Abstract
The major barrier to eradication of HIV infection is the latent viral reservoir that persists despite long-term highly active antiretroviral therapy (HAART). The main reason for the existence of latently infected cells is that proviral DNA becomes integrated into the cellular genome. Theoretically, the elimination of proviral DNA from every infected cell should therefore be able to cure HIV infection. This concept has been tested in studies that employed designed recombinases [1], zinc finger nucleases (ZFNs) and transcription activator-like effector nucleases (TALENs) bearing sequence-specific DNA-binding modules that recognize HIV DNA sequences [2]. In addition, the recent development of the bacterial adaptive immune system CRISPR/Cas9 for editing of genes in mammalian cells [3, 4] quickly led to the use of this new genome editing technology to try to inhibit and eliminate infection by different viruses, including HIV-1 [5].
Highlights
The major barrier to eradication of HIV infection is the latent viral reservoir that persists despite long-term highly active antiretroviral therapy (HAART)
*Correspondence: chen.liang@mcgill.ca 1 McGill University AIDS Centre, Lady Davis Institute, Jewish General Hospital, Montreal, QC H3T1E2, Canada Full list of author information is available at the end of the article question is whether and how HIV-1 might escape from the programmed CRISPR/Cas9 attack, a topic that is fundamental to attempts aimed at HIV treatment and prevention, including the use of small molecule-based antiretroviral therapy and HIV vaccines
It could be expected that HIV-1 would change the sequence of the viral DNA that is targeted by single guide RNA (sgRNA) or the PAM sequence, knowing how HIV-1 escapes from a sequence-specific RNA interference attack [14,15,16]
Summary
The major barrier to eradication of HIV infection is the latent viral reservoir that persists despite long-term highly active antiretroviral therapy (HAART). In addition to this single guide RNA (sgRNA), Cas9 needs to recognize a multinucleotide region that is adjacent to the 3′ end of the target DNA, which is termed PAM (protospacer adjacent motif ). Despite the promising possibility that CRISPR/Cas9 could be used to inactivate or even delete proviral DNA from HIV-1 infected cells, an important unanswered
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