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Previous Volume 348:2228-2238 May 29, 2003 Number 22 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Infection with human immunodeficiency virus type 1 (HIV-1), the retrovirus that causes the acquired immunodeficiency syndrome (AIDS), is one of the leading causes of death worldwide. All currently available antiretroviral agents inhibit essential HIV-1 enzymes — either the reverse transcriptase or the protease (Figure 1). Recent advances have markedly improved the outcome for many patients who receive these classes of antiretroviral drugs. However, the success of current therapy is limited by the emergence of drug-resistant viruses, the necessity of sustained adherence to complex regimens, and the potential for toxic effects. Novel classes of safe and effective agents with . . . [Full Text of this Article]

HIV-1 Binding and Entry

Early Characterization of the Viral Envelope and CD4+ T-Cell Tropism

The Search for Entry Cofactors

Chemokine Coreceptors (Cc Chemokine Receptor 5 and CXC Chemokine Receptor 4)

Membrane Fusion

Crystallizing the Dynamic Roles of the Viral Envelope Proteins

Inhibition of Viral Entry

Inhibiting the Interaction of GP120 with the CD4 Molecule

Nonspecific Interference with Attachment

Blocking Chemokine-Receptor Binding

Blocking the Fusion of Virus with the Cell Membrane

T-20 (Enfuvirtide)

T-1249

Resistance to Enfuvirtide and T-1249

Future Considerations

Source Information

From the Department of Medicine, University of Alabama, Birmingham (J.M.K.); and the Department of Medicine, University of North Carolina, Chapel Hill (J.J.E.).

Address reprint requests to Dr. Kilby at 908 20th St. S., UAB, Birmingham, AL 35294-2050, or at mkilby@uab.edu.

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Enfuvirtide for Prophylaxis against HIV Infection
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N Engl J Med 2003; 349:815, Aug 21, 2003. Correspondence

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