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Статті в журналах з теми "Lentiviruses"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 31 липня 2024

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1

Clements, J. E., and M. C. Zink. "Molecular biology and pathogenesis of animal lentivirus infections." Clinical Microbiology Reviews 9, no. 1 (January 1996): 100–117. http://dx.doi.org/10.1128/cmr.9.1.100.

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Lentiviruses are a subfamily of retroviruses that are characterized by long incubation periods between infection of the host and the manifestation of clinical disease. Human immunodeficiency virus type 1, the causative agent of AIDS, is the most widely studied lentivirus. However, the lentiviruses that infect sheep, goats, and horses were identified and studied prior to the emergence of human immunodeficiency virus type 1. These and other animal lentiviruses provide important systems in which to investigate the molecular pathogenesis of this family of viruses. This review will focus on two animal lentivirus models: the ovine lentivirus visna virus; and the simian lentivirus, simian immunodeficiency virus. These animal lentiviruses have been used to examine, in particular, the pathogenesis of lentivirus-induced central nervous system disease as models for humans with AIDS as well as other chronic diseases.

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2

Lairmore, M. D., S. T. Butera, G. N. Callahan, and J. C. DeMartini. "Spontaneous interferon production by pulmonary leukocytes is associated with lentivirus-induced lymphoid interstitial pneumonia." Journal of Immunology 140, no. 3 (February 1, 1988): 779–85. http://dx.doi.org/10.4049/jimmunol.140.3.779.

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Abstract Ovine lentiviruses share genome sequence, structural features, and replicative mechanisms with HIV, the etiologic agent of AIDS. A lamb model of lentivirus-induced lymphoid interstitial pneumonia, comparable to lymphoid interstitial pneumonia associated with pediatric AIDS, was used to investigate production of leukocyte-soluble mediators. Lentivirus-infected lambs and adult sheep with severe lymphoid interstitial pneumonia had significantly elevated levels of spontaneous interferon (IFN) production from pulmonary leukocytes compared with ovine lentiviruses-infected animals with mild or no lesions of lymphoid interstitial pneumonia or non-infected controls. However, peripheral blood mononuclear cells from lentivirus-infected lambs did not spontaneously release significant amounts of IFN. IFN production by pulmonary lymph node lymphocytes was enhanced in the presence of lentivirus-infected alveolar macrophages. Animals with lentivirus-induced disease and spontaneous IFN production had enhanced virus replication within tissues. The ovine lentiviruses-induced IFN had a m.w. of between 25,000 and 35,000 and was resistant to freeze/thawing procedures. The IFN activity was sensitive to trypsin and stable to low pH and heat. IFN with similar physical and biochemical properties was produced when ovine lentiviruses was added to control leukocyte cultures. IL-2 and PGE2 production and responses to mitogen by pulmonary lymph node lymphocytes of lentivirus-diseased lambs were not statistically different from control animals. Increased local production of IFN in lentivirus-infected host tissues may serve to accelerate the entry of leukocytes into virus-induced lesions promoting cell-mediated tissue damage and also provide increased numbers of cells for virus replication.

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3

Hötzel, Isidro, and William P. Cheevers. "Conservation of Human Immunodeficiency Virus Type 1 gp120 Inner-Domain Sequences in Lentivirus and Type A and B Retrovirus Envelope Surface Glycoproteins." Journal of Virology 75, no. 4 (February 15, 2001): 2014–18. http://dx.doi.org/10.1128/jvi.75.4.2014-2018.2001.

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ABSTRACT We recently described a sequence similarity between the small ruminant lentivirus surface unit glycoprotein (SU) gp135 and the second conserved region (C2) of the primate lentivirus gp120 which indicates a structural similarity between gp135 and the inner proximal domain of the human immunodeficiency virus type 1 gp120 (I. Hötzel and W. P. Cheevers, Virus Res. 69:47–54, 2000). Here we found that the seven-amino-acid sequence of the gp120 strand β25 in the C5 region, which is also part of the inner proximal domain, was conserved in the SU of all lentiviruses in similar or identical positions relative to the carboxy terminus of SU. Sequences conforming to the gp135-gp120 consensus for β-strand 5 in the C2 region, which is antiparallel to β25, were then sought in the SU of other lentiviruses and retroviruses. Except for the feline immunodeficiency virus, sequences similar to the gp120-gp135 consensus for β5 and part of the preceding strand β4 were present in the SU of all lentiviruses. This motif was highly conserved among strains of each lentivirus and included a strictly conserved cysteine residue in β4. In addition, the β4/β5 consensus motif was also present in the conserved carboxy-terminal region of all type A and B retroviral envelope surface glycoproteins analyzed. Thus, the antiparallel β-strands 5 and 25 of gp120 form an SU surface highly conserved among the lentiviruses and at least partially conserved in the type A and B retroviral envelope glycoproteins.

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4

Courgnaud, Valérie, Xavier Pourrut, Frédéric Bibollet-Ruche, Eitel Mpoudi-Ngole, Anke Bourgeois, Eric Delaporte, and Martine Peeters. "Characterization of a Novel Simian Immunodeficiency Virus from Guereza Colobus Monkeys (Colobus guereza) in Cameroon: a New Lineage in the Nonhuman Primate Lentivirus Family." Journal of Virology 75, no. 2 (January 15, 2001): 857–66. http://dx.doi.org/10.1128/jvi.75.2.857-866.2001.

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ABSTRACT Exploration of the diversity among primate lentiviruses is necessary to elucidate the origins and evolution of immunodeficiency viruses. During a serological survey in Cameroon, we screened 25 wild-born guereza colobus monkeys (Colobus guereza) and identified 7 with HIV/SIV cross-reactive antibodies. In this study, we describe a novel lentivirus, named SIVcol, prevalent in guereza colobus monkeys. Genetic analysis revealed that SIVcol was very distinct from all other known SIV/HIV isolates, with average amino acid identities of 40% for Gag, 50% for Pol, 28% for Env, and around 25% for proteins encoded by five other genes. Phylogenetic analyses confirmed that SIVcol is genetically distinct from other previously characterized primate lentiviruses and clusters independently, forming a novel lineage, the sixth in the current classification.Cercopithecidae monkeys (Old World monkeys) are subdivided into two subfamilies, the Colobinae and theCercopithecinae, and, so far, allCercopithecidae monkeys from which lentiviruses have been isolated belong to the Cercopithecinae subfamily. Therefore, SIVcol from guereza colobus monkeys (C. guereza) is the first primate lentivirus identified in the Colobinaesubfamily and the divergence of SIVcol may reflect divergence of the host lineage.

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5

Chen, Jianbo, Douglas Powell, and Wei-Shau Hu. "High Frequency of Genetic Recombination Is a Common Feature of Primate Lentivirus Replication." Journal of Virology 80, no. 19 (October 1, 2006): 9651–58. http://dx.doi.org/10.1128/jvi.00936-06.

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ABSTRACT Recent studies indicate that human immunodeficiency virus type 1 (HIV-1) recombines at exceedingly high rates, approximately 1 order of magnitude more frequently than simple gammaretroviruses such as murine leukemia virus and spleen necrosis virus. We hypothesize that this high frequency of genetic recombination is a common feature of primate lentiviruses. Alternatively, it is possible that HIV-1 is unique among primate lentiviruses in possessing high recombination rates. Among other primate lentiviruses, only the molecular mechanisms of HIV-2 replication have been extensively studied. There are reported differences between the replication mechanisms of HIV-1 and those of HIV-2, such as preferences for RNA packaging in cis and properties of reverse transcriptase and RNase H activities. These biological disparities could lead to differences in recombination rates between the two viruses. Currently, HIV-1 is the only primate lentivirus in which recombination rates have been measured. To test our hypothesis, we established recombination systems to measure the recombination rates of two other primate lentiviruses, HIV-2 and simian immunodeficiency virus from African green monkeys (SIVagm), in one round of viral replication. We determined that, for markers separated by 588, 288, and 90 bp, HIV-2 recombined at rates of 7.4%, 5.5%, and 2.4%, respectively, whereas SIVagm recombined at rates of 7.8%, 5.6%, and 2.7%, respectively. These high recombination rates are within the same range as the previously measured HIV-1 recombination rates. Taken together, our results indicate that HIV-1, HIV-2, and SIVagm all possess high recombination frequencies; hence, the high recombination potential is most likely a common feature of primate lentivirus replication.

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6

de Pablo-Maiso, Lorena, Ana Doménech, Irache Echeverría, Carmen Gómez-Arrebola, Damián de Andrés, Sergio Rosati, Esperanza Gómez-Lucia, and Ramsés Reina. "Prospects in Innate Immune Responses as Potential Control Strategies against Non-Primate Lentiviruses." Viruses 10, no. 8 (August 17, 2018): 435. http://dx.doi.org/10.3390/v10080435.

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Lentiviruses are infectious agents of a number of animal species, including sheep, goats, horses, monkeys, cows, and cats, in addition to humans. As in the human case, the host immune response fails to control the establishment of chronic persistent infection that finally leads to a specific disease development. Despite intensive research on the development of lentivirus vaccines, it is still not clear which immune responses can protect against infection. Viral mutations resulting in escape from T-cell or antibody-mediated responses are the basis of the immune failure to control the infection. The innate immune response provides the first line of defense against viral infections in an antigen-independent manner. Antiviral innate responses are conducted by dendritic cells, macrophages, and natural killer cells, often targeted by lentiviruses, and intrinsic antiviral mechanisms exerted by all cells. Intrinsic responses depend on the recognition of the viral pathogen-associated molecular patterns (PAMPs) by pathogen recognition receptors (PRRs), and the signaling cascades leading to an antiviral state by inducing the expression of antiviral proteins, including restriction factors. This review describes the latest advances on innate immunity related to the infection by animal lentiviruses, centered on small ruminant lentiviruses (SRLV), equine infectious anemia virus (EIAV), and feline (FIV) and bovine immunodeficiency viruses (BIV), specifically focusing on the antiviral role of the major restriction factors described thus far.

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7

St-Louis, Marie-Claude, Mihaela Cojocariu, and Denis Archambault. "The molecular biology of bovine immunodeficiency virus: a comparison with other lentiviruses." Animal Health Research Reviews 5, no. 2 (December 2004): 125–43. http://dx.doi.org/10.1079/ahr200496.

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AbstractBovine immunodeficiency virus (BIV) was first isolated in 1969 from a cow, R-29, with a wasting syndrome. The virus isolated induced the formation of syncytia in cell cultures and was structurally similar to maedi-visna virus. Twenty years later, it was demonstrated that the bovine R-29 isolate was indeed a lentivirus with striking similarity to the human immunodeficiency virus. Like other lentiviruses, BIV has a complex genomic structure characterized by the presence of several regulatory/accessory genes that encode proteins, some of which are involved in the regulation of virus gene expression. This manuscript aims to review biological and, more particularly, molecular aspects of BIV, with emphasis on regulatory/accessory viral genes/proteins, in comparison with those of other lentiviruses.

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8

Miyazawa, Takayuki. "Receptors for Lentiviruses." MEMBRANE 30, no. 2 (2005): 73–77. http://dx.doi.org/10.5360/membrane.30.73.

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9

Pomerantz, Roger J. "Replication of lentiviruses." Frontiers in Bioscience 8, no. 6 (2003): s156–174. http://dx.doi.org/10.2741/935.

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10

Dunbar, Cynthia. "Lentiviruses get specific." Blood 99, no. 2 (January 15, 2002): 397. http://dx.doi.org/10.1182/blood.v99.2.397.

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11

Emerman, Michael. "Learning from lentiviruses." Nature Genetics 24, no. 1 (January 2000): 8–9. http://dx.doi.org/10.1038/71740.

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12

Narayan, O., D. Sheffer, J. E. Clements, and G. Tennekoon. "Restricted replication of lentiviruses. Visna viruses induce a unique interferon during interaction between lymphocytes and infected macrophages." Journal of Experimental Medicine 162, no. 6 (December 1, 1985): 1954–69. http://dx.doi.org/10.1084/jem.162.6.1954.

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Lentivirus infections are characterized by a persistent, restricted type of virus replication in tissues. Using sheep and goat lentiviruses, whose target cells in vivo are macrophages, we explored virus-host cell interactions to determine whether an interferon (IFN) is produced during virus replication in vivo which causes restricted replication. We show that the lentiviruses were incapable of inducing IFN directly in any infected cell, including macrophages and lymphocytes. However, after infection with these viruses, sheep and goat macrophages acquired a factor that triggered IFN production by T lymphocytes. Only sheep/goat lentiviruses were capable of inducing the factor and, although these viruses replicated productively in various cell cultures of the natural host animal, only infected macrophages developed the IFN-inducing factor. The factor was produced continuously and was strictly cell associated, requiring direct contact with lymphocytes. The lymphocytes responded with a single, sudden release of IFN beginning 7 h after cocultivation and reaching peak values at 48 h, after which they ceased production and became refractory. IFN production was not immunologically specific and did not require histocompatibility between donors of the two cell types. The IFN is a nonglycosylated protein of molecular weight 54,000-64,000, and is stable to heat and acid treatments. These findings identify a unique IFN and a new method for virus induction of IFN. The novel two-stage process of induction provides a mechanism for local amplification and continuity of production of IFN in vivo. This is compatible with infection in the animal whose lentivirus-induced pathologic lesions consist of accumulations of lymphocytes and infected macrophages in target tissues.

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13

Hatziioannou, Theodora, Simone Cowan, and Paul D. Bieniasz. "Capsid-Dependent and -Independent Postentry Restriction of Primate Lentivirus Tropism in Rodent Cells." Journal of Virology 78, no. 2 (January 15, 2004): 1006–11. http://dx.doi.org/10.1128/jvi.78.2.1006-1011.2004.

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ABSTRACT Retrovirus tropism can be restricted by cellular factors such as Fv1, Ref1, and Lv1 that inhibit infection by targeting the incoming viral capsid. Here, we show that rodent cells exhibit differential sensitivity to infection by vesicular stomatitis virus G-pseudotyped lentiviruses and that differences between human immunodeficiency virus type 1 and simian immunodeficiency virus (SIVmac) infectivity are sometimes, but not always, governed by determinants in capsid-p2. In at least one case, resistance to SIVmac infection could be eliminated by saturation of target cells with noninfectious SIVmac particles. However, cross-saturation experiments and analysis of Fv1-null cells engineered to express natural or artificial Fv1 proteins revealed that lentivirus restriction in mouse cells is independent of Fv1. Overall, these findings indicate that novel restriction factors in rodents can modulate sensitivity to specific primate lentiviruses.

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14

Armimi, Anastasia, Afina Firdaus Syuaib, Katherine Vanya, Marselina Irasonia Tan, Dessy Natalia, David Virya Chen, Chikako Ono, Yoshiharu Matsuura, Anita Artarini, and Ernawati Arifin Giri-Rachman. "SARS-CoV-2 Neutralization Assay System using Pseudo-lentivirus." Indonesian Biomedical Journal 15, no. 2 (April 18, 2023): 179–86. http://dx.doi.org/10.18585/inabj.v15i2.2212.

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BACKGROUND: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infects humans' lower respiratory tracts and causes coronavirus disease-2019 (COVID-19). Neutralizing antibodies is one of the adaptive immune system responses that can reduce SARS-CoV-2 infection. This study aimed to develop a SARS-CoV-2 neutralization assay system using pseudo-lentivirus.METHODS: The plasmid used for pseudo-lentivirus production was characterized using restriction analysis. The gene encoding for SARS-CoV-2 spike protein was confirmed using sequencing. The transfection pseudo-lentivirus optimal condition was determined by choosing the transfection reagents and adding centrifugation step. Optimal pseudo-lentivirus infection was analysed using fluorescent assay and luciferase assay. The optimal condition of pseudo-lentivirus infection was determined by the target cell type and the number of pseudo-lentiviruses used for neutralization test. SARS-CoV-2 pseudo-lentivirus was used to detect neutralizing antibodies from serum samples.RESULTS: The plasmid used for pseudo-lentivirus production was characterized and confirmed to have no mutations. Lipofectamine 2000 reagent generated pseudo-lentivirus with a higher ability to infect target cells, as indicated by a percentage green fluorescent protein (GFP) of 12.68%. Pseudo-lentivirus centrifuged obtained more stable results in luciferase expression. Optimal pseudo-lentivirus infection conditions were obtained using puromycin-selected HEK 293T-ACE2 cells as target cells. The number of pseudo-lentiviruses used in the neutralization assay system was multiplicity of infection (MOI) 0.075. Serum A samples with a 1:10 dilution had the highest neutralizing antibody activity.CONCLUSION: This study shows that SARS-CoV-2 neutralization assay system using pseudo-lentivirus successfully detected neutralizing antibodies in human serum, which were indicated by a decrease in the percentage of pseudo-lentivirus infections.KEYWORDS: COVID-19, neutralizing antibody, neutralization assay, pseudo-lentivirus, SARS-COV-2

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15

Rosati, Sergio, Jimmy Kwang, and James E. Keen. "Genome Analysis of North American Small Ruminant Lentiviruses by Polymerase Chain Reaction and Restriction Enzyme Analysis." Journal of Veterinary Diagnostic Investigation 7, no. 4 (October 1995): 437–43. http://dx.doi.org/10.1177/104063879500700403.

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The polymerase chain reaction (PCR) was used to amplify portions of the gag and env structural genes of 8 ovine and 1 caprine lentivirus isolates of North American origin. Three sets of primers were used to amplify p16, p25, and Nî-gp40 gene fragments, and 1 set, annealing highly conserved portions of long terminal repeat (LTR) among small ruminant lentiviruses, was used as a positive control. Variable PCR amplification efficiency was observed. Different stringency conditions of hybridization with specific DNA probes were used to maximize detection of the PCR product. The p25 primers detected all strains, the gp40 primers detected 1 ovine and the caprine strain, and the p16 primers detected only 1 ovine isolate. All strains were detected by LTR primers. Restriction endonuclease analysis of 5 amplified p25 and 2 Nî-gp40 gene fragments revealed extensive heterogeneity among these North American small ruminant lentiviruses.

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16

Barnass, Stella. "Lentiviruses and mycobacterial diseases." Immunology Today 8, no. 1 (January 1987): 9. http://dx.doi.org/10.1016/0167-5699(87)90822-x.

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17

Breckpot, Karine, and K. Thielemans. "Lentiviruses in cancer immunotherapy." Future Virology 2, no. 6 (November 2007): 597–606. http://dx.doi.org/10.2217/17460794.2.6.597.

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18

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) is becoming the lentivirus of choice for human gene transfer systems. However, the safety of FIV-based vector systems has not been tested experimentally. Since lentiviruses such as HIV-1 and SIV have been shown to cross-package their RNA genomes, we tested the ability of FIV RNA to get cross-packaged into primate lentivirus particles such as HIV-1 and SIV, as well as a nonlentiviral retrovirus such as Mason-Pfizer monkey virus (MPMV), and vice versa. Our results reveal that FIV RNA can be cross-packaged by primate lentivirus particles such as HIV-1 and SIV and vice versa; however, a nonlentivirus particle such as MPMV is unable to package FIV RNA. Interestingly, FIV particles can package MPMV RNA but cannot propagate the vector RNA further for other steps of the retrovirus life cycle. These findings reveal that diverse retroviruses are functionally more similar than originally thought and suggest that upon coinfection of the same host, cross- or copackaging may allow distinct retroviruses to generate chimeric variants with unknown pathogenic potential.

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19

Baccam, Prasith, Robert J. Thompson, Yuxing Li, Wendy O. Sparks, Michael Belshan, Karin S. Dorman, Yvonne Wannemuehler, J. Lindsay Oaks, James L. Cornette, and Susan Carpenter. "Subpopulations of Equine Infectious Anemia Virus Rev Coexist In Vivo and Differ in Phenotype." Journal of Virology 77, no. 22 (November 15, 2003): 12122–31. http://dx.doi.org/10.1128/jvi.77.22.12122-12131.2003.

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ABSTRACT Lentiviruses exist in vivo as a population of related, nonidentical genotypes, commonly referred to as quasispecies. The quasispecies structure is characteristic of complex adaptive systems and contributes to the high rate of evolution in lentiviruses that confounds efforts to develop effective vaccines and antiviral therapies. Here, we describe analyses of genetic data from longitudinal studies of genetic variation in a lentivirus regulatory protein, Rev, over the course of disease in ponies experimentally infected with equine infectious anemia virus. As observed with other lentivirus data, the Rev variants exhibited a quasispecies character. Phylogenetic and partition analyses suggested that the Rev quasispecies comprised two distinct subpopulations that coexisted during infection. One subpopulation appeared to accumulate changes in a linear, time-dependent manner, while the other evolved radially from a common variant. Over time, the two subpopulations cycled in predominance coincident with changes in the disease state, suggesting that the two groups differed in selective advantage. Transient expression assays indicated the two populations differed significantly in Rev nuclear export activity. Chimeric proviral clones containing Rev genotypes representative of each population differed in rate and overall level of virus replication in vitro. The coexistence of genetically distinct viral subpopulations that differ in phenotype provides great adaptability to environmental changes within the infected host. A quasispecies model with multiple subpopulations may provide additional insight into the nature of lentivirus reservoirs and the evolution of antigenic and drug-resistant variants.

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20

Jin, Jing, Timothy Sturgeon, Chaoping Chen, Simon C. Watkins, Ora A. Weisz, and Ronald C. Montelaro. "Distinct Intracellular Trafficking of Equine Infectious Anemia Virus and Human Immunodeficiency Virus Type 1 Gag during Viral Assembly and Budding Revealed by Bimolecular Fluorescence Complementation Assays." Journal of Virology 81, no. 20 (August 8, 2007): 11226–35. http://dx.doi.org/10.1128/jvi.00431-07.

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ABSTRACT Retroviral Gag polyproteins are necessary and sufficient for virus budding. Numerous studies of human immunodeficiency virus type 1 (HIV-1) Gag assembly and budding mechanisms have been reported, but relatively little is known about these fundamental pathways among animal lentiviruses. While there may be a general assumption that lentiviruses share common assembly mechanisms, studies of equine infectious anemia virus (EIAV) have indicated alternative cellular pathways and cofactors employed among lentiviruses for assembly and budding. In the current study, we used bimolecular fluorescence complementation to characterize and compare assembly sites and budding efficiencies of EIAV and HIV-1 Gag in both human and rodent cells. The results of these studies demonstrated that replacing the natural RNA nuclear export element (Rev-response element [RRE]) used by HIV-1 and EIAV with the hepatitis B virus posttranscriptional regulatory element (PRE) altered HIV-1, but not EIAV, Gag assembly sites and budding efficiency in human cells. Consistent with this novel observation, different assembly sites were revealed in human cells for Rev-dependent EIAV and HIV-1 Gag polyproteins. In rodent cells, Rev-dependent HIV-1 Gag assembly and budding were blocked, but changing RRE to PRE rescued HIV-1 Gag assembly and budding. In contrast, EIAV Gag polyproteins synthesized from mRNA exported via either Rev-dependent or PRE-dependent mechanisms were able to assemble and bud efficiently in rodent cells. Taken together, our results suggest that lentivirus assembly and budding are regulated by the RNA nuclear export pathway and that alternative cellular pathways can be adapted for lentiviral Gag assembly and budding.

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21

Wolf, Cindy. "Update on Small Ruminant Lentiviruses." Veterinary Clinics of North America: Food Animal Practice 37, no. 1 (March 2021): 199–208. http://dx.doi.org/10.1016/j.cvfa.2020.12.003.

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22

Nandi, Jayashree S., Anil K. Chhangani, Shravan Singh Rathore, and Bajrang Raj J. Mathur. "Diversity of Primate Lentiviruses Rebooted." Journal of Biosciences and Medicines 07, no. 12 (2019): 126–38. http://dx.doi.org/10.4236/jbm.2019.712011.

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23

Reina, Ramsés, Damián Andrés, and Beatriz Amorena. "Immunization against Small Ruminant Lentiviruses." Viruses 5, no. 8 (August 2, 2013): 1948–63. http://dx.doi.org/10.3390/v5081948.

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24

Ruprecht, Ruth M., Timothy W. Baba, Vladimir Liska, Nancy B. Ray, Louis N. Martin, Michael Murphey‐Corb, Tahir A. Rizvi, et al. "Oral Transmission of Primate Lentiviruses." Journal of Infectious Diseases 179, s3 (May 1999): S408—S412. http://dx.doi.org/10.1086/314794.

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25

Holmes, E. C. "Ancient lentiviruses leave their mark." Proceedings of the National Academy of Sciences 104, no. 15 (April 2, 2007): 6095–96. http://dx.doi.org/10.1073/pnas.0701578104.

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26

Cross, James C. "Lentiviruses to the placental rescue." Nature Biotechnology 25, no. 2 (February 2007): 190–91. http://dx.doi.org/10.1038/nbt0207-190.

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27

Dove, Alan. "Lentiviruses for stable gene therapy." Nature Biotechnology 18, no. 8 (August 2000): 813. http://dx.doi.org/10.1038/78375.

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28

Narayan, O., and J. E. Clements. "Biology and Pathogenesis of Lentiviruses." Journal of General Virology 70, no. 7 (July 1, 1989): 1617–39. http://dx.doi.org/10.1099/0022-1317-70-7-1617.

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29

Federico, M. "Lentiviruses as gene delivery vectors." Current Opinion in Biotechnology 10, no. 5 (October 1, 1999): 448–53. http://dx.doi.org/10.1016/s0958-1669(99)00008-7.

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30

TRISTEM, MICHAEL, CRAIG MARSHALL, ABRAHAM KARPAS, JURAJ PETRIK, and FERGAL HILL. "Origin of vpx in lentiviruses." Nature 347, no. 6291 (September 1990): 341–42. http://dx.doi.org/10.1038/347341b0.

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31

Blacklaws, B. A., E. Berriatua, S. Torsteinsdottir, N. J. Watt, D. de Andres, D. Klein, and G. D. Harkiss. "Transmission of small ruminant lentiviruses." Veterinary Microbiology 101, no. 3 (July 2004): 199–208. http://dx.doi.org/10.1016/j.vetmic.2004.04.006.

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32

Davis, Jennifer L., and Janice E. Clements. "Complex gene expression of lentiviruses." Microbial Pathogenesis 4, no. 4 (April 1988): 239–45. http://dx.doi.org/10.1016/0882-4010(88)90084-8.

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33

Chastel, C. "Points: Lentiviruses, AIDS, and insects." BMJ 293, no. 6539 (July 12, 1986): 140. http://dx.doi.org/10.1136/bmj.293.6539.140-f.

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34

Schneider, Josef, and Gerhard Hunsmann. "Simian lentiviruses — the SIV group." AIDS 2, no. 1 (February 1988): 1–10. http://dx.doi.org/10.1097/00002030-198802000-00001.

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35

Denman, A. M. "Induction of interferon by lentiviruses." Immunology Today 7, no. 7-8 (July 1986): 201–2. http://dx.doi.org/10.1016/0167-5699(86)90103-9.

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36

Da Silva Teixeira, Maria Fatima, Véronique Lambert, Laila Mselli-Lakahl, Abdelkamel Chettab, Yahia Chebloune, and Jean-François Mornex. "Immortalization of caprine fibroblasts permissive for replication of small ruminant lentiviruses." American Journal of Veterinary Research 58, no. 6 (June 1, 1997): 579–84. http://dx.doi.org/10.2460/ajvr.1997.58.06.579.

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Abstract Objective To establish immortalized caprine fibroblastic cell lines permissive for replication of small ruminant lentiviruses. Animals Carpal synovial membrane explants collected aseptically from a surgically delivered fetus of a lentivirus-seronegative goat. Procedure Immortalization of goat embryonic fibroblasts was performed by DNA transfection with plasmids coding for simian virus 40 large T antigen. The generated cell lines were phenotypically characterized. Cytogenetics, growth pattern, and sensitivity to viral infection were studied. Results 3 cell lines, designated TIGEF, mMTSV-54, and mMTSV-93, were generated. They had a more rapid doubling time than did fibroblasts from which they were derived, and retained morphologic and phenotypic fibroblastic characteristics. They were immortalized but not transformed because tumor formation was not promoted after their SC injection into athymic nude mice. The 3 cell lines were susceptible to caprine arthritisencephalitis virus and visna-maedi virus infections, and supported a complete virus replication cycle. Conclusions Cultured caprine fibroblastic cells were immortalized, using simian virus 40 large T antigen. The TIGEF, mMTSV-54, and mMTSV-93 immortalized cell lines were permissive to in vitro small ruminant lentivirus replication. Clinical Relevance Because lentivirus detection, as well as detailed studies of host-lentivirus interactions, are hampered by differences in viral susceptibility of each primary culture, permanent cell lines are essential tools for such analysis. (Am J Vet Res 1997;58:579–584)

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37

Soares, Rafael Rodrigues, Francisco Alberto Moraes Viana Júnior, Diego Moraes Soares, Thais Bastos Rocha, Leandro Henrique Veiga de Sousa, Hamilton Pereira Santos, and Helder de Moraes Pereira. "Serological evidence and spatial analysis of small ruminant lentiviruses in herds in Maranhão, Brazil." Acta Veterinaria Brasilica 14, no. 4 (December 29, 2020): 244–51. http://dx.doi.org/10.21708/avb.2020.14.4.9001.

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Caprine arthritis encephalitis and Maedi-Visnaare lentiviruses affecting goats and sheep, respectively. Despite the literature having studies about these diseases, there is a constant demand and the need to study the health status of flocks that exploit economically. Therefore, this study aimed to assess the frequency of small ruminant lentiviruses explored in regional locations of Chapadinha and Itapecuru Mirim, that compose the microregion of Low Parnaíba, Maranhão, Brazil, as well as analyze the spatial distribution of outbreaks in the studied regions. Therefore, 241 properties were visited, where blood was collected in 1150 sheep and 1260 goats and tested by agar gel immunodiffusion (AGID). Epidemiological questionnaire was applied and collected the geographic coordinates. There was a low frequencyfor lentivirus, with 0.39% (5/1260) of goats and 0.08% (1/1150) of sheep. Regarding the spatial analysis, the reagent flocks were distributed in strategic cities for commercialization throughout the microregion. There was a low occurrence of lentiviruses.The municipalities of Cantanhede and Pirapemas of the regional of Itapecuru Mirimand Brejo and Magalhães de Almeida had reagent flocks for CAE. Whereas the municipality of Matões do Norte presented flock reagent to Maedi-Visna, this belonging to the regional of Chapadinha.

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38

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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39

Han, Guan-Zhu, and Michael Worobey. "A Primitive Endogenous Lentivirus in a Colugo: Insights into the Early Evolution of Lentiviruses." Molecular Biology and Evolution 32, no. 1 (October 27, 2014): 211–15. http://dx.doi.org/10.1093/molbev/msu297.

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40

Johnston, J. B., Y. Jiang, G. van Marle, M. B. Mayne, W. Ni, J. Holden, J. C. McArthur, and C. Power. "Lentivirus Infection in the Brain Induces Matrix Metalloproteinase Expression: Role of Envelope Diversity." Journal of Virology 74, no. 16 (August 15, 2000): 7211–20. http://dx.doi.org/10.1128/jvi.74.16.7211-7220.2000.

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ABSTRACT Infection of the brain by lentiviruses, including human immunodeficiency virus (HIV) and feline immunodeficiency virus (FIV), causes inflammation and results in neurodegeneration. Molecular diversity within the lentivirus envelope gene has been implicated in the regulation of cell tropism and the host response to infection. Here, we examine the hypothesis that envelope sequence diversity modulates the expression of host molecules implicated in lentivirus-induced brain disease, including matrix metalloproteinases (MMP) and related transcription factors. Infection of primary macrophages by chimeric HIV clones containing brain-derived envelope fragments from patients with HIV-associated dementia (HAD) or nondemented AIDS patients (HIV-ND) showed that MMP-2 and -9 levels in conditioned media were significantly higher for the HAD clones. Similarly, STAT-1 and JAK-1 levels were higher in macrophages infected by HAD clones. Infections of primary feline macrophages by the neurovirulent FIV strain (V1CSF), the less neurovirulent strain (Petaluma), and a chimera containing the V1CSF envelope in a Petaluma background (FIV-Ch) revealed that MMP-2 and -9 levels were significantly higher in conditioned media from V1CSF- and FIV-Ch-infected macrophages, which was associated with increased intracellular STAT-1 and JAK-1 levels. The STAT-1 inhibitor fludarabine significantly reduced MMP-2 expression, but not MMP-9 expression, in FIV-infected macrophages. Analysis of MMP mRNA and protein levels in brain samples from HIV-infected persons or FIV-infected cats showed that MMP-2 and -9 levels were significantly increased in lentivirus-infected brains compared to those of uninfected controls. Elevated MMP expression was accompanied by significant increases in STAT-1 and JAK-1 mRNA and protein levels in the same brain samples. The present findings indicate that two lentiviruses, HIV and FIV, have common mechanisms of MMP-2 and -9 induction, which is modulated in part by envelope sequence diversity and the STAT-1/JAK-1 signaling pathway.

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41

Compton, Alex A., Harmit S. Malik, and Michael Emerman. "Host gene evolution traces the evolutionary history of ancient primate lentiviruses." Philosophical Transactions of the Royal Society B: Biological Sciences 368, no. 1626 (September 19, 2013): 20120496. http://dx.doi.org/10.1098/rstb.2012.0496.

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Simian immunodeficiency viruses (SIVs) have infected primate species long before human immunodeficiency virus has infected humans. Dozens of species-specific lentiviruses are found in African primate species, including two strains that have repeatedly jumped into human populations within the past century. Traditional phylogenetic approaches have grossly underestimated the age of these primate lentiviruses. Instead, here we review how selective pressures imposed by these viruses have fundamentally altered the evolutionary trajectory of hosts genes and, even in cases where there now remains no trace of the viruses themselves, these evolutionary signatures can reveal the types of viruses that were once present. Examination of selection by ancient viruses on the adaptive evolution of host genes has been used to derive minimum age estimates for modern primate lentiviruses. This type of data suggests that ancestors of modern SIV existed in simian primates more than 10 Ma. Moreover, examples of host resistance and viral adaptation have implications not only for estimating the age and host range of ancient primate lentiviruses, but also the pathogenic potential of their modern counterparts.

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42

Wang, Chu, Kaikai Zhang, Lina Meng, Xin Zhang, Yanan Song, Ying Zhang, Yanxin Gai, et al. "The C-terminal domain of feline and bovine SAMHD1 proteins has a crucial role in lentiviral restriction." Journal of Biological Chemistry 295, no. 13 (February 19, 2020): 4252–64. http://dx.doi.org/10.1074/jbc.ra120.012767.

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SAM and HD domain-containing protein 1 (SAMHD1) is a host factor that restricts reverse transcription of lentiviruses such as HIV in myeloid cells and resting T cells through its dNTP triphosphohydrolase (dNTPase) activity. Lentiviruses counteract this restriction by expressing the accessory protein Vpx or Vpr, which targets SAMHD1 for proteasomal degradation. SAMHD1 is conserved among mammals, and the feline and bovine SAMHD1 proteins (fSAM and bSAM) restrict lentiviruses by reducing cellular dNTP concentrations. However, the functional regions of fSAM and bSAM that are required for their biological functions are not well-characterized. Here, to establish alternative models to investigate SAMHD1 in vivo, we studied the restriction profile of fSAM and bSAM against different primate lentiviruses. We found that both fSAM and bSAM strongly restrict primate lentiviruses and that Vpx induces the proteasomal degradation of both fSAM and bSAM. Further investigation identified one and five amino acid sites in the C-terminal domain (CTD) of fSAM and bSAM, respectively, that are required for Vpx-mediated degradation. We also found that the CTD of bSAM is directly involved in mediating bSAM's antiviral activity by regulating dNTPase activity, whereas the CTD of fSAM is not. Our results suggest that the CTDs of fSAM and bSAM have important roles in their antiviral functions. These findings advance our understanding of the mechanism of fSAM- and bSAM-mediated viral restriction and might inform strategies for improving HIV animal models.

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43

van der Loo, W., J. Abrantes, and P. J. Esteves. "Sharing of Endogenous Lentiviral Gene Fragments among Leporid Lineages Separated for More than 12 Million Years." Journal of Virology 83, no. 5 (December 24, 2008): 2386–88. http://dx.doi.org/10.1128/jvi.01116-08.

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ABSTRACT Lentiviruses are causal agents of severe pathologies of a variety of mammals, including cattle and humans (e.g., AIDS and different types of lymphoma). While endogenous forms of lentivirus do not occur in these species, A. Katzourakis and coworkers (A. Katzourakis, M. Tristem, O. G. Pybus, and R. J. Gifford, Proc. Natl. Acad. Sci. USA 104:6261-6265, 2007) recently reported the presence in the genome of the European rabbit (Oryctolagus cuniculus) of multiple sequences defining a lentiviral subgroup elegantly referred to as RELIK (rabbit endogenous lentivirus type K). Sequence comparisons indicated that the RELIK ancestor may have integrated into the rabbit lineage more than 7 million years ago. We have substantiated this by producing sequence data certifying the sharing of RELIK sequences among leporid lineages that diverged some 12 million years ago.

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44

MIYAZAWA, Takayuki. "Evolution of lentiviruses and receptor specificity." Uirusu 55, no. 1 (2005): 27–34. http://dx.doi.org/10.2222/jsv.55.27.

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45

DESROSIERS, RONALD C., MUTHIAH D. DANIEL, and YEN LI. "HIV-Related Lentiviruses of Nonhuman Primates." AIDS Research and Human Retroviruses 5, no. 5 (October 1989): 465–73. http://dx.doi.org/10.1089/aid.1989.5.465.

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46

Willett, Brian J., Margaret J. Hosie, James C. Neil, Julie D. Turner, and James A. Hoxie. "Common mechanism of infection by lentiviruses." Nature 385, no. 6617 (February 1997): 587. http://dx.doi.org/10.1038/385587a0.

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47

Connolly, J. B. "Lentiviruses in gene therapy clinical research." Gene Therapy 9, no. 24 (November 29, 2002): 1730–34. http://dx.doi.org/10.1038/sj.gt.3301893.

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48

Cui, J., and E. C. Holmes. "Endogenous Lentiviruses in the Ferret Genome." Journal of Virology 86, no. 6 (January 11, 2012): 3383–85. http://dx.doi.org/10.1128/jvi.06652-11.

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49

HU, SHIU-LOK. "Recombinant Subunit Vaccines against Primate Lentiviruses." AIDS Research and Human Retroviruses 12, no. 5 (March 20, 1996): 451–53. http://dx.doi.org/10.1089/aid.1996.12.451.

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50

Campbell, R. S. F., and W. F. Robinson. "The comparative pathology of the lentiviruses." Journal of Comparative Pathology 119, no. 4 (November 1998): 333–95. http://dx.doi.org/10.1016/s0021-9975(98)80033-9.

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