Integrating the extracellular, intracellular, and intercellular pathogenic processes of the microbiome through glucose saturation, inhibition of the acetyl-CoA carboxylase subunit accA with asRNA, and through quantifying cell-to-cell quorum sensing

Hillman, Tatiana

doi:10.7287/peerj.preprints.27459v1

Cited by 2 publications

(2 citation statements)

References 3 publications

(3 reference statements)

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“…The ultimate purpose of this review was to present possible alternative ways and means to overcome the obstacles for targeting HIV-1 with CRISPR-Cas9 editing of CCR5 of T-cells. HIV-1 infects T cells, which are cells that largely populate the GI tract and more specifically reside in the Peyer's patches of the small intestines, approximately 70% of the immune system is within the GI tract (Hillman, 2018). The degradation of the GI tract can create more space for developing larger HIV reservoirs.…”

Section: Resultsmentioning

confidence: 99%

HIV-1: Tackling the Obstacles that Limit the Effectiveness of CRISPR-Cas9 Gene Editing of the T Cell Co-receptor CCR5

Hillman¹

2020

Preprint

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HIV-1 is a complicated and perplexing virus. It infects T cells, reverse transcribes its RNA into DNA, utilizes its host DNA machinery to replicate its HIV-DNA, translates the HIV-DNA into proteins, assembles itself for a budding escape from the T cell, and rapidly mutates its conformation. Partially, due to its complexity, there remains no cure for HIV or AIDs. However, recently with the discovery of TALENs, the use of zinc fingers, and most of all the applications of CRISPR-Cas9 technology, has given researchers new hope in finding alternative gene therapies and treatments for diseases. With more focus on CRISPR-Cas9, this new and novel technology uses a guiding RNA, sgRNA, to lead a Cas9 nuclease to its target for deletion or to change that DNA site. CRISPR-Cas9 can delete point mutations and multiple DNA sites. Because CRISPR can alter DNA sequences, several scientists have conducted research into CRISPR, possibly treating more diseases such as cancer, diabetes, and even HIV. HIV-1 drew the focus of a researcher named Dr. Ebina in 2013 when he was the first to design and apply CRISPR-Cas9 to genes found in the binding sites of HIV-1, inhibiting HIV-1 gene expression. Since 2013, several other researchers have blocked HIV replication and infection through CRISPR-Cas9 targeting the receptors of T cells called the CC chemokine receptor 5 or CCR5. HIV-1 binds to the CD4 receptor of T cells, which consists of co-receptors CCR5 and CXCR4. If CCR5 expression can be removed, the HIV virus cannot bind to T-cells, blocking the initial attachment stage, and discontinuing the infection. However, there remain obstacles and issues for the CRISPR deletion of CCR5 for treating HIV-1. The issues include: 1) finding new and safe methods of CRISPR-Cas9 delivery, 2) clearing the latent HIV reservoirs, 3) improving the sgRNA design to avoid off-target mutations or deletions, and 4) effectively analyze the viral escape of HIV from CRISPR-Cas9 modifications. Therefore, the purpose of this review is to discuss possible techniques for removing the obstacles that can lessen the potential of CRISPR to delete CCR5, repressing HIV-1 into long-term remission or a functional cure.

show abstract

Section: Resultsmentioning

confidence: 99%

HIV-1: Tackling the Obstacles that Limit the Effectiveness of CRISPR-Cas9 Gene Editing of the T Cell Co-receptor CCR5

Hillman¹

2020

Preprint

Self Cite

View full text Add to dashboard Cite

show abstract

“…The ultimate purpose for this review was to present possible alternative ways and means to overcome the obstacles for targeting HIV-1 with the CRISPR-Cas9 editing of CCR5 of Tcells. HIV-1 infects T cells, which are cells that largely populate the GI tract and more specifically reside in the Peyer's patches of the small intestines, approximately 70% of the immune system is within the GI tract (Hillman, 2018). The degradation of the GI tract can create more space for developing larger HIV reservoirs.…”

Section: Resultsmentioning

confidence: 99%

HIV-1: Tackling the Obstacles, Which Limit the Effectiveness of the CRISPR-Cas9 Gene Editing of the T Cell Co-Receptor, CCR5<strong> </strong>

Hillman¹

2019

Preprint

Self Cite

View full text Add to dashboard Cite

HIV-1 is a complicated and perplexing virus. It infects T cells, reverse transcribes its RNA into DNA, utilizes its host DNA machinery to replicate its HIV-DNA, translates the HIV-DNA into proteins, assembles itself for a budding escape from the T cell, and rapidly mutates its conformation. Partially, due to its complexity, there remains no cure for HIV or AIDs. However, recently with the discovery of TALENs, the use of Zinc fingers, and most of all the application of CRISPR-Cas9 technology, has given researchers a new hope in finding alternative gene therapies and treatments for diseases. With more focus on CRISPR-Cas9, this new and novel technology uses a guiding RNA, sgRNA, to lead a Cas9 nuclease to its target for deletion or to change that DNA site. The CRISPR-Cas9 can delete point mutations and multiple DNA sites. Because CRISPR can alter DNA sequences, several scientists have conducted research into CRISPR possibly curing more diseases as cancer, diabetes, and even HIV. HIV-1 drew the focus of a researcher named Dr. Ebina in 2013 when he was the first to design and apply CRISPR-Cas9 to genes found in the binding sites of the HIV-1, inhibiting HIV-1 gene expression. Since 2013 several other researchers have blocked HIV replication and infection through the CRISPR-Cas9 targeting the receptors of T cells called the CC chemokine receptor 5 or CCR5. HIV-1 binds to the CD4 receptor of T cells that consists of co-receptors CCR5 and CXCR4. If CCR5 expression can be removed, the HIV virus can not bind to T-cells, blocking the initial attachment stage, discontinuing the infection. However, there remain obstacles and issues for the CRISPR deletion of CCR5 for treating HIV-1. The issues include: 1) finding new and safe methods of CRISPR-Cas9 delivery, 2) clearing the latent HIV reservoirs, 3) improve the sgRNA design to avoid off-target mutations or deletions, and 4) effectively analyze the viral escape of HIV from CRISPR-Cas9 modifications. Therefore, the purpose of this review is to discuss possible techniques for removing the obstacles that can lessen the potential of CRISPR to delete CCR5, repressing HIV-1 into long-term remission.

show abstract

Integrating the extracellular, intracellular, and intercellular pathogenic processes of the microbiome through glucose saturation, inhibition of the acetyl-CoA carboxylase subunit accA with asRNA, and through quantifying cell-to-cell quorum sensing

Cited by 2 publications

References 3 publications

HIV-1: Tackling the Obstacles that Limit the Effectiveness of CRISPR-Cas9 Gene Editing of the T Cell Co-receptor CCR5

HIV-1: Tackling the Obstacles that Limit the Effectiveness of CRISPR-Cas9 Gene Editing of the T Cell Co-receptor CCR5

HIV-1: Tackling the Obstacles, Which Limit the Effectiveness of the CRISPR-Cas9 Gene Editing of the T Cell Co-Receptor, CCR5<strong> </strong>

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