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Reducing HIV replication with CRISPR could lead to effective cure

This article or excerpt is included in the GLP’s daily curated selection of ideologically diverse news, opinion and analysis of biotechnology innovation.

Scientists in Japan have used CRISPR-Cas9 technology to stop human immunodeficiency virus type 1 (HIV-1) replication in latently infected T cells that can’t be controlled using existing drug treatments. The gene-editing approach effectively disrupts two regulatory HIV-1 genes, tat and rev, which are essential for viral replication.

[W]hile lifelong antiretroviral therapy (ART) can help convert what is otherwise a deadly infection into a more “manageable chronic disease,” current treatments are not a cure because they can’t completely eradicate the virus, which inserts its genes into the host cells’ DNA, the authors explain. Despite treatment using ART, HIV-1 continues to replicate at a very low level in some latently infected immune system cell types, such as CD4+ cells, macrophages, and follicular dendritic cells. ”

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The scientists generated six guide RNAs (gRNAs)—three targeting tat and three targeting rev—to direct the DNA-cleaving Cas9 enzyme to the relevant sites in the proviral DNA. They packaged gRNAs and the Cas9 enzyme system into a lentiviral vector, which they could then introduce into cultured cells.

They claim that the ability to transduce nondividing cells, such as resting CD4+ T cells, using lentiviral constructs and achieve long-term Cas9 transgene expression supports the feasibility of using the system to eradicate cells that act as latent reservoirs of HIV-1.

Editor’s note: Read full study

Read full, original post: CRISPR Eradicates Latent HIV-1, Offering Hope of “Functional Cures”

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