase, Env; envelope, Tat; trans-activator of transcription, Rev; regulator of expression of virion proteins, Nef; negative effector, Vif; virion infectivity factor, Vpr; viral protein r, Vpu; viral protein u, LTR; long terminal repeat.