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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.
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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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.
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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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.
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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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.
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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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.
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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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.
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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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.
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.
Dissertations / Theses on the topic "Lentiviruses":
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Robertson, David L. "Recombination in primate lentiviruses." Thesis, University of Nottingham, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336866.
Bailes, Elizabeth. "Origins and evolution of primate lentiviruses." Thesis, University of Nottingham, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246384.
Kelly, Maureen C. "Parallels in tRNA primer acquisition by lentiviruses." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2009r/kelly.pdf.
Li, Li. "Short-term and long-term evolution of lentiviruses." Thesis, University of Nottingham, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.575475.
Lentiviruses have paradoxically fast short-term rate of evolution and slow long-term rate of evolution, which differ by several orders of magnitude. In this thesis, with a new method called truncated tree analysis, slower rates of evolution of transmitted viruses were estimated. However, the rate decline of the transmitted viruses is limited, and is not sufficient to explain the dramatic difference between the short-term and long-term evolutionary rates. These dramatically different rates were reconciled by an S shaped curve based on the new trend observed from this thesis. In the middle part of this new trend, the rate of evolution decreases as the time of divergence increases. Using this new trend, the time scale of HIV -1 and their closest related SIV found in apes were set. The SIV cpzPtt and SIV cpzPts isolated from the two subspecies of chimpanzees shared the most recent common ancestor around 25.2 thousand years ago. This is younger than the estimated date of these two host subspecies split, and suggests that the SIV cpz is relatively new to the chimpanzees. The second chapter of this thesis further explores lentiviral evolution by examining the feline immunodeficiency viruses (FIV's). An American origin scenario of the FIV s was proposed. In this scenario the ancestor of FIV first the invaded the ancestors of the puma lineage living in American, and then as the ancient puma lineage speciated and migrated FIV spread out to many other felids. The final chapter of this thesis further explores the evolutionary rate decline as the time span extends by introducing the idea of flip- flop sites that undergo negative frequency dependent selection pressures. Theoretical simulations confirmed that in the short time span, the presence of the flip-flop sites results in overestimation of the evolutionary rate, but in longer time spans, opposite effects of flip-flop sites were observed.
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Broughton-Neiswanger, Liam E. "Maternal transmission is the major mode of ovine lentivirus transmission in a ewe flock a molecular epidemiology study /." Pullman, Wash. : Washington State University, 2010. http://www.dissertations.wsu.edu/Thesis/Spring2010/L_Broughton_042010.pdf.
Thesis (M.S. in veterinary science)--Washington State University, May 2010. Title from PDF title page (viewed on June 29, 2010). "College of Veterinary Medicine." Includes bibliographical references (p. 20-26).
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Stewart, Meredith Ellen. "An investigation into aspects of the replication of Jembrana disease virus /." Access via Murdoch University Digital Theses Project, 2005. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20051222.104106.
Harris, Matthew E. "Analysis of post-transcriptional regulation of lentiviruses and mammalian hepadnaviruses /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1999. http://wwwlib.umi.com/cr/ucsd/fullcit?p9935471.
Ditcham, William. "The development of recombinant vaccines against Jembrana disease." Thesis, Ditcham, William (2007) The development of recombinant vaccines against Jembrana disease. PhD thesis, Murdoch University, 2007. https://researchrepository.murdoch.edu.au/id/eprint/438/.
Jembrana disease virus (JDV) is a lentivirus causing an acute infection with a 17% case fatality rate in Bali cattle in Indonesia. Control of the disease is currently achieved by identification of infected areas and restriction of cattle movement. A detergent-inactivated whole virus tissue-derived vaccine is sometimes employed in affected areas.
This thesis reports initial attempts to produce genetically engineered vaccines to replace the inactivated tissue-derived vaccine, which as it is made from homogenised spleen of infected animals, is expensive to produce and could contain adventitious agents present in the donor animals.
4 potential DNA vaccine constructs were created containing the JDV genes coding for the Tat, capsid (CA), transmembrane (TM) and surface unit (SU) proteins in a commercially available vaccine plasmid. These were assessed for functionality in a range of in vitro and in vivo assays. All proteins were expressed in vitro and administration of 2 of the constructs by a commercial 'gene gun' into the epidermis of mice resulted in antibody production to the appropriate protein. Due to the difficulties of licensing such a DNA vaccine in Indonesia, these vaccines were not progressed further.
A mathematical model was developed to describe the progression of the acute phase of Jembrana disease following experimental infection with JDV. The model divided the disease into 6 phases based on the rates of viral replication and clearance calculated from data on sequential plasma viral RNA load detected by quantitative reverse-transcription polymerase chain reaction. This allowed statistical comparison of each phase of the disease and comparison of the severity of the disease process in groups of animals. The use of the model overcame the difficulty of comparing the disease in different animals as a consequence of the animal-to-animal variation in the disease process.
The mathematical model was used to identify differences in the pathogenicity of 2 strains of JDV. One strain, JDVTAB caused a more rapid onset of disease in non-vaccinated controls, a significantly higher virus load at the onset of the febrile period and a higher peak viraemia than in animals infected with JDVPUL. This provided the first evidence of variation in pathogenicity of JDV strains.
The measurement of virus load also demonstrated that some JDV infected animals developed a clinical disease that was not typical of that which had been reported previously. When infected with less than 1,000 infectious virus particles, up to 20% of infected animals failed to develop a febrile response. Infection of these animals was confirmed, however, by the detection of a high titre of circulating virus particles in plasma. These atypical infections had not been reported previously.
Application of the mathematical model describing the progression of the disease in individual animals was used to examine the effect of vaccination with the inactivated tissue-derived vaccine on the progression of the disease. Several effects were noted in vaccinated animals that were subsequently infected with JDV: a reduction in the duration of the febrile response, a reduction in the severity of the febrile response in the early phases of the acute disease, and a reduction in virus load in the early and later phases of the disease process.
The effect of vaccination with recombinant Tat, matrix (MA) and CA protein vaccines expressed in a bacterial expression system on subsequent JDV infection was also examined. A vaccine incorporating recombinant Tat and CA vaccine emulsified with Freund's incomplete adjuvant decreased the febrile response particularly in the later stages of the acute disease process, decreased the severity of the leucopenia in the later phases of the acute disease, and decreased the virus load in some but not all phases of the acute disease process. Vaccines administered with Freund's incomplete adjuvant were more efficacious than vaccines administered with QuilA, the latter actually exacerbating the disease process in vaccinated animals.
E, Wilcox G., Soeharsono S, Dharma D. M. N, Copland J. W, AustralianCentre for International Agricultural Research., Indonesia Direktorat Jenderal Petermakan, and Bali Cattle Disease Investigation Unit., eds. Jembrana disease and the bovine lentiviruses: Proceedings of a workshop 10-13 June 1996, Bali, Indonesia. Canberra: Australian Centre for International Agricultural Research in association with Direktorat Jenderal Petermakan and the Bali Cattle Disease Investigation Unit, 1997.
Milne, Catherine E. Maedi visna: The disease, its potential impact on the UK sheep industry and a cost benefit appraisal ofcontrol strategies. [Aberdeen]: SAC, 1993.
Gonda, Matthew A. "The Lentiviruses of Cattle." In The Retroviridae, 83–109. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4899-1730-0_3.
Déglon, N., and P. Aebischer. "Lentiviruses as Vectors for CNS Diseases." In Current Topics in Microbiology and Immunology, 191–209. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-56114-6_10.
Huso, David L., and Opendra Narayan. "Escape of Lentiviruses from Immune Surveillance." In Virus Variability, Epidemiology and Control, 61–73. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4757-9271-3_5.
Lin, Yuan, Amar Desai, and Stanton L. Gerson. "Lentiviruses: Vectors for Cancer Gene Therapy." In Gene-Based Therapies for Cancer, 155–79. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6102-0_10.
Narayan, Opendra, Mary C. Zink, Mark Gorrell, Sharon Crane, David Huso, Pauline Jolly, Mary Saltarelli, Robert J. Adams, and Janice E. Clements. "The Lentiviruses of Sheep and Goats." In The Retroviridae, 229–55. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4899-1627-3_4.
Pancino, G., H. Ellerbrok, M. Sitbon, and P. Sonigo. "Conserved Framework of Envelope Glycoproteins Among Lentiviruses." In Current Topics in Microbiology and Immunology, 77–105. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78536-8_5.
Jeang, K. T., and A. Gatignol. "Comparison of Regulatory Features Among Primate Lentiviruses." In Current Topics in Microbiology and Immunology, 123–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78536-8_7.
Gelderblom, Hans R., Preston A. Marx, Muhsin Özel, Dirk Gheysen, Robert J. Munn, Kenneth I. Joy, and Georg Pauli. "Morphogenesis, Maturation and Fine Structure of Lentiviruses." In Retroviral Proteases, 159–80. London: Macmillan Education UK, 1990. http://dx.doi.org/10.1007/978-1-349-11907-3_17.
Pyper, J. M., J. E. Clements, J. L. Davis, and O. Narayan. "Variations in Clinical Disease During Replication of Lentiviruses." In Maedi-Visna and Related Diseases, 129–56. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-1613-8_8.
Xiao, Yun-Feng. "Label-free Detection of Single Nanoparticles and Lentiviruses Using an Optical Microcavity." In Optical Sensors. Washington, D.C.: OSA, 2013. http://dx.doi.org/10.1364/sensors.2013.st2b.3.
Hoffman, Robert M., Hiroyuki Kishimoto, and Toshiyoshi Fujiwara. "Specific in vivo labeling with GFP retroviruses, lentiviruses, and adenoviruses for imaging." In Biomedical Optics (BiOS) 2008, edited by Alexander P. Savitsky, Robert E. Campbell, and Robert M. Hoffman. SPIE, 2008. http://dx.doi.org/10.1117/12.773308.
Tapanes-Castillo, Alexis, Derek Dykxhoorn, Leana Ramos, Milagros Mulero, Deliabell Hernandez, and Vadym Trokhymchuk. "Culturing Human Neural Stem Cells and Quantifying Lentiviruses to Study Autism." In MOL2NET 2016, International Conference on Multidisciplinary Sciences, 2nd edition. Basel, Switzerland: MDPI, 2016. http://dx.doi.org/10.3390/mol2net-02-07008.
Zhang, Dongming, Frederic Vigant, Qun He, Anirban Kundu, Wei Zhang, Hongliang Zong, Ewa Jaruga-Killeen, et al. "Abstract 1511: Subcutaneous injection of total nucleated cells rapidly isolated following four-hour peripheral whole blood exposure to CD3-directed CAR-T lentiviruses with a synthetic driver results in robust CAR-T proliferation and anti-tumor immunity." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1511.
Tulio, Robertha, and Rômulo Machado Balmant. "Dental care for HIV positive patients - care and importance - case report." In II INTERNATIONAL SEVEN MULTIDISCIPLINARY CONGRESS. Seven Congress, 2023. http://dx.doi.org/10.56238/homeinternationalanais-087.
Abstract Acquired immunodeficiency syndrome (AIDS) is caused by the "Lentivirus" family of retroviruses, called HIV-1. This syndrome is defined as an infectious disease of viral origin, with its manifestation interspersed in peaks and troughs, with a pathophysiology involving the compromising of the immune system, causing the defense system to not operate correctly, leaving the patient susceptible to the development of infections.
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Alton, EWFW, AC Boyd, JC Davies, DR Gill, U. Griesenbach, TE Harman, SC Hyde, and G. McLachlan. "S68 Towards a first-in-human trial with a pseudotyped lentivirus." In British Thoracic Society Winter Meeting, Wednesday 17 to Friday 19 February 2021, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2021. http://dx.doi.org/10.1136/thorax-2020-btsabstracts.73.
Lund-Palau, H., C. Meng, A. Pilou, N. Atsumi, A. Bhargava, M. Chan, A. Byrne, et al. "T2 Lentivirus GM-CSF gene therapy ameliorates autoimmune pulmonary alveolar proteinosis." In British Thoracic Society Winter Meeting 2018, QEII Centre, Broad Sanctuary, Westminster, London SW1P 3EE, 5 to 7 December 2018, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2018. http://dx.doi.org/10.1136/thorax-2018-212555.2.
Burke, David, Kristine Drafahl, Clark Fjeld, Chad Galderisi, and Cindy Spittle. "Abstract 896: Enhanced sensitivity detection of replication competent lentivirus by qPCR." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-896.
Wilson, AA, GJ Murphy, H. Hamakawa, L. Kwok, S. Srinivasan, A. Hovav, RC Mulligan, S. Amar, B. Suki, and DN Kotton. "Lentivirus-Based Expression of Human Alpha-1 Antitrypsin Ameliorates Emphysema in Mice." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3509.
Marcotte, Richard, Azin Sayad, Maliha Haider, Kevin Brown, Troy Ketela, Jason Moffat, and Benjamin G. Neel. "Abstract PR01: Functional characterization of breast cancer using pooled lentivirus shRNA screens." In Abstracts: AACR Precision Medicine Series: Synthetic Lethal Approaches to Cancer Vulnerabilities - May 17-20, 2013; Bellevue, WA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.pms-pr01.
Lindner, Daniel. Complementation of Myelodysplastic Syndrome Clones with Lentivirus Expression Libraries. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada566912.
Lindner, Daniel J. Complementation of Myelodysplastic Syndrome Clones with Lentivirus Expression Libraries. Fort Belvoir, VA: Defense Technical Information Center, January 2013. http://dx.doi.org/10.21236/ada581503.
Lindner, Daniel. Complementation of Myelodysplastic Syndrome Clones with Lentivirus Expression Libraries. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada581646.
DeMartini, James C., Abraham Yaniv, Jonathan O. Carlson, Arnona Gazit, Leonard E. Pearson, Kalman Perk, J. K. Young, Noam Safran, and A. Friedman. Evaluation of Naked Proviral DNA as a Vaccine for Ovine Lentivirus Infection. United States Department of Agriculture, September 1994. http://dx.doi.org/10.32747/1994.7570553.bard.
Ovine lentivirus (OvLV) infection is widespread in sheep of the United States and Israel and is responsible for substantial economic losses. The primary goal of this project was to evaluate naked proviral DNA as a vaccine to induce protective immunity in sheep in endemic areas. Contrary to expectations, inoculation of sheep with proviral DNA derived from the full length OvLV molecular clone pkv72 did not result in detectable OvLV infection, but infectious virus was recovered from transfected ovine cells. Kv72 virus produced by these cells infected sheep and induced antibody responses, and was used as a viral challenge in subsequent experiments. To improve in vivo transfection efficiency and compare the viral LTR with other romoters, expression of reporter genes was studied in sheep transfected in vivo by injection of cationic liposome-DNA complexes; one formulation produced gene expression in a sheep for 4 months following a single intravenous injection. Since the pol-deleted OvLV construct was not stable in vivo, twelve lambs were injected with plasmids containing the Kv72 gag region (pCMVgag) or env region (pCMVenv), or saline. Prior to challenge, no detectable anti-OvLV immune responses were detected. Following homologous challenge with OvLV. Although the naked DNA approach to vaccination holds promise for control of ovine lentivirus-induced disease, further work needs to be done to develop more effective methods of transfecting sheep with DNA.
