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Journal of Undergraduate Research

Keywords

HIV, retrovirus, drug treatment, drug resistance, protease inhibitors

College

Life Sciences

Department

Physiology and Developmental Biology

Abstract

The human immunodeficiency virus (HIV) is a retrovirus with RNA as its genetic material. During the replication cycle, the enzyme reverse transcriptase uses the RNA template to transcribe a complementary DNA copy. Because of the significant infidelity of reverse transcriptase, mutations accumulate within the viral genome at a rate approximately a million times higher than that of a typical host genome (3). This high mutation rate leads to a heterogeneous population in which viral isolates are closely related and evolutionary pathways can be discerned from molecular data. In addition, high mutation rates allow for accelerated evolution, especially under selective conditions. The protease gene has been the target of recent drug therapies attempting to reduce viral load within infected individuals. Protease inhibitors, in combination with traditional reverse transcriptase inhibitors, have proven to be an effective drug therapy, with results as remarkable as 99% decreases in viral load within the first two weeks of treatment (1). However, continued success with such drug regimes is hindered when even 1% of the virus survives. HIV not eradicated by drug treatment is known to hide out in tissues, creating latent reservoirs of virus. My research analyzed HIV evolution before and after drug treatment with emphasis placed on instances of convergent evolution indicative of drug resistance.

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