scholarly journals DNA repair and gene editing: the director’s cut

2021 ◽  
Author(s):  
Kelly Doughty ◽  
Robert A. Baldock
Keyword(s):  
Biological Sciences ◽  
Human Immunodeficiency Virus ◽  
Dna Repair ◽  
Gene Editing ◽  
Genetic Diseases ◽  
Theme Parks ◽  
Macaque Monkeys ◽  
Origin Stories ◽  
Immunodeficiency Virus ◽  
New Gene

Novelists and screenwriters have bombarded our imaginations with the idea of genetic engineering. From superhero origin stories to theme parks inhabited by dinosaurs, the prospect of re-writing the genetic code has inspired many and raised many ethical questions. The potential for these tools in medicine and biological sciences to prevent genetic diseases is readily being explored. Recent successes include destruction of simian immunodeficiency virus DNA from infected rhesus macaque monkeys (synonymous to the human immunodeficiency virus). The diverse power of these tools is also helping to control mosquito populations and supress the spread of malaria. New gene-editing tools have made genome editing faster, more accurate and cheaper than ever before, but how do they work? And how do we know whether the desired edits will be made?

scholarly journals Induction of immune response in macaque monkeys infected with simian–human immunodeficiency virus having the TNF-α gene at an early stage of infection

Virology ◽  
2005 ◽  
Vol 343 (2) ◽  
pp. 151-161 ◽  
Author(s):  
Yuya Shimizu ◽  
Yasuyuki Miyazaki ◽  
Kentaro Ibuki ◽  
Hajime Suzuki ◽  
Kentaro Kaneyasu ◽  
...  
Keyword(s):  
Immune Response ◽  
Human Immunodeficiency Virus ◽  
Early Stage ◽  
Macaque Monkeys ◽  
Tnf Α ◽  
Immunodeficiency Virus

scholarly journals The Use of CRISPR/Cas9 as a Tool to Study Human Infectious Viruses

2021 ◽  
Vol 11 ◽  
Author(s):  
Huafeng Lin ◽  
Gang Li ◽  
Xiangwen Peng ◽  
Aimin Deng ◽  
Lei Ye ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Infectious Diseases ◽  
Food Industry ◽  
Gene Editing ◽  
Agricultural Practices ◽  
Clinical Settings ◽  
Future Perspectives ◽  
Biological Feature ◽  
B Virus ◽  
Immunodeficiency Virus

Clustered regularly interspaced short palindromic repeats (CRISPR) systems are a set of versatile gene-editing toolkit that perform diverse revolutionary functions in various fields of application such as agricultural practices, food industry, biotechnology, biomedicine, and clinical research. Specially, as a novel antiviral method of choice, CRISPR/Cas9 system has been extensively and effectively exploited to fight against human infectious viruses. Infectious diseases including human immunodeficiency virus (HIV), hepatitis B virus (HBV), human papillomavirus (HPV), and other viruses are still global threats with persistent potential to probably cause pandemics. To facilitate virus removals, the CRISPR/Cas9 system has already been customized to confer new antiviral capabilities into host animals either by modifying host genome or by directly targeting viral inherent factors in the form of DNA. Although several limitations and difficulties still need to be conquered, this technology holds great promises in the treatment of human viral infectious diseases. In this review, we will first present a brief biological feature of CRISPR/Cas9 systems, which includes a description of CRISPR/Cas9 structure and composition; thereafter, we will focus on the investigations and applications that employ CRISPR/Cas9 system to combat several human infectious viruses and discuss challenges and future perspectives of using this new platform in the preclinical and clinical settings as an antiviral strategy.

CRISPR Genome Editing Technology and its Application in Genetic Diseases: A Review

2020 ◽  
Vol 21 ◽  
Author(s):  
Sepideh Khatibi ◽  
Amirhossein Sahebkar ◽  
Seyed Hamid Aghaee Bakhtiari
Keyword(s):  
Cystic Fibrosis ◽  
Human Immunodeficiency Virus ◽  
Genetic Diseases ◽  
Human Diseases ◽  
Live Cells ◽  
Single Nucleotide ◽  
Rna Sequence ◽  
Immunodeficiency Virus ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome

: Gene therapy has been a long-lasting goal of scientists and there are many ideal methods and tools that have been developed to correct disease-causing mutations in human. Recently, Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) technology has been progressively used for the assessment or treatment of human diseases, including Thalassemia, Parkinson disease, Cystic Fibrosis, Glaucoma, Huntington’s disease and Human Immunodeficiency Virus/Acquired Immunodeficiency Syndrome (HIV/AIDS). CRISPR sequences is a part of the bacterial immune system, which includes nuclease Cas enzyme and a RNA sequence. The RNA sequence is unique and pathogen-specific, which identifies and binds to the DNA of invasive viruses, and allows the nuclease Cas enzyme to cut identified DNA and destroy the invasive viruses. This feature provides a possibility to edit mutations in DNA sequence of live cells through replacement of a specific targeted RNA sequence with the RNA sequence in the CRISPR system. Previous studies showed the improvement steps in confrontation to human diseases caused by single nucleotide mutations using this system. In this review, we first concisely introduce CRISPR and its functions, and next study the use of CRISPR in the treatment of human diseases.

scholarly journals DNA Repair Enzyme Uracil DNA Glycosylase Is Specifically Incorporated into Human Immunodeficiency Virus Type 1 Viral Particles through a Vpr-Independent Mechanism

1999 ◽  
Vol 73 (2) ◽  
pp. 1682-1688 ◽  
Author(s):  
Karen E. Willetts ◽  
Françoise Rey ◽  
Isabelle Agostini ◽  
Jean-Marc Navarro ◽  
Yves Baudat ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Dna Repair ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Repair Enzyme ◽  
Uracil Dna Glycosylase ◽  
Viral Particles ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT The Vpr protein, encoded by the human immunodeficiency virus type 1 (HIV-1) genome, is one of the nonstructural proteins packaged in large amounts into viral particles. We have previously reported that Vpr associates with the DNA repair enzyme uracil DNA glycosylase (UDG). In this study, we extended these observations by investigating whether UDG is incorporated into virions and whether this incorporation requires the presence of Vpr. Our results, with highly purified viruses, show that UDG is efficiently incorporated either into wild-type virions or into Vpr-deficient HIV-1 virions, indicating that Vpr is not involved in UDG packaging. Using an in vitro protein-protein binding assay, we reveal a direct interaction between the precursor form of UDG and the viral integrase (IN). Finally, we demonstrate that IN-defective viruses fail to incorporate UDG, indicating that IN is required for packaging of UDG into virions.

scholarly journals The Presence of Human Immunodeficiency Virus Type 1 Vpr Correlates with a Decrease in the Frequency of Mutations in a Plasmid Shuttle Vector

1999 ◽  
Vol 73 (9) ◽  
pp. 7132-7137 ◽  
Author(s):  
Jeremy B. Jowett ◽  
Yi-ming Xie ◽  
Irvin S. Y. Chen
Keyword(s):  
Human Immunodeficiency Virus ◽  
Dna Repair ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Excision Repair ◽  
Shuttle Vector ◽  
Vector System ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT The human immunodeficiency virus type 1 (HIV-1) Vpr protein induces cell cycle arrest at the border of G2 and M similar to the arrest caused by agents which damage DNA. We determined whether the presence of Vpr would affect the ability of cells to repair DNA. We developed a shuttle vector system to analyze the effect of Vpr upon the repair of UV-damaged DNA. Our results demonstrated that the presence of Vpr decreased the rate of deletions in this system. Of note, cells arrested in G2 by other genotoxic agents also increased the frequency of DNA repair of UV-damaged shuttle vectors. We did not observe any direct effect of Vpr upon the rate of double-strand break repair and/or nucleotide excision repair of genomic DNA in cells. Our results suggest a role for HIV-1 Vpr in altering the frequency of DNA repair, a property which may have importance for HIV-1 replication and pathogenesis.

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