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Статті в журналах з теми "HIV (Viruses) Gene therapy"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 1 лютого 2022

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1

Hu, JinTing, YeWen Feng, Ping Ma, and Yu Lai. "Coreceptor-Based Hematopoietic Stem Cell Gene Therapy for HIV Disease." Current Stem Cell Research & Therapy 14, no. 7 (September 23, 2019): 591–97. http://dx.doi.org/10.2174/1574888x14666190523094556.

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: Combination antiretroviral therapy (cART) has significantly reduced the mortality rate and morbidity, and has increased the life expectancy of the human immunodeficiency virus (HIV) infected patients. However, the current cART is incapable of eradicating viruses from the human body, and HIV remains one of the most notorious viruses mankind has ever faced. HIV-1 enters target cells through the binding of gp120 viral protein to a CD4 receptor and then to a coreceptor, C-C chemokine receptor 5 (CCR5) or C-X-C chemokine receptor type 4 (CXCR4). Individuals homozygous for a 32-bp deletion in the

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2

Weinberger, Leor S., David V. Schaffer, and Adam P. Arkin. "Theoretical Design of a Gene Therapy To Prevent AIDS but Not Human Immunodeficiency Virus Type 1 Infection." Journal of Virology 77, no. 18 (September 15, 2003): 10028–36. http://dx.doi.org/10.1128/jvi.77.18.10028-10036.2003.

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ABSTRACT Recent reports confirm that, due to the presence of long-lived, latently infected cell populations, eradication of human immunodeficiency virus type 1 (HIV-1) from infected patients by using antiretroviral drugs will be exceedingly difficult. An alternative to virus eradication may be to use gene therapy to induce a pseudo-latent state in virus-producing cells, thus transforming HIV-1 into a lifelong, but manageable, virus. Conditionally replicating HIV-1 (crHIV-1) gene therapy vectors provide an avenue for subduing HIV-1 expression in infected cells (by creating a parasite, crHIV-1,

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3

Das, Atze T., Thijn R. Brummelkamp, Ellen M. Westerhout, Monique Vink, Mandy Madiredjo, René Bernards, and Ben Berkhout. "Human Immunodeficiency Virus Type 1 Escapes from RNA Interference-Mediated Inhibition." Journal of Virology 78, no. 5 (March 1, 2004): 2601–5. http://dx.doi.org/10.1128/jvi.78.5.2601-2605.2004.

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ABSTRACT Short-term assays have suggested that RNA interference (RNAi) may be a powerful new method for intracellular immunization against human immunodeficiency virus type 1 (HIV-1) infection. However, RNAi has not yet been shown to protect cells against HIV-1 in long-term virus replication assays. We stably introduced vectors expressing small interfering RNAs (siRNAs) directed against the HIV-1 genome into human T cells by retroviral transduction. We report here that an siRNA directed against the viral Nef gene (siRNA-Nef) confers resistance to HIV-1 replication. This block in replication is

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4

Bacheler, Lee, Susan Jeffrey, George Hanna, Richard D'Aquila, Lany Wallace, Kelly Logue, Beverly Cordova, et al. "Genotypic Correlates of Phenotypic Resistance to Efavirenz in Virus Isolates from Patients Failing Nonnucleoside Reverse Transcriptase Inhibitor Therapy." Journal of Virology 75, no. 11 (June 1, 2001): 4999–5008. http://dx.doi.org/10.1128/jvi.75.11.4999-5008.2001.

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ABSTRACT Efavirenz (also known as DMP 266 or SUSTIVA) is a potent nonnucleoside inhibitor of human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) activity and of HIV-1 replication in vitro and in vivo. Most patients on efavirenz-containing regimens have sustained antiviral responses; however, rebounds in plasma viral load have been observed in some patients in association with the emergence of mutant strains of HIV-1. Virus isolates from the peripheral blood mononuclear cells (PBMCs) of patients with such treatment failures, as well as recombinant viruses incorporating viral

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5

Sakkhachornphop, Supachai, Sudarat Hadpech, Tanchanok Wisitponchai, Chansunee Panto, Doungnapa Kantamala, Utaiwan Utaipat, Jutarat Praparattanapan, et al. "Broad-Spectrum Antiviral Activity of an Ankyrin Repeat Protein on Viral Assembly against Chimeric NL4-3 Viruses Carrying Gag/PR Derived from Circulating Strains among Northern Thai Patients." Viruses 10, no. 11 (November 13, 2018): 625. http://dx.doi.org/10.3390/v10110625.

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Certain proteins have demonstrated proficient human immunodeficiency virus (HIV-1) life cycle disturbance. Recently, the ankyrin repeat protein targeting the HIV-1 capsid, AnkGAG1D4, showed a negative effect on the viral assembly of the HIV-1NL4-3 laboratory strain. To extend its potential for future clinical application, the activity of AnkGAG1D4 in the inhibition of other HIV-1 circulating strains was evaluated. Chimeric NL4-3 viruses carrying patient-derived Gag/PR-coding regions were generated from 131 antiretroviral drug-naïve HIV-1 infected individuals in northern Thailand during 2001–20

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6

Manisha. B. Shinde, Dr. Archana D. Kajale, Dr. Madhuri A. Channawar, and Dr. Shilpa R. Gawande. "Vector-mediated cancer gene therapy: A review." GSC Biological and Pharmaceutical Sciences 13, no. 2 (November 30, 2020): 152–65. http://dx.doi.org/10.30574/gscbps.2020.13.2.0368.

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Gene therapy is the transfer of genetic material to cure a disease or at least to improve the clinical status of a patient. One of the basic concepts of gene therapy is to transform viruses into genetic shuttles, which will deliver the gene of interest into the target cells. Safe methods have been devised to do this, using several viral and non-viral vectors. Two main approaches emerged: in vivo modification and ex vivo modification. Retrovirus, adenovirus, adenoassociated virus are suitable for gene therapeutic approaches which are based on permanent expression of the therapeutic gene. Non-vi

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7

Martinez, Miguel Angel, Maria Nevot, Ana Jordan-Paiz, and Sandra Franco. "Similarities between Human Immunodeficiency Virus Type 1 and Hepatitis C Virus Genetic and Phenotypic Protease Quasispecies Diversity." Journal of Virology 89, no. 19 (July 15, 2015): 9758–64. http://dx.doi.org/10.1128/jvi.01097-15.

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ABSTRACTHuman immunodeficiency virus type 1 (HIV-1) and hepatitis C virus (HCV) are two highly variable RNA viruses that cause chronic infections in humans. Although HCV likely preceded the AIDS epidemic by some decades, the global spread of both viruses is a relatively recent event. Nevertheless, HCV global diversity is higher than that of HIV-1. To identify differences in mutant diversity, we compared the HIV-1 protease and HCV NS3 protease quasispecies. Three protease gene quasispecies samples per virus, isolated from a total of six infected patients, were genetically and phenotypically ana

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8

Bailey, Justin R., Ahmad R. Sedaghat, Tara Kieffer, Timothy Brennan, Patricia K. Lee, Megan Wind-Rotolo, Christine M. Haggerty, et al. "Residual Human Immunodeficiency Virus Type 1 Viremia in Some Patients on Antiretroviral Therapy Is Dominated by a Small Number of Invariant Clones Rarely Found in Circulating CD4+ T Cells." Journal of Virology 80, no. 13 (July 1, 2006): 6441–57. http://dx.doi.org/10.1128/jvi.00591-06.

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ABSTRACT Antiretroviral therapy can reduce human immunodeficiency virus type 1 (HIV-1) viremia to below the detection limit of ultrasensitive clinical assays (50 copies of HIV-1 RNA/ml). However, latent HIV-1 persists in resting CD4+ T cells, and low residual levels of free virus are found in the plasma. Limited characterization of this residual viremia has been done because of the low number of virions per sample. Using intensive sampling, we analyzed residual viremia and compared these viruses to latent proviruses in resting CD4+ T cells in peripheral blood. For each patient, we found some v

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9

Saunders, Kevin O., Lingshu Wang, M. Gordon Joyce, Zhi-Yong Yang, Alejandro B. Balazs, Cheng Cheng, Sung-Youl Ko, et al. "Broadly Neutralizing Human Immunodeficiency Virus Type 1 Antibody Gene Transfer Protects Nonhuman Primates from Mucosal Simian-Human Immunodeficiency Virus Infection." Journal of Virology 89, no. 16 (June 3, 2015): 8334–45. http://dx.doi.org/10.1128/jvi.00908-15.

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ABSTRACTBroadly neutralizing antibodies (bnAbs) can prevent lentiviral infection in nonhuman primates and may slow the spread of human immunodeficiency virus type 1 (HIV-1). Although protection by passive transfer of human bnAbs has been demonstrated in monkeys, durable expression is essential for its broader use in humans. Gene-based expression of bnAbs provides a potential solution to this problem, although immune responses to the viral vector or to the antibody may limit its durability and efficacy. Here, we delivered an adeno-associated viral vector encoding a simianized form of a CD4bs bn

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10

Styczyński, Jan. "ABC of viral infections in hematology: focus on herpesviruses." Acta Haematologica Polonica 50, no. 3 (September 28, 2019): 159–66. http://dx.doi.org/10.2478/ahp-2019-0026.

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AbstractViruses are a form of life that possess genes but do not have a cellular structure. Viruses do not have their own metabolism, and they require a host cell to make new products; therefore, they cannot naturally reproduce outside a host cell. The objective of this paper is to present the basic practical clinical roles of viruses in patients with hematological diseases including malignancies and non-malignan- cies, as well as those undergoing hematopoietic cell transplantation (HCT), with the focus on herpesviruses causing latent infections in severely immunocompromised patients. From the

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11

Palker, T. J. "Human T-cell Lymphotropic Viruses: Review and Prospects for Antiviral Therapy." Antiviral Chemistry and Chemotherapy 3, no. 3 (June 1992): 127–39. http://dx.doi.org/10.1177/095632029200300301.

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The human T-cell lymphotropic viruses types I and II (HTLV-I, II) pose challenges to researchers and clinicians who seek to unveil mechanisms of viral transformation and pathogenesis. HTLV-I infection in humans is associated with a wide array of primary and secondary diseases ranging from mild immunosuppression to adult T-cell leukaemia/lymphoma and HTLV-associated myelopathy/tropical spastic paraparesis (HAM/TSP), a neurological degenerative syndrome. As retroviruses, HTLV-I and II share similar replicative cycles with human immunodeficiency virus (HIV), the causative agent of acquired immuno

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12

Appelt, Jens U., Frank A. Giordano, Marcel Zimmermann, Stephan Weinhard, Nadja Grund, Agnes Hotz-Wagenblatt, W. Jens Zeller, Heike Allgayer, Stefan Fruehauf, and Stephanie Laufs. "Genes Involved in Acute Leukemias Are Favored Targets of HIV Vector Integration." Blood 110, no. 11 (November 16, 2007): 3738. http://dx.doi.org/10.1182/blood.v110.11.3738.3738.

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Abstract Insertional mutagenesis and development of leukemia following retroviral gene therapy has created intense interest in assessing the safety of viral vectors for further gene therapy trials. Using the gtsg.org database we analyzed more than 14,900 different viral integration sites of ASLV, FIV, FV, HIV, MLV and SIV based vectors in terms of insertions into fragile sites, cancer genes, transcription factor binding sites, CpG islands, and repetitive elements (SINE, LINE, LTR elements). When we compared these data with our newly generated random set, containing 1,000,000 random integration

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13

Schopman, Nick C. T., Anja Braun, and Ben Berkhout. "Directed HIV-1 Evolution of Protease Inhibitor Resistance by Second-Generation Short Hairpin RNAs." Antimicrobial Agents and Chemotherapy 56, no. 1 (November 7, 2011): 479–86. http://dx.doi.org/10.1128/aac.05491-11.

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ABSTRACTDespite the success of antiretroviral drugs in decreasing AIDS-related mortality, a substantial fraction of HIV-infected patients experience therapy failure due to the emergence of drug-resistant virus variants. For durable inhibition of HIV-1 replication, the emergence of such escape viruses must be controlled. In addition to antiretroviral drugs, RNA interference (RNAi)-based gene therapy can be used to inhibit HIV-1 replication by targeting the viral RNA genome. RNAi is an evolutionary conserved gene silencing mechanism that mediates the sequence-specific breakdown of the targeted m

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14

Martin, Supang A., Patricia A. Cane, Deenan Pillay, and Jean L. Mbisa. "Coevolved Multidrug-Resistant HIV-1 Protease and Reverse Transcriptase Influences Integrase Drug Susceptibility and Replication Fitness." Pathogens 10, no. 9 (August 24, 2021): 1070. http://dx.doi.org/10.3390/pathogens10091070.

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Integrase strand transfer inhibitors (InSTIs) are recommended agents in first-line combination antiretroviral therapy (cART). We examined the evolution of drug resistance mutations throughout HIV-1 pol and the effects on InSTI susceptibility and viral fitness. We performed single-genome sequencing of full-length HIV-1 pol in a highly treatment-experienced patient, and determined drug susceptibility of patient-derived HIV-1 genomes using a phenotypic assay encompassing full-length pol gene. We show the genetic linkage of multiple InSTI-resistant haplotypes containing major resistance mutations

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15

Tonkinson, J. L., and C. A. Stein. "Antisense Nucleic Acids — Prospects for Antiviral Intervention." Antiviral Chemistry and Chemotherapy 4, no. 4 (August 1993): 193–200. http://dx.doi.org/10.1177/095632029300400401.

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Antisense oligodeoxynucleotides are a promising new class of antiviral agent. Because they bind in a sequence-specific manner to complementary regions of mRNA, oligos can inhibit gene expression in a sequence-specific manner. The ‘antisense’ approach has been used successfully to block cellular expression and replication of several viruses including Human Immunodeficiency Virus-1 (HIV-1), and Herpes Simplex Virus (HSV). However, the antiviral effect of oligodeoxynucleotides is not limited to sequence-specific inhibition of gene expression. Non sequence-specific effects are frequently observed,

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16

Kim, Sanggu, Yun-Cheol Kim, Hangfei Qi, Kunkai Su, Sherie L. Morrison, and Samson A. Chow. "Efficient Identification of Human Immunodeficiency Virus Type 1 Mutants Resistant to a Protease Inhibitor by Using a Random Mutant Library." Antimicrobial Agents and Chemotherapy 55, no. 11 (August 29, 2011): 5090–98. http://dx.doi.org/10.1128/aac.00687-11.

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ABSTRACTEmergence of drug-resistant mutant viruses during the course of antiretroviral therapy is a major hurdle that limits the success of chemotherapeutic treatment to suppress human immunodeficiency virus type 1 (HIV-1) replication and AIDS progression. Development of new drugs and careful patient management based on resistance genotyping data are important for enhancing therapeutic efficacy. However, identifying changes leading to drug resistance can take years of clinical studies, and conventionalin vitroassays are limited in generating reliable drug resistance data. Here we present an ef

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17

Ahlenstiel, Golo, Kirsten Roomp, Martin Däumer, Jacob Nattermann, Martin Vogel, Jürgen K. Rockstroh, Niko Beerenwinkel, et al. "Selective Pressures of HLA Genotypes and Antiviral Therapy on Human Immunodeficiency Virus Type 1 Sequence Mutation at a Population Level." Clinical and Vaccine Immunology 14, no. 10 (August 22, 2007): 1266–73. http://dx.doi.org/10.1128/cvi.00169-07.

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ABSTRACT The objective of this study was a comprehensive analysis of the immune-driven evolution of viruses of human immunodeficiency virus type 1 (HIV-1) clade B in a large patient cohort treated at a single hospital in Germany and its implications for antiretroviral therapy. We examined the association of the HLA-A, HLA-B, and HLA-DRB1 alleles with the emergence of mutations in the complete protease gene and the first 330 codons of the reverse transcriptase (RT) gene of HIV-1, studying their distribution and persistence and their impact on antiviral drug therapy. The clinical data for 179 HI

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18

Charpentier, Charlotte, Tamara Nora, Olivier Tenaillon, François Clavel, and Allan J. Hance. "Extensive Recombination among Human Immunodeficiency Virus Type 1 Quasispecies Makes an Important Contribution to Viral Diversity in Individual Patients." Journal of Virology 80, no. 5 (March 1, 2006): 2472–82. http://dx.doi.org/10.1128/jvi.80.5.2472-2482.2006.

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ABSTRACT Although recombination during human immunodeficiency virus type 1 (HIV-1) replication in vitro and in vivo has been documented, little information is available concerning the extent that recombination contributes to the diversity of HIV-1 quasispecies in the course of infection in individual patents. To investigate the impact of recombination on viral diversity, we developed a technique that permits the isolation of contemporaneous clonal viral populations resulting from single infectious events by plasma-derived viruses, thereby permitting the assessment of recombination throughout t

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19

Browning, Matthew T., Russell D. Schmidt, Kathy A. Lew, and Tahir A. Rizvi. "Primate and Feline Lentivirus Vector RNA Packaging and Propagation by Heterologous Lentivirus Virions." Journal of Virology 75, no. 11 (June 1, 2001): 5129–40. http://dx.doi.org/10.1128/jvi.75.11.5129-5140.2001.

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ABSTRACT Development of safe and effective gene transfer systems is critical to the success of gene therapy protocols for human diseases. Currently, several primate lentivirus-based gene transfer systems, such as those based on human and simian immunodeficiency viruses (HIV/SIV), are being tested; however, their use in humans raises safety concerns, such as the generation of replication-competent viruses through recombination with related endogenous retroviruses or retrovirus-like elements. Due to the greater phylogenetic distance from primate lentiviruses, feline immunodeficiency virus (FIV)

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20

Miyoshi, Hiroyuki, Ulrike Blömer, Masayo Takahashi, Fred H. Gage, and Inder M. Verma. "Development of a Self-Inactivating Lentivirus Vector." Journal of Virology 72, no. 10 (October 1, 1998): 8150–57. http://dx.doi.org/10.1128/jvi.72.10.8150-8157.1998.

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ABSTRACT We have constructed a new series of lentivirus vectors based on human immunodeficiency virus type 1 (HIV-1) that can transduce nondividing cells. The U3 region of the 5′ long terminal repeat (LTR) in vector constructs was replaced with the cytomegalovirus (CMV) promoter, resulting in Tat-independent transcription but still maintaining high levels of expression. A self-inactivating (SIN) vector was constructed by deleting 133 bp in the U3 region of the 3′ LTR, including the TATA box and binding sites for transcription factors Sp1 and NF-κB. The deletion is transferred to the 5′ LTR aft

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21

Boucher, C. A., W. Keulen, T. van Bommel, M. Nijhuis, D. de Jong, M. D. de Jong, P. Schipper, and N. K. Back. "Human immunodeficiency virus type 1 drug susceptibility determination by using recombinant viruses generated from patient sera tested in a cell-killing assay." Antimicrobial Agents and Chemotherapy 40, no. 10 (October 1996): 2404–9. http://dx.doi.org/10.1128/aac.40.10.2404.

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A simple approach for the determination of drug susceptibilities by using human immunodeficiency virus type 1 (HIV-1) RNA from the sera of patients is described. HIV-1 RNA was extracted from patient sera, and the 5' part of the reverse transcriptase (RT) gene was transcribed into DNA and amplified in a nested PCR. The amplified fragment covers the 3' part of the protease gene and amino acids 1 to 304 of the RT gene. This fragment can be introduced through homologous recombination, as described previously, into a novel HIV-1 reference strain (pHXB2 delta 2-261RT) from which amino acids 2 to 261

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22

Bacheler, Lee T., Elizabeth D. Anton, Phil Kudish, David Baker, Julie Bunville, Karen Krakowski, Laura Bolling, et al. "Human Immunodeficiency Virus Type 1 Mutations Selected in Patients Failing Efavirenz Combination Therapy." Antimicrobial Agents and Chemotherapy 44, no. 9 (September 1, 2000): 2475–84. http://dx.doi.org/10.1128/aac.44.9.2475-2484.2000.

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ABSTRACT Efavirenz is a potent and selective nonnucleoside inhibitor of human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT). Nucleotide sequence analyses of the protease and RT genes (coding region for amino acids 1 to 229) of multiple cloned HIV-1 genomes from virus found in the plasma of patients in phase II clinical studies of efavirenz combination therapy were undertaken in order to identify the spectrum of mutations in plasma-borne HIV-1 associated with virological treatment failure. A K103N substitution was the HIV-1 RT gene mutation most frequently observed among plas

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23

von Eije, Karin Jasmijn, Olivier ter Brake, and Ben Berkhout. "Human Immunodeficiency Virus Type 1 Escape Is Restricted When Conserved Genome Sequences Are Targeted by RNA Interference." Journal of Virology 82, no. 6 (December 12, 2007): 2895–903. http://dx.doi.org/10.1128/jvi.02035-07.

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ABSTRACT RNA interference (RNAi) is a cellular mechanism in which small interfering RNAs (siRNAs) mediate sequence-specific gene silencing by cleaving the targeted mRNA. RNAi can be used as an antiviral approach to silence the human immunodeficiency virus type 1 (HIV-1) through stable expression of short-hairpin RNAs (shRNAs). We previously reported efficient HIV-1 inhibition by an shRNA against the nonessential nef gene but also described viral escape by mutation or deletion of the nef target sequence. The objective of this study was to obtain insight in the viral escape routes when essential

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24

Biswas, Preetha, Xi Jiang, Annmarie L. Pacchia, Joseph P. Dougherty, and Stuart W. Peltz. "The Human Immunodeficiency Virus Type 1 Ribosomal Frameshifting Site Is an Invariant Sequence Determinant and an Important Target for Antiviral Therapy." Journal of Virology 78, no. 4 (February 15, 2004): 2082–87. http://dx.doi.org/10.1128/jvi.78.4.2082-2087.2004.

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ABSTRACT Human immunodeficiency virus type 1 (HIV-1) utilizes a distinctive form of gene regulation as part of its life cycle, termed programmed −1 ribosomal frameshifting, to produce the required ratio of the Gag and Gag-Pol polyproteins. We carried out a sequence comparison of 1,000 HIV-1 sequences at the slippery site (UUUUUUA) and found that the site is invariant, which is somewhat surprising for a virus known for its variability. This prompted us to prepare a series of mutations to examine their effect upon frameshifting and viral infectivity. Among the series of mutations were changes of

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25

Salomon, H., Z. Gu, Q. Gao, K. Nagai, J. Hiscott, and M. A. Wainberg. "Host Cell Dependence of Human Immunodeficiency Virus Type-1 Drug Resistance Profiles and Tissue Culture Selection Patterns." Antiviral Chemistry and Chemotherapy 6, no. 4 (August 1995): 222–29. http://dx.doi.org/10.1177/095632029500600404.

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Clinical isolates of the human immunodeficiency virus type 1 (HIV-1) displayed differential sensitivity to antiviral nucleosides depending on the type of host cell employed for viral propagation. Viruses derived from the peripheral blood mononuclear cells (PBMC) of subjects on prolonged 3′-azido-3′-deoxythymidine (AZT) therapy behaved as AZT-resistant when tested in either cord blood mononuclear cells or MT-4 cells but as relatively drug-sensitive in the U-937 monocytic cell line. Viruses derived from monocytes/ macrophages of the same individuals behaved as drug-sensitive in all cells tested.

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Patton, Gillian S., Otto Erlwein, and Myra O. McClure. "Cell-cycle dependence of foamy virus vectors." Journal of General Virology 85, no. 10 (October 1, 2004): 2925–30. http://dx.doi.org/10.1099/vir.0.80210-0.

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Retroviruses differ in the extent to which they are dependent on host-cell proliferation for their replication, an aspect of their replication that impacts on their vector potential. Foamy viruses offer distinct advantages over other retroviruses for development as vectors for gene therapy. A vector derived from the prototypic foamy virus (PFV), formerly known as human foamy virus (HFV), transduced aphidicolin-arrested cells five- to tenfold more efficiently than one derived from murine leukemia virus (MLV), but several-fold less efficiently than a human immunodeficiency virus type 1 (HIV-1) v

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27

Servais, Jean, Christine Lambert, Elodie Fontaine, Jean-Marc Plesséria, Isabelle Robert, Vic Arendt, Thérèse Staub, et al. "Variant Human Immunodeficiency Virus Type 1 Proteases and Response to Combination Therapy Including a Protease Inhibitor." Antimicrobial Agents and Chemotherapy 45, no. 3 (March 1, 2001): 893–900. http://dx.doi.org/10.1128/aac.45.3.893-900.2001.

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ABSTRACT The objective of this observational study was to assess the genetic variability in the human immunodeficiency virus (HIV) protease gene from HIV type 1 (HIV-1)-positive (clade B), protease inhibitor-naı̈ve patients and to evaluate its association with the subsequent effectiveness of a protease inhibitor-containing triple-drug regimen. The protease gene was sequenced from plasma-derived virus from 116 protease inhibitor-naı̈ve patients. The virological response to a triple-drug regimen containing indinavir, ritonavir, or saquinavir was evaluated every 3 months for as long as 2 years (n

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28

Ariffin, Tengku Ahmad Akram Tengku Mohd, Suharni Mohamad, Wan Nazirah Wan Yusuf, and Rafidah Hanim Shueb. "Antiretroviral drug resistance and HIV-1 subtypes among treatment-naive prisoners in Kelantan, Malaysia." Journal of Infection in Developing Countries 8, no. 08 (August 13, 2014): 1063–67. http://dx.doi.org/10.3855/jidc.4095.

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Introduction: The widespread use of highly active antiretroviral therapy (HAART) and continuous reports of HIV-1 strains developing resistance to these drugs is rather alarming, as transmission of resistant viruses to newly infected persons is possible. This study aimed to determine HIV-1 subtypes and the prevalence of primary mutations associated with antiretroviral (ARV) resistance among treatment-naive prisoners on the east coast of Malaysia. Methodology: Viral RNA was extracted from plasma samples of 21 treatment-naive prisoners. Protease (PR) and reverse transcriptase (RT) regions were am

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Price, David A., George Scullard, Annette Oxenius, Ruth Braganza, Simon A. Beddows, Shamim Kazmi, John R. Clarke, Gabriele E. Johnson, Jonathan N. Weber, and Rodney E. Phillips. "Discordant Outcomes following Failure of Antiretroviral Therapy Are Associated with Substantial Differences in Human Immunodeficiency Virus-Specific Cellular Immunity." Journal of Virology 77, no. 10 (May 15, 2003): 6041–49. http://dx.doi.org/10.1128/jvi.77.10.6041-6049.2003.

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ABSTRACT Many individuals chronically infected with human immunodeficiency virus type 1 (HIV-1) experience a recrudescence of plasma virus during continuous combination antiretroviral therapy (ART) due either to the emergence of drug-resistant viruses or to poor compliance. In most cases, virologic failure on ART is associated with a coincident decline in CD4+ T lymphocyte levels. However, a proportion of discordant individuals retain a stable or even increasing CD4+ T lymphocyte count despite virological failure. In order to address the nature of these different outcomes, we evaluated virolog

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Winters, M. A., R. W. Shafer, R. A. Jellinger, G. Mamtora, T. Gingeras, and T. C. Merigan. "Human immunodeficiency virus type 1 reverse transcriptase genotype and drug susceptibility changes in infected individuals receiving dideoxyinosine monotherapy for 1 to 2 years." Antimicrobial Agents and Chemotherapy 41, no. 4 (April 1997): 757–62. http://dx.doi.org/10.1128/aac.41.4.757.

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The genetic mechanisms of human immunodeficiency virus type 1 (HIV-1) resistance to dideoxyinosine (ddI) in vivo have been described based on data from primary HIV-1 isolates. To better define the spectrum of HIV-1 reverse transcriptase (RT) changes occurring during ddI therapy, we determined the genotype and ddI susceptibility of the RT gene of HIV RNA isolated from the plasma of 23 patients who had received 1 to 2 years (mean, 87 +/- 16 weeks) of ddI monotherapy. Population-based sequencing of plasma virus showed that 12 of 23 (52%) patients developed known ddI resistance mutations: L74V (7

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Vasudevachari, M. B., Y. M. Zhang, H. Imamichi, T. Imamichi, J. Falloon, and N. P. Salzman. "Emergence of protease inhibitor resistance mutations in human immunodeficiency virus type 1 isolates from patients and rapid screening procedure for their detection." Antimicrobial Agents and Chemotherapy 40, no. 11 (November 1996): 2535–41. http://dx.doi.org/10.1128/aac.40.11.2535.

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Patient human immunodeficiency virus type 1 (HIV-1) isolates that are resistant to protease inhibitors may contain amino acid substitutions L10I/V, M46L/I, G-48V, L63P, V82A/F/T, I84V, and L90M in the protease gene. Substitutions at positions 82 and/or 90 occur in variants that display high levels of resistance to certain protease inhibitors. Nucleotide substitutions at these two sites also lead to the loss of two HindII restriction enzyme digestion sites, and these changes make possible a rapid procedure for the detection of drug-resistant variants in patients on protease inhibitor therapy. T

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Hoeben, RC, FJ Fallaux, SJ Cramer, DJ van den Wollenberg, H. van Ormondt, E. Briet, and AJ van der Eb. "Expression of the blood-clotting factor-VIII cDNA is repressed by a transcriptional silencer located in its coding region." Blood 85, no. 9 (May 1, 1995): 2447–54. http://dx.doi.org/10.1182/blood.v85.9.2447.bloodjournal8592447.

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Hemophilia A is caused by a deficiency of factor-VIII procoagulant (fVIII) activity. The current treatment by frequent infusions of plasma-derived fVIII concentrates is very effective but has the risk of transmittance of blood-borne viruses (human immunodeficiency virus [HIV], hepatitis viruses). Use of recombinant DNA-derived fVIII as well as gene therapy could make hemophilia treatment independent of blood-derived products. So far, the problematic production of the fVIII protein and the low titers of the fVIII retrovirus stocks have prevented preclinical trials of gene therapy for hemophilia

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Susser, Simone, Mathieu Flinders, Henk W. Reesink, Stefan Zeuzem, Glenn Lawyer, Anne Ghys, Veerle Van Eygen, James Witek, Sandra De Meyer, and Christoph Sarrazin. "Evolution of Hepatitis C Virus Quasispecies during Repeated Treatment with the NS3/4A Protease Inhibitor Telaprevir." Antimicrobial Agents and Chemotherapy 59, no. 5 (February 23, 2015): 2746–55. http://dx.doi.org/10.1128/aac.04911-14.

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ABSTRACTIn treating hepatitis B virus (HBV) and human immunodeficiency virus (HIV) infections, the rapid reselection of resistance-associated variants (RAVs) is well known in patients with repeated exposure to the same class of antiviral agents. For chronic hepatitis C patients who have experienced virologic failure with direct-acting antiviral drugs, the potential for the reselection of persistent RAVs is unknown. Nine patients who received 14 days of telaprevir monotherapy were retreated with telaprevir-based triple therapy 4.3 to 5.7 years later. In four patients with virologic failure with

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Persaud, Deborah, George K. Siberry, Aima Ahonkhai, Joleen Kajdas, Daphne Monie, Nancy Hutton, Douglas C. Watson, Thomas C. Quinn, Stuart C. Ray, and Robert F. Siliciano. "Continued Production of Drug-Sensitive Human Immunodeficiency Virus Type 1 in Children on Combination Antiretroviral Therapy Who Have Undetectable Viral Loads." Journal of Virology 78, no. 2 (January 15, 2004): 968–79. http://dx.doi.org/10.1128/jvi.78.2.968-979.2004.

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ABSTRACT Highly active antiretroviral therapy (HAART) can suppress plasma human immunodeficiency virus type 1 (HIV-1) levels to below the detection limit of ultrasensitive clinical assays. However, HIV-1 persists in cellular reservoirs, and in adults, persistent low-level viremia is detected with more sensitive assays. The nature of this viremia is poorly understood, and it is unclear whether viremia persists in children on HAART, particularly those who start therapy shortly after birth. We therefore developed a reverse transcriptase PCR (RT-PCR) assay that allows genotyping of HIV-1 protease

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Goujon, Caroline, Loraine Jarrosson-Wuilleme, Jeanine Bernaud, Dominique Rigal, Jean-Luc Darlix, and Andrea Cimarelli. "Heterologous Human Immunodeficiency Virus Type 1 Lentiviral Vectors Packaging a Simian Immunodeficiency Virus-Derived Genome Display a Specific Postentry Transduction Defect in Dendritic Cells." Journal of Virology 77, no. 17 (September 1, 2003): 9295–304. http://dx.doi.org/10.1128/jvi.77.17.9295-9304.2003.

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ABSTRACT Heterologous lentiviral vectors (LVs) represent a way to address safety concerns in the field of gene therapy by decreasing the possibility of genetic recombination between vector and packaging constructs and the generation of replication-competent viruses. Using described LVs based on human immunodeficiency virus type 1 (HIV-1) and simian immunodeficiency virus MAC251 (SIVMAC251), we asked whether heterologous virion particles in which trans-acting factors belonged to HIV-1 and cis elements belonged to SIVMAC251 (HIV-siv) would behave as parental homologous vectors in all cell types.

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Indriati, Dwi Wahyu, Tomohiro Kotaki, Siti Qamariyah Khairunisa, Adiana Mutamsari Witaningrum, Muhammad Qushai Yunifiar Matondang, Shuhei Ueda, Nasronudin, Asep Purnama, Dwi Kurniawan, and Masanori Kameoka. "Appearance of Drug Resistance Mutations Among the Dominant HIV-1 Subtype, CRF01_AE in Maumere, Indonesia." Current HIV Research 16, no. 2 (August 15, 2018): 158–66. http://dx.doi.org/10.2174/1570162x16666180502114344.

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Background and Objectives:Human Immunodeficiency Virus (HIV) is still a major health issue in Indonesia. In recent years, the appearance of drug resistance-associated mutations has reduced the effectiveness of Antiretroviral Therapy (ART). We conducted genotypic studies, including the detection of drug resistance-associated mutations (from first-line regimen drugs), on HIV-1 genes derived from infected individuals in Maumere, West Nusa Tenggara. Maumere, a transit city in West Nusa Tenggara, which has a high HIV-1 transmission rate.Method:We collected 60 peripheral blood samples from 53 ART-ex

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Weber, Jan, Ana C. Vazquez, Dane Winner, Justine D. Rose, Doug Wylie, Ariel M. Rhea, Kenneth Henry, et al. "Novel Method for Simultaneous Quantification of Phenotypic Resistance to Maturation, Protease, Reverse Transcriptase, and Integrase HIV Inhibitors Based on 3′Gag(p2/p7/p1/p6)/PR/RT/INT-Recombinant Viruses: a Useful Tool in the Multitarget Era of Antiretroviral Therapy." Antimicrobial Agents and Chemotherapy 55, no. 8 (May 31, 2011): 3729–42. http://dx.doi.org/10.1128/aac.00396-11.

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ABSTRACTTwenty-six antiretroviral drugs (ARVs), targeting five different steps in the life cycle of the human immunodeficiency virus type 1 (HIV-1), have been approved for the treatment of HIV-1 infection. Accordingly, HIV-1 phenotypic assays based on common cloning technology currently employ three, or possibly four, different recombinant viruses. Here, we describe a system to assess HIV-1 resistance to all drugs targeting the three viral enzymes as well as viral assembly using a single patient-derived, chimeric virus. Patient-derived p2-INT (gag-p2/NCp7/p1/p6/pol-PR/RT/IN) products were PCR

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Kaltenbach, Robert F., George Trainor, Daniel Getman, Greg Harris, Sena Garber, Beverly Cordova, Lee Bacheler, et al. "DPC 681 and DPC 684: Potent, Selective Inhibitors of Human Immunodeficiency Virus Protease Active against Clinically Relevant Mutant Variants." Antimicrobial Agents and Chemotherapy 45, no. 11 (November 1, 2001): 3021–28. http://dx.doi.org/10.1128/aac.45.11.3021-3028.2001.

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ABSTRACT Human immunodeficiency virus (HIV) protease inhibitors (PIs) are important components of many highly active antiretroviral therapy regimens. However, development of phenotypic and/or genotypic resistance can occur, including cross-resistance to other PIs. Development of resistance takes place because trough levels of free drug are inadequate to suppress preexisting resistant mutant variants and/or to inhibit de novo-generated resistant mutant variants. There is thus a need for new PIs, which are more potent against mutant variants of HIV and show higher levels of free drug at the trou

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39

Lohrengel, Sabine, Felix Hermann, Isabel Hagmann, Heike Oberwinkler, Laura Scrivano, Caroline Hoffmann, Dorothee von Laer, and Matthias T. Dittmar. "Determinants of Human Immunodeficiency Virus Type 1 Resistance to Membrane-Anchored gp41-Derived Peptides." Journal of Virology 79, no. 16 (August 15, 2005): 10237–46. http://dx.doi.org/10.1128/jvi.79.16.10237-10246.2005.

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ABSTRACT The expression of a membrane-anchored gp41-derived peptide (M87) has been shown to confer protection from infection through human immunodeficiency virus type 1 (HIV-1) (Hildinger et al., J. Virol. 75:3038-3042, 2001). In an effort to characterize the mechanism of action of this membrane-anchored peptide in comparison to the soluble peptide T-20, we selected resistant variants of HIV-1NL4-3 and HIV-1BaL by serial virus passage using PM1 cells stably expressing peptide M87. Sequence analysis of the resistant isolates showed different patterns of selected point mutations in heptad repeat

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Pluta, Aneta, Juan P. Jaworski, and César N. Cortés-Rubio. "Balance between Retroviral Latency and Transcription: Based on HIV Model." Pathogens 10, no. 1 (December 29, 2020): 16. http://dx.doi.org/10.3390/pathogens10010016.

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The representative of the Lentivirus genus is the human immunodeficiency virus type 1 (HIV-1), the causative agent of acquired immunodeficiency syndrome (AIDS). To date, there is no cure for AIDS because of the existence of the HIV-1 reservoir. HIV-1 infection can persist for decades despite effective antiretroviral therapy (ART), due to the persistence of infectious latent viruses in long-lived resting memory CD4+ T cells, macrophages, monocytes, microglial cells, and other cell types. However, the biology of HIV-1 latency remains incompletely understood. Retroviral long terminal repeat regio

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Vassilopoulos, George, Grant Trobridge, Neil C. Josephson, and David W. Russell. "Gene transfer into murine hematopoietic stem cells with helper-free foamy virus vectors." Blood 98, no. 3 (August 1, 2001): 604–9. http://dx.doi.org/10.1182/blood.v98.3.604.

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Abstract Gene transfer into hematopoietic stem cells (HSCs) is an ideal treatment strategy for many genetic and hematologic diseases. However, progress has been limited by the low HSC transduction rates obtained with retroviral vectors based on murine leukemia viruses. This study examined the potential of vectors derived from the nonpathogenic human foamy virus (HFV) to transduce human CD34+ cells and murine HSCs. More than 80% of human hematopoietic progenitors present in CD34+ cell preparations derived from cord blood were transduced by a single overnight exposure to HFV vector stocks. Mice

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Holterman, Lennart, Ronald Vogels, Remko van der Vlugt, Martijn Sieuwerts, Jos Grimbergen, Jorn Kaspers, Eric Geelen, et al. "Novel Replication-Incompetent Vector Derived from Adenovirus Type 11 (Ad11) for Vaccination and Gene Therapy: Low Seroprevalence and Non-Cross-Reactivity with Ad5." Journal of Virology 78, no. 23 (December 1, 2004): 13207–15. http://dx.doi.org/10.1128/jvi.78.23.13207-13215.2004.

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ABSTRACT A novel plasmid-based adenovirus vector system that enables manufacturing of replication-incompetent (ΔE1) adenovirus type 11 (Ad11)-based vectors is described. Ad11 vectors are produced on PER.C6/55K cells yielding high-titer vector batches after purification. Ad11 seroprevalence proves to be significantly lower than that of Ad5, and neutralizing antibody titers against Ad11 are low. Ad11 seroprevalence among human immunodeficiency virus-positive (HIV+) individuals is as low as that among HIV− individuals, independent of the level of immune suppression. The low level of coinciding se

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Hill, Claire L., Paul D. Bieniasz, and Myra O. McClure. "Properties of human foamy virus relevant to its development as a vector for gene therapy." Journal of General Virology 80, no. 8 (August 1, 1999): 2003–9. http://dx.doi.org/10.1099/0022-1317-80-8-2003.

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The Spumaviridae (foamy viruses) are increasingly being considered as potential vectors for gene therapy, yet little has been documented of their basic cell biology. This study demonstrates that human foamy virus (HFV) has a broad tropism and that the receptor for HFV is expressed not only on many mammalian, but on avian and reptilian cells. Receptor interference assays using an envelope-expressing cell line and a vesicular stomatitis virus/HFV pseudotype virus demonstrate that the cellular receptor is common to all primate members of the genus. The majority of foamy virus particles assemble a

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Swan, Christina H., Bernd Buhler, Mario P. Tschan, Carlos F. Barbas, and Bruce E. Torbett. "Lentiviral CCR5 Intrabody Gene Delivery Provides Protection and Enrichment during CCR5-Tropic Infection." Blood 104, no. 11 (November 16, 2004): 1755. http://dx.doi.org/10.1182/blood.v104.11.1755.1755.

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Abstract The molecular mechanism of human immunodeficiency virus type 1 (HIV-1) entry into target cells is a multistep mechanism. The viral envelope glycoproteins (env) binds first to CD4 and subsequently interacts with the V3 loop with a chemokine receptor, CCR5 or CXCR4, triggering the fusion event. Several findings suggest that viruses using CCR5 for entry (R5-tropic HIV-1) is the predominant species transmitted among patients. Importantly, CCR5 expression levels determine disease progression. CCR5 does not seem to be necessary for normal cell function, since individuals with a homozygous m

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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 immunodef

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Gu, Zhengxian, Hengsheng Fang, Horacio Salomon, Qing Gao, and Mark A. Wainberg. "Identification of Mutations that Encode Drug Resistance in the Polymerase Gene of the Human Immunodeficiency Virus." Canadian Journal of Infectious Diseases 5, suppl e (1994): 29E—33E. http://dx.doi.org/10.1155/1994/826340.

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In vitro selection in MT-4 cells was used to generate human immunodeficiency virus-type 1 (HIV 1) variants that are resistant to 2',3'-dideoxycytidine (ddC), 2',3'-didcoxyinosine (ddI) and the (-) enantiomer of 2' ,3'-dideoxy-3'-thiacytidine (3TC). The complete reverse transcriptase open reading frames of these viruses, and portions of flanking protease and integrase within the pol gene, were cloned and sequenced by polymerase chain reaction (PCR) techniques. Mulalions were observed at each of amino acid sites 65 (Lys → Arg: AAA → AGA) and 184 (Met → Val: ATG → GTG) when ddC was used in this p

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De Bolle, Leen, Lieve Naesens, and Erik De Clercq. "Update on Human Herpesvirus 6 Biology, Clinical Features, and Therapy." Clinical Microbiology Reviews 18, no. 1 (January 2005): 217–45. http://dx.doi.org/10.1128/cmr.18.1.217-245.2005.

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SUMMARY Human herpesvirus 6 (HHV-6) is a betaherpesvirus that is closely related to human cytomegalovirus. It was discovered in 1986, and HHV-6 literature has expanded considerably in the past 10 years. We here present an up-to-date and complete overview of the recent developments concerning HHV-6 biological features, clinical associations, and therapeutic approaches. HHV-6 gene expression regulation and gene products have been systematically characterized, and the multiple interactions between HHV-6 and the host immune system have been explored. Moreover, the discovery of the cellular recepto

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Kapoor, Amit, Morris Jones, R. W. Shafer, Soo-Yon Rhee, Powel Kazanjian, and Eric L. Delwart. "Sequencing-Based Detection of Low-Frequency Human Immunodeficiency Virus Type 1 Drug-Resistant Mutants by an RNA/DNA Heteroduplex Generator-Tracking Assay." Journal of Virology 78, no. 13 (July 1, 2004): 7112–23. http://dx.doi.org/10.1128/jvi.78.13.7112-7123.2004.

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ABSTRACT Drug-resistant viruses may be present as minority variants during early treatment failures or following discontinuation of failed antiretroviral regimens. A limitation of the traditional direct PCR population sequencing method is its inability to detect human immunodeficiency virus type 1 (HIV-1) variants present at frequencies lower than 20%. A drug resistance genotyping assay based on the isolation and DNA sequencing of minority HIV protease variants is presented here. A multiple-codon-specific heteroduplex generator probe was constructed to improve the separation of HIV protease ge

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Hué, Stéphane, Robert J. Gifford, David Dunn, Esther Fernhill, and Deenan Pillay. "Demonstration of Sustained Drug-Resistant Human Immunodeficiency Virus Type 1 Lineages Circulating among Treatment-Naïve Individuals." Journal of Virology 83, no. 6 (January 21, 2009): 2645–54. http://dx.doi.org/10.1128/jvi.01556-08.

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ABSTRACT Transmission of human immunodeficiency virus (HIV) drug resistance is well-recognized and compromises response to first-line therapy. However, the population dynamics of transmitted resistance remains unclear, although previous models have assumed that such transmission reflects direct infection from treated individuals. We investigated whether population-based phylogenetic analyses would uncover lineages of resistant viruses circulating in untreated individuals. Through the phylogenetic analysis of 14,061 HIV type 1 (HIV-1) pol gene sequences generated in the United Kingdom from both

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Vergne, Laurence, Martine Peeters, Eitel Mpoudi-Ngole, Anke Bourgeois, Florian Liegeois, Coumba Toure-Kane, Souleymane Mboup, et al. "Genetic Diversity of Protease and Reverse Transcriptase Sequences in Non-Subtype-B Human Immunodeficiency Virus Type 1 Strains: Evidence of Many Minor Drug Resistance Mutations in Treatment-Naive Patients." Journal of Clinical Microbiology 38, no. 11 (2000): 3919–25. http://dx.doi.org/10.1128/jcm.38.11.3919-3925.2000.

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Most human immunodeficiency virus (HIV) drug susceptibility studies have involved subtype B strains. Little information on the impact of viral diversity on natural susceptibility to antiretroviral drugs has been reported. However, the prevalence of non-subtype-B (non-B) HIV type 1 (HIV-1) strains continues to increase in industrialized countries, and antiretroviral treatments have recently become available in certain developing countries where non-B subtypes predominate. We sequenced the protease and reverse transcriptase (RT) genes of 142 HIV-1 isolates from antiretroviral-naive patients: 4 b

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