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Journal articles on the topic 'HIV pathogenicity; Gene therapy'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Munis, Altar M. "Gene Therapy Applications of Non-Human Lentiviral Vectors." Viruses 12, no. 10 (September 29, 2020): 1106. http://dx.doi.org/10.3390/v12101106.

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Recent commercialization of lentiviral vector (LV)-based cell therapies and successful reports of clinical studies have demonstrated the untapped potential of LVs to treat diseases and benefit patients. LVs hold notable and inherent advantages over other gene transfer agents based on their ability to transduce non-dividing cells, permanently transform target cell genome, and allow stable, long-term transgene expression. LV systems based on non-human lentiviruses are attractive alternatives to conventional HIV-1-based LVs due to their lack of pathogenicity in humans. This article reviews non-human lentiviruses and highlights their unique characteristics regarding virology and molecular biology. The LV systems developed based on these lentiviruses, as well as their successes and shortcomings, are also discussed. As the field of gene therapy is advancing rapidly, the use of LVs uncovers further challenges and possibilities. Advances in virology and an improved understanding of lentiviral biology will aid in the creation of recombinant viral vector variants suitable for translational applications from a variety of lentiviruses.

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2

White, Sarah M., Matthew Renda, Na-Yon Nam, Ekaterina Klimatcheva, Yonghong Zhu, Jennifer Fisk, Mark Halterman, et al. "Lentivirus Vectors Using Human and Simian Immunodeficiency Virus Elements." Journal of Virology 73, no. 4 (April 1, 1999): 2832–40. http://dx.doi.org/10.1128/jvi.73.4.2832-2840.1999.

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ABSTRACT Lentivirus vectors based on human immunodeficiency virus (HIV) type 1 (HIV-1) constitute a recent development in the field of gene therapy. A key property of HIV-1-derived vectors is their ability to infect nondividing cells. Although high-titer HIV-1-derived vectors have been produced, concerns regarding safety still exist. Safety concerns arise mainly from the possibility of recombination between transfer and packaging vectors, which may give rise to replication-competent viruses with pathogenic potential. We describe a novel lentivirus vector which is based on HIV, simian immunodeficiency virus (SIV), and vesicular stomatitis virus (VSV) and which we refer to as HIV/SIVpack/G. In this system, an HIV-1-derived genome is encapsidated by SIVmac core particles. These core particles are pseudotyped with VSV glycoprotein G. Because the nucleotide homology between HIV-1 and SIVmac is low, the likelihood of recombination between vector elements should be reduced. In addition, the packaging construct (SIVpack) for this lentivirus system was derived from SIVmac1A11, a nonvirulent SIV strain. Thus, the potential for pathogenicity with this vector system is minimal. The transduction ability of HIV/SIVpack/G was demonstrated with immortalized human lymphocytes, human primary macrophages, human bone marrow-derived CD34+ cells, and primary mouse neurons. To our knowledge, these experiments constitute the first demonstration that the HIV-1-derived genome can be packaged by an SIVmac capsid. We demonstrate that the lentivirus vector described here recapitulates the biological properties of HIV-1-derived vectors, although with increased potential for safety in humans.

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3

Morice, Yoann, Dominique Roulot, Véronique Grando, Jérome Stirnemann, Elyanne Gault, Vincent Jeantils, Michelle Bentata, et al. "Phylogenetic analyses confirm the high prevalence of hepatitis C virus (HCV) type 4 in the Seine-Saint-Denis district (France) and indicate seven different HCV-4 subtypes linked to two different epidemiological patterns." Journal of General Virology 82, no. 5 (May 1, 2001): 1001–12. http://dx.doi.org/10.1099/0022-1317-82-5-1001.

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Hepatitis C virus (HCV) has been classified into six clades as a result of high genetic variability. In the Seine-Saint-Denis district of north-east Paris, the prevalence of HCV-4, which usually infects populations from Africa or the Middle East, is twice as high as that recorded for the whole of continental France (10·2 versus 4·5%). Although the pathogenicity of HCV-4 remains unknown, resistance of HCV-4 to therapy appears to be similar to that observed for HCV-1. In order to characterize the epidemiology of HCV-4 in Paris, sequences of the non-structural 5B gene (332 bp) were obtained from 38 HCV-4-infected patients. Extensive phylogenetic analyses indicated seven different HCV-4 subtypes. Moreover, phylogenetic tree topologies clearly distinguished two epidemiological profiles. The first profile (52·6% of patients) reflects the intra-suburban emergence of two distinct HCV-4 subclades occurring mainly among intravenous drug users (65% of patients). The second profile shows six subclades [HCV-4a, -4f, -4h, -4k, -4a(B) and a new sequence] and accounts for patients from Africa (Egypt and sub-Saharan countries) who have unknown risk factors (77·8% of patients) and in whom no recent diffusion of HCV-4 is evident. This study indicates the high diversity of HCV-4 and the extension of HCV-4a and -4d subclades among drug users in France.

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4

&NA;. "Gene therapy for HIV?" Inpharma Weekly &NA;, no. 1128 (March 1998): 11. http://dx.doi.org/10.2165/00128413-199811280-00019.

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5

Voelker, R. "Gene therapy for HIV." JAMA: The Journal of the American Medical Association 275, no. 20 (May 22, 1996): 1533. http://dx.doi.org/10.1001/jama.275.20.1533.

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6

Voelker, Rebecca. "Gene Therapy for HIV." JAMA: The Journal of the American Medical Association 275, no. 20 (May 22, 1996): 1533. http://dx.doi.org/10.1001/jama.1996.03530440011009.

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7

Minton, Kirsty. "Gene therapy for HIV." Nature Reviews Immunology 4, no. 6 (June 2004): 400. http://dx.doi.org/10.1038/nri1386.

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8

Bird, Lucy. "Gene therapy for HIV?" Nature Reviews Immunology 14, no. 4 (March 25, 2014): 215. http://dx.doi.org/10.1038/nri3655.

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9

Lever, A. M. L. "Gene therapy for HIV." Sexually Transmitted Infections 77, no. 2 (April 1, 2001): 93–96. http://dx.doi.org/10.1136/sti.77.2.93.

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10

Crenshaw, Brennetta J., Leandra B. Jones, Courtnee’ R. Bell, Sanjay Kumar, and Qiana L. Matthews. "Perspective on Adenoviruses: Epidemiology, Pathogenicity, and Gene Therapy." Biomedicines 7, no. 3 (August 19, 2019): 61. http://dx.doi.org/10.3390/biomedicines7030061.

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Human adenoviruses are large (150 MDa) doubled-stranded DNA viruses that cause respiratory infections. These viruses are particularly pathogenic in healthy and immune-compromised individuals, and currently, no adenovirus vaccine is available for the general public. The purpose of this review is to describe (i) the epidemiology and pathogenicity of human adenoviruses, (ii) the biological role of adenovirus vectors in gene therapy applications, and (iii) the potential role of exosomes in adenoviral infections.

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11

Jacobson, Jeffrey M. "HIV gene therapy research advances." Blood 121, no. 9 (February 28, 2013): 1483–84. http://dx.doi.org/10.1182/blood-2013-01-475921.

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12

Didigu, Chuka, and Robert Doms. "Gene Therapy Targeting HIV Entry." Viruses 6, no. 3 (March 21, 2014): 1395–409. http://dx.doi.org/10.3390/v6031395.

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13

Clayton, Julie. "Gene therapy progress for HIV." Drug Discovery Today 7, no. 16 (August 2002): 841–42. http://dx.doi.org/10.1016/s1359-6446(02)02418-2.

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14

Hardy, Leslie M. "Gene Therapy for HIV Infection." JAMA: The Journal of the American Medical Association 272, no. 6 (August 10, 1994): 423. http://dx.doi.org/10.1001/jama.1994.03520060021009.

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15

de Mendoza, Carmen, Pablo Barreiro, Laura Benitez, and Vicente Soriano. "Gene therapy for HIV infection." Expert Opinion on Biological Therapy 15, no. 3 (October 17, 2014): 319–27. http://dx.doi.org/10.1517/14712598.2015.967208.

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16

Lever, A. M. L. "Gene therapy for HIV infection." British Medical Bulletin 51, no. 1 (January 1995): 149–66. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072944.

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17

Chadwick, David R., and Andrew ML Lever. "Gene therapy for HIV infection." Expert Opinion on Therapeutic Patents 8, no. 8 (August 1998): 983–90. http://dx.doi.org/10.1517/13543776.8.8.983.

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18

Medina, M., A. Ramezani, and S. Joshi. "Anti-HIV-1 gene therapy." Transfusion Science 17, no. 1 (March 1996): 109–20. http://dx.doi.org/10.1016/0955-3886(95)00064-x.

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19

Calenda, V., P. Leissner, M. Marigliano, and M. Mehtali. "Gene therapy for HIV infection." Hematology and Cell Therapy 38, no. 2 (April 1996): 211–13. http://dx.doi.org/10.1007/s00282-996-0211-9.

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20

McCarthy, Michael. "Gene therapy for HIV infection." Lancet 342, no. 8874 (September 1993): 799. http://dx.doi.org/10.1016/0140-6736(93)91558-4.

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21

Lisziewicz, J., L. Galluzzi, and F. Lori. "Gene therapy for HIV-1." Bundesgesundheitsblatt - Gesundheitsforschung - Gesundheitsschutz 44, no. 11 (November 1, 2001): 1071–75. http://dx.doi.org/10.1007/s00103-001-0281-3.

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22

Sheykhhasan, Mohsen, Aidin Foroutan, Hamed Manoochehri, Saeideh Gholamzadeh Khoei, Naresh Poondla, and Massoud Saidijam. "Could gene therapy cure HIV?" Life Sciences 277 (July 2021): 119451. http://dx.doi.org/10.1016/j.lfs.2021.119451.

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23

Battaglia, Piero A., Santina Zito, Antonella Macchini, and Franca Gigliani. "A Drosophila model of HIV-Tat-related pathogenicity." Journal of Cell Science 114, no. 15 (August 1, 2001): 2787–94. http://dx.doi.org/10.1242/jcs.114.15.2787.

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To analyze the mechanism of Tat-mediated HIV pathogenicity, we produced a Drosophila melanogaster strain transgenic for HIV-tat gene and induced the expression of the protein during Drosophila development. By in vitro and in vivo experiments, we demonstrated that Tat specifically binds to tubulin via the MAP-binding domain of tubulin, and that this interaction delays the polymerization of tubulin and induces a premature stop to microtubule-dependent cytoplasmic streaming. The delay in the polymerization of microtubules, the tracks for the transport of the axes determinants, alters the positioning of the dorso-ventral axis as shown by the mislocalization of Gurken and Kinesin in oocyte of Drosophila after Tat induction. These results validate the use of Drosophila as a tool to study the molecular mechanism of viral gene products and suggest that Tat-tubulin interaction is responsible for neurodegenerative diseases associated with AIDS.

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24

Manjunath, N., Guohua Yi, Ying Dang, and Premlata Shankar. "Newer Gene Editing Technologies toward HIV Gene Therapy." Viruses 5, no. 11 (November 14, 2013): 2748–66. http://dx.doi.org/10.3390/v5112748.

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25

&NA;. "Gene therapy to limit HIV infection?" Inpharma Weekly &NA;, no. 1013 (November 1995): 11. http://dx.doi.org/10.2165/00128413-199510130-00023.

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26

&NA;. "A possible anti-HIV gene therapy." Inpharma Weekly &NA;, no. 972 (February 1995): 11. http://dx.doi.org/10.2165/00128413-199509720-00021.

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27

Jolly, Douglas J. "HIV Infection and Gene Transfer Therapy." Human Gene Therapy 2, no. 2 (July 1991): 111–12. http://dx.doi.org/10.1089/hum.1991.2.2-111.

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28

Pennisi, E. "HIV Provides Tools for Gene Therapy." Science News 143, no. 24 (June 12, 1993): 372. http://dx.doi.org/10.2307/3977264.

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29

Lori, Franco, Paola Guallini, Luca Galluzzi, and Julianna Lisziewicz. "Gene Therapy Approaches to HIV Infection." American Journal of PharmacoGenomics 2, no. 4 (2002): 245–52. http://dx.doi.org/10.2165/00129785-200202040-00004.

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30

Fox, Jeffrey L. "HIV vector challenges gene therapy oversight." Nature Biotechnology 15, no. 9 (September 1997): 832. http://dx.doi.org/10.1038/nbt0997-832.

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31

Dey, R., and B. Pillai. "Cell-based gene therapy against HIV." Gene Therapy 22, no. 11 (June 16, 2015): 851–55. http://dx.doi.org/10.1038/gt.2015.58.

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32

Berkhout, Ben. "HIV-based lentiviral vectors for anti-HIV gene therapy." Future Virology 5, no. 4 (July 2010): 367–69. http://dx.doi.org/10.2217/fvl.10.30.

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33

Poeschla, E., P. Corbeau, and F. Wong-Staal. "Development of HIV vectors for anti-HIV gene therapy." Proceedings of the National Academy of Sciences 93, no. 21 (October 15, 1996): 11395–99. http://dx.doi.org/10.1073/pnas.93.21.11395.

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34

Gürtler, Lutz G. "Effect of Antiretroviral HIV Therapy on Hepatitis B Virus Replication and Pathogenicity." Intervirology 57, no. 3-4 (2014): 212–17. http://dx.doi.org/10.1159/000360942.

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35

Kalomoiris, Stefanos, Je'Tai Lawson, Rachel X. Chen, Gerhard Bauer, Jan A. Nolta, and Joseph S. Anderson. "CD25 Preselective Anti-HIV Vectors for Improved HIV Gene Therapy." Human Gene Therapy Methods 23, no. 6 (December 2012): 366–75. http://dx.doi.org/10.1089/hgtb.2012.142.

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36

Travis, J. "Crippled HIV Debuts as Gene Therapy Tool." Science News 149, no. 15 (April 13, 1996): 229. http://dx.doi.org/10.2307/3979870.

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37

Olszko, Miles, and Grant Trobridge. "Foamy Virus Vectors for HIV Gene Therapy." Viruses 5, no. 10 (October 22, 2013): 2585–600. http://dx.doi.org/10.3390/v5102585.

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38

Herrera-Carrillo, Elena, and Ben Berkhout. "Bone Marrow Gene Therapy for HIV/AIDS." Viruses 7, no. 7 (July 17, 2015): 3910–36. http://dx.doi.org/10.3390/v7072804.

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39

Macpherson, Janet, L. "Ribozymes in gene therapy of HIV-1." Frontiers in Bioscience 4, no. 1-3 (1999): d497. http://dx.doi.org/10.2741/macpherson.

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40

Lin, Min-Hsuan, Haran Sivakumaran, and David Harrich. "HIV gene therapy that’s not a SIN." HIV Therapy 4, no. 4 (July 2010): 395–98. http://dx.doi.org/10.2217/hiv.10.32.

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41

&NA;. "Gene therapy: HIV shows promise as vector." Inpharma Weekly &NA;, no. 1037 (May 1996): 8. http://dx.doi.org/10.2165/00128413-199610370-00017.

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42

Hattori, Toshio, Ryo Yamada, and Mitsuo Honda. "Gene therapy against AIDS : Anti-HIV ribozyme." Japanese Journal of Pharmacology 71 (1996): 5. http://dx.doi.org/10.1016/s0021-5198(19)33968-x.

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43

Kitchen, Scott G., Saki Shimizu, and Dong Sung An. "Stem cell-based anti-HIV gene therapy." Virology 411, no. 2 (March 2011): 260–72. http://dx.doi.org/10.1016/j.virol.2010.12.039.

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44

Whelan, Jo. "Gene therapy alternative to HAART for HIV." Drug Discovery Today 5, no. 7 (July 2000): 269–70. http://dx.doi.org/10.1016/s1359-6446(00)01520-8.

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45

Piché, Alain. "Gene Therapy for HIV Infections: Intracellular Immunization." Canadian Journal of Infectious Diseases 10, no. 4 (1999): 307–12. http://dx.doi.org/10.1155/1999/914379.

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Despite significant advances in the treatment of human immunodeficiency virus (HIV) infection in the past 10 years, it remains an incurable disease. The inability of traditional drug-based therapies to inhibit HIV replication effectively for extended periods of time has stimulated intense research to develop novel approaches for this disease. Current understanding of HIV molecular biology and pathogenesis has opened the way for the development of gene therapy strategies for HIV infections. In this context, a number of intracellular immunization-based strategies have been evaluated, and some of them have reached the stage of phase I/II human clinical trials. These strategies include the use of single-chain antibodies, capsid-targeted viral inactivation, transdominant negative mutants, ribozymes, antisense oligonucleotides and RNA decoys. While a number of issues remain to be studied before intracellular immunization can be applied to the treatment of HIV infections, the significant progress already made in this field is likely to lead to clinical applications.

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46

Symonds, Geoff P. "Ribozymes in gene therapy of HIV-1." Frontiers in Bioscience 4, no. 4 (1999): d497–505. http://dx.doi.org/10.2741/a444.

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47

Pennisi, E. "High-Tech Gene Therapy to Target HIV." Science News 144, no. 12 (September 18, 1993): 182. http://dx.doi.org/10.2307/3977480.

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48

Cotton, P. "High-tech assault on HIV: gene therapy." JAMA: The Journal of the American Medical Association 272, no. 16 (October 26, 1994): 1235–36. http://dx.doi.org/10.1001/jama.272.16.1235.

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49

Cotton, Paul. "High-tech Assault on HIV: Gene Therapy." JAMA: The Journal of the American Medical Association 272, no. 16 (October 26, 1994): 1235. http://dx.doi.org/10.1001/jama.1994.03520160017007.

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50

Hayafune, Masaaki, Naoko Miyano-Kurosaki, Akiko Kusunoki, Yuka Mouri, and Hiroshi Takaku. "HIV gene therapy using RNA virus systems." Nucleic Acids Symposium Series 50, no. 1 (November 1, 2006): 79–80. http://dx.doi.org/10.1093/nass/nrl039.

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