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WIREs Nanomed Nanobiotechnol
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Nanotechnology and HIV: potential applications for treatment and prevention

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Abstract HIV/AIDS is a global pandemic and is the leading infectious cause of death among adults. Although antiretroviral (ARV) therapy has dramatically improved the quality of life and increased the life expectancy of those infected with HIV, life‐long suppressive treatment is required and a cure for HIV infection remains elusive; frequency of dosing and drug toxicity as well as the development of viral resistance pose additional limitations. Furthermore, preventative measures such as a vaccine or microbicide are urgently needed to curb the rate of new infections. The capabilities inherent to nanotechnology hold much potential for impact in the field of HIV treatment and prevention. This article reviews the potential for the multidisciplinary field of nanotechnology to advance the fields of HIV treatment and prevention. WIREs Nanomed Nanobiotechnol 2010 2 693–702 This article is categorized under: Therapeutic Approaches and Drug Discovery > Nanomedicine for Infectious Disease

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HIV LIFECYCLE AND ARV DRUG TARGETS

Viral entry requires binding of viral gp120 to the cellular receptor CD4 and a co‐receptor (CCR5 or CXCR4). Co‐receptor binding initiates changes to gp120 and an intramembrane peptide gp41 that result in membrane fusion. CCR5 inhibitors such as maraviroc prevent viral binding to the CCR5 co‐receptor. The fusion inhibitor enfuvirtide binds to gp41 and prevents the conformational changes required for viral fusion with the cell.

Inside the cytoplasmic compartment, the viral core uncoats and the viral enzyme reverse transcriptase (RT) copies the viral RNA into a double stranded DNA copy which is transported into the nucleus. Nucleoside reverse transcriptase inhibitors (NRTIs) and non‐nucleoside reverse transcriptase inhibitors (NNRTI) inhibit reverse transcription of the viral RNA.

Inside the nucleus, viral integrase incorporates viral DNA into the host cell genome, a step blocked by integrase inhibitors.

The integrated proviral DNA is transcribed to generate full‐length viral RNA and multiple spliced mRNA transcripts that are translated into proteins (e.g., Gag and Gag‐Pol precursors and gp160) by cellular machinery.

The viral proteins and viral RNA are transported to a site near the plasma membrane where they are assembled together with a number of host cell factors into a viral particle.

Budding of the viral particle occurs in conjunction with cleavage of the Gag and Gag‐Pol precursors by viral protease which results in a mature virion. Protease inhibitors block the cleavage step and prevent formation of mature virions.12

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