The Human Immunodeficiency Virus, Type 2 (HIV-2) emerged in the US in 1987 and since then it has presented a problem to medical science as it is more resistant to the drugs used in Highly Active Antiretroviral Therapy (HAART). Computational simulations of the various enzymes associated with HIV-2 purport to yield data regarding the efficacy of known HAART drugs. Specifically targeting HIV-2 protease, simulations have yielded results indicating ID50 values for five selected HIV protease inhibitor drugs – Amprenavir (APV), Darunavir (DRV), Indinavir (IDV), Lopinavir (LPV), and Saquinavir (SQV). These drugs were chosen based on previous research which indicated the relative inhibition to range from highly inhibitory to weakly inhibitory; not respective to listed order. Current computational studies were done in order to investigate and compare the binding of these ligands to HIV-2 protease. Docking studies revealed that in addition to known active sites, other potential allosteric sites were available. Binding energy and inhibition constant values revealed a slightly different pattern of affinity than prior research suggested. APV ranked lowest in affinity, agreeing with research and showed weak affinity for active site binding and potential allosteric site binding. IDV showed significantly stronger affinity for active site binding than existing research suggests. Further simulations including MD simulations will be completed to further investigate this binding activity.

Computational studies of inhibitor binding to human immunodeficiency virus, Type 2 (HIV-2) protease

249th National Meeting (2015)

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