Anne Sutherland's Journal

HIV Meds
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Figure 1. The Life Cycle of Human Immunodeficiency Virus Type 1 (HIV-1), Showing Potential Targets for Antiretroviral Therapy.

HIV-1 binds to receptors on the cell surface, undergoes membrane fusion, and then releases copies of the RNA genome into the cytoplasm. After successful invasion of the cell, the viral reverse-transcriptase enzyme transcribes single-stranded viral RNA into double-stranded DNA that can be integrated into the genetic material of the human host. Reverse-transcriptase inhibitors were the first agents approved for the treatment of HIV-1; currently available inhibitors of this enzyme are nucleoside antagonists (zidovudine, didanosine, zalcitabine, lamivudine, stavudine, abacavir, and combined formulations), nonnucleoside competitive inhibitors (nevirapine, delavirdine, and efavirenz), and one nucleotide analogue (tenofovir). The viral integrase enzyme is required for the integration of proviral DNA into the host genome before replication. Investigational integrase inhibitors are currently in early clinical trials. When the infected cell synthesizes new protein, integrated proviral DNA is also translated into the protein building blocks of new viral progeny. The viral components then assemble on the cell surface and bud out as immature viral particles. The final maturation of newly formed viruses requires the HIV-1 protease to digest larger components into the intricate pieces that make up an infectious virion. Several protease inhibitors (ritonavir, indinavir, nelfinavir, amprenavir, lopinavir–ritonavir, and two formulations of saquinavir) are currently in clinical use.

T-20 or Enfuvirtide - recently published study in NEJM

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