Current antiretroviral agents target enzymatic functions of the virus such as reverse transcription (nonnucleoside or nucleoside reverse transcriptase inhibitors; NNRTI and NRTI), protease processing of viral polyporoteins (protease inhibitors), viral membrane fusion (fusion inhibitors) and viral DNA integration (integarase inhibitors). Drug cocktail (a combination of nonnucleoside and nucleoside reverse transcriptase inhibitors as well as protease inhibitors) is effective in suppressing viral infection into a chronic condition which rarely progresses to AIDS, many of the inhibitors have adverse side effects. For example, NRTIs can interfere with mitochondrial DNA synthesis and cause hypersensitivity, anemia, diarrhea, neuropathy, nausea, and fatigue in patients. NNRTI may cause severe liver damage or psychological disorders such as depression and insomnia. Protease inhibitors may cause numerous drug-drug interaction, elevated lipodystrophy, and elevated risk of heart attack. Lastly, integrase inhibitors only have short and medium term medical outcomes but are not suitable for long-term use. Therefore there is a need to search for a different class of HIV inhibitors that are efficacious and better-tolerated by patients. HIV-1 encodes accessory proteins including vif, vpu, and nef; these proteins counteract cellular antiviral factors that otherwise would restrict viral replication. Necessary for the replication of HIV-1, vif promotes viral replication by targeting host antiviral protein apobec 3 for degradation. Apobec 3 is a cytidine deaminase that introduces catastrophic levels of G to A hypermutations in viral cDNA, thus yielding biologically incompetent viral genomes. As viral replication is absolutely dependent on the ability of vif to neutralize apobec 3, the vif-apobec axis is an attractive antiviral target. Currently, there are no compounds that target the vif/apobec axis.