Relevant bibliographies by topics / Human endogenous retroviruse

Academic literature on the topic 'Human endogenous retroviruse'

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Published: 9 March 2023

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Journal articles on the topic "Human endogenous retroviruse"

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Oppelt, Peter, Reiner Strick, Pamela L. Strissel, Kilian Winzierl, Matthias W. Beckmann, and Stefan P. Renner. "Expression of the human endogenous retroviruse-W envelope gene syncytin in endometriosis lesions." Gynecological Endocrinology 25, no. 11 (October 23, 2009): 741–47. http://dx.doi.org/10.3109/09513590903184142.

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Mang, Rui, Jolanda Maas, Xianghong Chen, Jaap Goudsmit, and Antoinette C. van der Kuyl. "Identification of a novel type C porcine endogenous retrovirus: evidence that copy number of endogenous retroviruses increases during host inbreeding." Journal of General Virology 82, no. 8 (August 1, 2001): 1829–34. http://dx.doi.org/10.1099/0022-1317-82-8-1829.

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Different classes of porcine endogenous retroviruses (PERVs), which have the potential to infect humans during xenotransplantation, have been isolated from the pig genome. Because vertebrate genomes may contain numerous endogenous retrovirus sequences, the pig genome was examined for additional endogenous retroviruses, resulting in the isolation of a novel, complete endogenous retrovirus genome, designated PERV-E. The gag, pol and env genes of PERV-E are closely related to those of human endogenous retrovirus (HERV) 4-1, which belongs to the HERV-E family. Results of studies to determine the presence and copy number of PERVs demonstrated that PERV-E and PERV-A/B-like proviruses were present in all genomes tested, but that PERV-C was not found in two of the species examined, including wild boar. Multiple copies of PERVs could be found in each pig genome. Among all of the pig genomes tested, the wild boar genome had the lowest copy number of all PERVs, suggesting that the number of integrations of complete endogenous retroviruses is increased by inbreeding.
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Mangeney, Marianne, Nathalie de Parseval, Gilles Thomas, and Thierry Heidmann. "The full-length envelope of an HERV-H human endogenous retrovirus has immunosuppressive properties." Journal of General Virology 82, no. 10 (October 1, 2001): 2515–18. http://dx.doi.org/10.1099/0022-1317-82-10-2515.

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We have demonstrated previously that the envelope proteins of a murine retrovirus (Moloney murine leukaemia virus) and a simian retrovirus (Mason–Pfizer monkey virus) have immunosuppressive properties in vivo. This property was manifested by the ability of the proteins, when expressed by tumour cells normally rejected by engrafted mice, to allow the envelope-expressing cells to escape immune rejection and to proliferate. Here, it is shown that this property is not restricted to the envelope of infectious retroviruses, but is also shared by the envelope protein encoded by an endogenous retrovirus of humans belonging to the HERV-H family. These results emphasize the close relationship between endogenous and infectious retroviruses and might be important in relation to the process of tumour progression in humans.
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Lezhnyova, Vera R., Ekaterina V. Martynova, Timur I. Khaiboullin, Richard A. Urbanowicz, Svetlana F. Khaiboullina, and Albert A. Rizvanov. "The Relationship of the Mechanisms of the Pathogenesis of Multiple Sclerosis and the Expression of Endogenous Retroviruses." Biology 9, no. 12 (December 11, 2020): 464. http://dx.doi.org/10.3390/biology9120464.

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Two human endogenous retroviruses of the HERV-W family can act as cofactors triggering multiple sclerosis (MS): MS-associated retrovirus (MSRV) and ERVWE1. Endogenous retroviral elements are believed to have integrated in our ancestors’ DNA millions of years ago. Their involvement in the pathogenesis of various diseases, including neurodegenerative pathologies, has been demonstrated. Numerous studies have shown a correlation between the deterioration of patients’ health and increased expression of endogenous retroviruses. The exact causes and mechanisms of endogenous retroviruses activation remains unknown, which hampers development of therapeutics. In this review, we will summarize the main characteristics of human endogenous W retroviruses and describe the putative mechanisms of activation, including epigenetic mechanisms, humoral factors as well as the role of the exogenous viral infections.
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Salmons, Brian, James S. Lawson, and Walter H. Günzburg. "Recent developments linking retroviruses to human breast cancer: infectious agent, enemy within or both?" Journal of General Virology 95, no. 12 (December 1, 2014): 2589–93. http://dx.doi.org/10.1099/vir.0.070631-0.

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Evidence is accumulating that one or more beta-retrovirus is associated with human breast cancer. Retroviruses can exist as an infectious (exogenous) virus or as a part of the genetic information of cells due to germline integration (endogenous). An exogenous virus with a genome that is highly homologous to mouse mammary tumour virus is gaining acceptance as possibly being associated with human breast cancer, and recently furnished evidence is discussed in this article, as is the evidence for involvement of an endogenous human beta-retrovirus, HERV-K. Modes of interaction are also reviewed and linkages to the APOBEC3 family are suggested.
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Patience, Clive, Yasuhiro Takeuchi, Francois-Loic Cosset, and Robin A. Weiss. "Packaging of Endogenous Retroviral Sequences in Retroviral Vectors Produced by Murine and Human Packaging Cells." Journal of Virology 72, no. 4 (April 1, 1998): 2671–76. http://dx.doi.org/10.1128/jvi.72.4.2671-2676.1998.

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ABSTRACT Interaction of retrovirus vectors and endogenous retroviruses present in packaging cell lines and target cells may result in unwanted events, such as the formation of recombinant viruses and the mobilization of therapeutic vectors. Using sensitive reverse transcriptase PCR assays, we investigated human and murine gene therapy packaging cell lines for incorporation of endogenous retrovirus transcripts into murine leukemia virus (MLV) vector particles and, conversely, whether vector genomes are incorporated into human endogenous retrovirus (HERV) particles. VL30 endogenous retrovirus sequences were efficiently packaged in particles produced by the murine AM12 packaging system. For every seven MLV-derived β-galactosidase (β-Gal) vector genomes present in the particles, one copy of VL30 was also packaged. Although human FLY packaging cells expressed several classes of HERV transcripts (HERV-K, HuRT, type C, and RTVL-H), none was detectable in the MLV vector particles released from the cells. Nonspecific packaging of the MLV Gag-Pol expression vector transcripts was detected in the FLY virions at a low level (1 in 17,000 sequences). These findings indicate that human packaging cells produce retrovirus particles far less contaminated by endogenous viral sequences than murine packaging cells. Human teratocarcinoma cells (GH cells), which produce HERV-K particles, were transduced with an MLV-derived β-Gal vector. Although both HERV-K and RTVL-H sequences were found in association with the particles, β-Gal transcripts were not detected, indicating that HERV Gag proteins do not efficiently package MLV-based vectors.
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Burmeister, Thomas, Stefan Schwartz, and Eckhard Thiel. "A PCR primer system for detecting oncoretroviruses based on conserved DNA sequence motifs of animal retroviruses and its application to human leukaemias and lymphomas." Journal of General Virology 82, no. 9 (September 1, 2001): 2205–13. http://dx.doi.org/10.1099/0022-1317-82-9-2205.

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Many C- and D-type retroviruses are known to cause a broad spectrum of malignant diseases in animals. Certain genome regions of these animal retroviruses are highly conserved between different animal species. It should be possible to detect new members of the retrovirus family with consensus PCR primers derived from these conserved sequence motifs. The consensus PCR primers developed in this study are generic enough to detect nearly all known oncogenic mammalian and avian exogenous C- and D-type retroviruses but do not amplify human endogenous retroviral sequences. In contrast to previous investigations, the present study involved highly stringent PCR conditions and truly generic PCR primers. Forty-four samples from patients with various immunophenotyped malignant diseases (acute and chronic T-/B-cell lymphocytic leukaemias, acute myeloid leukaemias, T-/B-cell lymphomas, chronic myeloproliferative disorders) and three cell lines (Hodgkin’s lymphoma, Burkitt’s lymphoma) have thus far been investigated using these PCR primers. The fact that no retroviruses have been found argues against an involvement of known animal oncoretroviruses or related hitherto undetected human retroviruses in the aetiopathogenesis of these diseases. The retrovirus detection system developed here may be used to confirm suspected retroviral involvement in other (malignant or nonmalignant) human diseases as well as to identify new animal retroviruses.
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Miller, A. Dusty, Ulla Bergholz, Marion Ziegler, and Carol Stocking. "Identification of the Myelin Protein Plasmolipin as the Cell Entry Receptor for Mus caroli Endogenous Retrovirus." Journal of Virology 82, no. 14 (May 7, 2008): 6862–68. http://dx.doi.org/10.1128/jvi.00397-08.

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ABSTRACT The Asian wild mouse species Mus caroli harbors an endogenous retrovirus (McERV) that is closely related to but distinct from the endogenous retrovirus family defined by the Mus dunni endogenous virus and the Mus musculus endogenous retrovirus. McERV could infect some cell types from humans, dogs, and rats, but not all, and did not infect any mouse cell line tested. Because of its interesting host range and proposed ancestral relationship to primate retroviruses and because none of the entry receptors for this family of retroviruses had been identified, we began a search for the McERV receptor. We determined the chromosomal location of the receptor gene in the human genome by phenotypic screening of the G3 human-hamster radiation hybrid cell line panel and confirmed the localization by assaying for receptor activity conferred by bacterial artificial chromosome (BAC) clones spanning the region. We next localized the gene more precisely in one positive BAC by assaying for receptor activity following BAC digestion with several restriction enzymes that cleaved different sets of genes, and we confirmed that the final candidate gene, plasmolipin (PLLP; TM4SF11), is the novel receptor by showing that the expression of the human PLLP cDNA renders hamster and mouse cells susceptible to McERV infection. PLLP functions as a voltage-dependent potassium ion channel and is expressed primarily in kidney and brain, helping to explain the limited range of cell types that McERV can infect. Interestingly, mouse PLLP also functioned well as a receptor for McERV but was simply not expressed in the mouse cell types that we originally tested.
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Çakmak Güner, Buket, and Nermin Gözükırmızı. "Human Endogenous Retroviruses." International Journal of Innovative Approaches in Science Research 2, no. 1 (March 29, 2018): 1–8. http://dx.doi.org/10.29329/ijiasr.2018.132.1.

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Michalski, F. "Human endogenous retroviruses." Clinical Microbiology Reviews 9, no. 4 (October 1996): 585. http://dx.doi.org/10.1128/cmr.9.4.585.

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Dissertations / Theses on the topic "Human endogenous retroviruse"

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DOLCI, MARIA. "UNRAVELING THE ROLE OF THE HUMAN ENDOGENOUS RETROVIRUSES IN THE PATHOGENESIS OF COLON CANCER." Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/703397.

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Background: Human endogenous retroviruses (HERV) are remnants of exogenous retroviral infections, representing 8% of the human genome. Their regulation is based on the DNA methylation of promoters, the long terminal repeats (LTRs). Transcripts from HERV have been associated with cancers, but reports concerning HERV expression in colorectal cancer remain sporadic. Methods: 63 Italian patients and 58 Tunisian patients with advanced stages of colorectal cancer were enrolled in this study. HERV-H, -K, -R, -P LTRs, and Alu, LINE-1 methylation levels, and the expressions of HERV env and pol gene were investigated by pyrosequencing and by RT qPCR, respectively, in the tumor, normal adjacent tissues, and, when possible, in the blood and plasmatic extracellular vesicles (EVs). Associations among clinical characteristics and HERV expression and methylation levels were also evaluated. The expression of the HERV-K Pol/Env proteins was also evaluated by Western Blot. Results: As for the Italians patients, Alu, LINE-1, HERV-H and -K LTRs were demethylated in the tumor tissues compared to the normal adjacent tissues (p<0.05), while no differences were observed in HERV env gene expression levels, among the clinical specimens. The env gene was expressed in the EVs (p<0.01) of 54% (-H), 38% (-K), 31% (-R) patients. Associations were found between HERV expression and right tumor colon location and between HERV methylation and vascular invasion (p<0.05). HERV K Pol protein was more expressed (p<0.01) in the adjacent normal tissues compared to the tumor tissues. The Env protein was only expressed in the tumor tissue. As for the Tunisian population, LINE-1 was less methylated in the tumor tissue compared to the adjacent normal tissue (p<0.05), while Alu, HERV-K and -H LTRs showed the same trends, but the difference was not significant. The expression of the HERV env and pol genes were similar in the biological samples. No association was found between the HERV expression/methylation and the clinical characteristics of the Tunisian patients. Conclusions: The changes in DNA methylation of retroelements are specific in colorectal cancer but do not correlate with viral overexpression. The Pol protein expression in the normal cells may induce the retrotrascription and the subsequent transfer of HERV sequences into other cells, possibly through EVs. HERV genome insertion might cause cells transformation. In the cancer cells, the Env protein may contribute to the cancer progression through cell to cell fusion.
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Katzourakis, Aris. "The evolution of human endogenous retroviruses." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497642.

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Muir, Alison. "Placental expression of human endogenous retroviruses." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.616115.

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Akleh, Rana Elias. "Developing a Single-Cycle Infectious System to Study an ERV-K Retroviral Envelope." Thesis, Boston College, 2017. http://hdl.handle.net/2345/bc-ir:107695.

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Thesis advisor: Welkin Johnson
Endogenous Retroviruses (ERVs) are “fossilized” retroviruses of a once exogenous retrovirus located in the genome of extant vertebrates. Retroviral infection results in a provirus integration into the host genome. An infection of a germline cell could lead to the provirus potentially being inherited by the offspring of the infected individual. Once in the genome, the provirus becomes subject to evolutionary processes and can become either lost or fixed in a population, remaining as “fossils” long after the exogenous retrovirus has gone extinct23. Notably, 8% of the human genome consists of ERVs30. Human Endogenous Retrovirus Type K (HERV-K)(HML-2) family is of particular interest. HERV-K integrations are as old as 30-35 million years, endogenizing before the separation of humans and Old World Monkeys. However, there are human specific insertions, some as young as 150,000 – 250,000 years, making them the youngest insertion in the human genome. There are over 90 insertions in the human genome; the bulk is shared by all humans44,47. Transcripts of HERV-K genes are upregulated in multiple cancer and tumor cell lines 14,39,46, as well as in HIV-1 infected patients 7,11,29. Just as there are human specific insertions of ERV-K, there are also Old World Monkey specific insertions44. I have identified an intact endogenous retroviral envelope open reading frame on chromosome 12 of the rhesus macaque genome. This viral envelope-encoding sequence, which I refer to as rhERV-K env, retains all the canonical features of a retroviral Env protein. An alignment between rhERV-K env and a consensus sequence of HERV-K, HERV-Kcon env, shows a 70% amino acid sequence identity. For experimental purposes, reconstructed HERV-K envelopes have been incorporated into virions of Human Immunodeficiency virus (HIV-1)19,26,49, Murine Leukemia Virus (MLV)12, and Vesicular stomatitis Virus (VSV)26,41,49. While these approaches have illuminated some aspects of HERV-K Env-mediated entry, to date a cell-surface receptor has not been identified for any ERV-K Env. This could be due to its low infectivity levels12,26,49, its seemingly broad cell tropism limiting identification of null cell lines26,49, or possibly the HERV-K consensus reconstructions are not an accurate representation of the progenitor HERV-K virus. I am interested in understanding how the ERV-K retrovirus accessed the human germline (some 150,000 – 250,000 years ago). To do this, I focused specifically on the envelope proteins of HERV-K and rhERV-K, with the goal of analyzing the ERV-K entry process. The identification and inclusion of rhERV-K Env in this study is meant to circumvent the possibility that the previously described consensus reconstructions of human HERV-K Env are not representative, and may also provide a means to compare the endogenization process in the human/ape and old-world monkey lineages. I focused on developing two systems for single-cycle infection, one based on Mason-Pfizer Monkey Virus (MPMV) (which has not been done before), and a second based on MLV, which has previously been reported on. MPMV, like HERV-K, is a betaretrovirus, and I reasoned that possibly using a betaretrovirus would overcome some of the low-infectivity issues associated with prior attempts using HIV and MLV. To develop a system for examining function of the ERV-K Env proteins, I addressed 3 issues: 1. Are the HERV-K Env and rhERV-K Env proteins expressed and properly processed? 2. Can they be incorporated into virions of a heterologous virus? 3. Are ERV-K pseudotyped virions infectious? I have answered these questions in the following thesis
Thesis (MS) — Boston College, 2017
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Biology
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Singh, Manvendra [Verfasser]. "Human endogenous retroviruses aid embryonic development / Manvendra Singh." Berlin : Freie Universität Berlin, 2019. http://d-nb.info/1181097703/34.

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Forrest, Graham Robert. "Human endogenous retrovirus 3 : evolutionary conservation and function." Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312093.

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Hu, Lijuan. "Endogenous Retroviral RNA Expression in Humans." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Universitetsbiblioteket [distributör], 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8213.

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Kowalski, Paul Edward. "Novel genetic effects of a human endogenous retrovirus insertion." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ34571.pdf.

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Singh, Sarita. "Human endogenous retrovirus K gene expression in cutaneous melanoma." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/10118.

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Introduction: In recent years, the key environmental and genomic changes that "drive" melanoma have become more clearly elucidated but much remains to be understood. Data published in 2003 demonstrated expression of Human Endogenous Retrovirus K (HERV-K) in melanomas but not in normal tissues, indicating a potential oncogenic role. Furthermore, HERV-K proviruses encode the putative oncogenic proteins Rec and Np9. In this work the feasibility of reliable detection of HERV-K expression from formalin-fixed paraffin-embedded (FFPE) tissue has been determined. Expression has been correlated with melanoma subtype and histological markers of poor outcome. Methods: HERV-K mRNA expression in melanoma cell lines (A375 and WM2664), FFPE primary melanoma (n=39), normal skin (n=31) and benign naevus (n=16) tissues was investigated by a novel real-time quantitative RT-PCR (qRT-PCR). Expressed HERVK env sequences were cloned and sequenced. Results: A375 cells expressed all HERV-K genes and produced putative viral particles. Full-length mRNA was expressed in all primary melanoma and control tissues investigated with no differences in expression levels between the groups (pol: n=47, p=0.267; unspliced env: n=40, p=0.823). No correlation was observed with melanoma subtype or stage (Breslow). A proportion of all tissue types expressed np9 with no differences in expression levels between them (p=0.964). Spliced env was expressed in 8/39 melanoma, compared with 1/16 benign naevus and 0/31 normal skin samples (p=0.003). Expression of rec was found in 9/39 melanomas but not in control samples (p=0.009) nor extra-lesional skin in five rec-positive cases (p=0.06). The rec-positive melanomas were histologically in vertical growth phase and thicker than rec-negative tumours (median Breslow 2.1mm versus 1.05mm, p=0.009). Sequencing of expressed env cDNA clones derived from melanoma and control samples (n=8) revealed expression of multiple HERV-K loci. Conclusions: Gene expression can be studied in FFPE tissue. The expression of potentially oncogenic rec in approximately 25% primary melanomas merits further evaluation.
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Al-Shamarti, Ibtihal I. A. "Epigenetic dynamics of Human Endogenous Retroviruses (HERVs) in human cancer cell lines." Thesis, University of Leicester, 2018. http://hdl.handle.net/2381/42767.

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Transposable elements (TEs) are endogenous components of eukaryotic genomes, constituting 45% of human DNA. The human genome project revealed that human endogenous retroviruses (HERVs) constitute about 8% of the sequence. HERVs are derived from sequences integrated into germ cells during retrovirus infections, up to 25 million years ago. However, most copies of HERVs are defective in multiple ways. The HERV-K family is the youngest family and likely has significant biological activity because of its protein coding capacity. HERV-K activity may be involved in a variety of cancers, and in particular may play an important role in human melanoma. In this project, HERV activity in melanoma and different cancer cell lines was investigated. Our results showed the HERV-K pol gene is expressed in melanoma and in breast, prostate and colon cancers. Furthermore, the response to serum starvation conditions is not simply related to increased expression of HERV-K genes, and changes in cellular phenotype under serum starvation are limited to particular melanoma cell lines, rather than being a general phenomenon. HERV-K env protein expression in melanoma cells was compared to normal primary melanocytes - 1% FBS serum starvation can increase expression of this protein in SKMel5 cells that retain an adherent phenotype. Moreover, env protein expression is significantly increased in T47D breast cancer cells under 1% FBS. The analysis of HERV-K LTR methylation state demonstrated that HERV K env and gag proteins in melanoma cells under 10% FBS and 1% FBS conditions decreased. The most interesting finding was the detection of 98 candidate loci as novel proviral insertions where previously these loci were annotated as solo LTRs. This result suggests that proviruses are systematically excluded from assemblies and the census of HERV-K proviruses is much greater than represented in assembled genomes. The Genome-wide amplification of proviral sequences combined with Next Generation Sequences (GAPS –NGS) is established as an effective approach to discover new proviral loci.
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Books on the topic "Human endogenous retroviruse"

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Yoshiki, Takashi. Molecular pathology of human retroviruses, HTLV-I and endogenous retroviruses. Sapporo, Japan: Hokkaido University Graduate School of Medicine, 2004.

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Svensson, Ann-Cathrin. Molecular analyses of human endogenous retrovirus ERV9: Marker for HLA-DR haplotype evolution. Uppsala: Sveriges Lantbruksuniversitet, 1996.

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Andersson, Ann-Catrin. Studies on Human Endogenous Retroviruses (Hervs) With Special Focus on Erv3. Uppsala Universitet, 2002.

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Sverdlov, Eugene D. Retroviruses and Primate Genome Evolution. Taylor & Francis Group, 2005.

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Sverdlov, Eugene D. Retroviruses and Primate Genome Evolution. Taylor & Francis Group, 2005.

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Sverdlov, Eugene D. Retroviruses and Primate Genome Evolution. Landes Bioscience, 2005.

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Book chapters on the topic "Human endogenous retroviruse"

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Wilkinson, David A., Dixie L. Mager, and Jo-Ann C. Leong. "Endogenous Human Retroviruses." In The Retroviridae, 465–535. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4899-1730-0_9.

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Brack-Werner, R., C. Leib-Mösch, T. Werner, V. Erfle, and R. Hehlmann. "Human Endogenous Retrovirus-like Sequences." In Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, 464–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74621-5_81.

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Schomburg, Dietmar, and Ida Schomburg. "human endogenous retrovirus K endopeptidase 3.4.23.50." In Class 3.4–6 Hydrolases, Lyases, Isomerases, Ligases, 127–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-36260-6_6.

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Nexø, B. A. "The Biology of Endogenous Leukemia Viruses: A Study of the DBA/2 Mouse." In International Symposium: Retroviruses and Human Pathology, 63–76. Totowa, NJ: Humana Press, 1985. http://dx.doi.org/10.1007/978-1-4612-5008-1_5.

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Toudic, Caroline, Xavier Elisseeff, Adjimon Gatien Lokossou, and Benoit Barbeau. "Roles of Endogenous Retrovirus-Encoded Syncytins in Human Placentation." In Human Retrotransposons in Health and Disease, 215–38. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-48344-3_9.

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Strick, Reiner, Matthias W. Beckmann, and Pamela L. Strissel. "Cell–Cell Fusions and Human Endogenous Retroviruses in Cancer." In Cell Fusions, 395–426. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9772-9_17.

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Garazha, Andrew, Maria Suntsova, and Anton Buzdin. "Structural and Functional Coevolution of Human Endogenous Retroviruses with Our Genome." In Genetics, Evolution and Radiation, 479–85. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-48838-7_38.

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Ay, Eva, Ferenc Banati, Katalin Turi-Balog, and Janos Minarovits. "The Role of Endogenous Retroviruses in the Formation of Syncytiotrophoblast and Materno-Fetal Barrier." In Maternal Fetal Transmission of Human Viruses and their Influence on Tumorigenesis, 83–104. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4216-1_3.

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Perron, Hervé, and Marion Leboyer. "Human Endogenous Retrovirus as Missing Link in the Global Etiopathogenesis of Schizophrenia and Bipolar Disorder." In Immuno-Psychiatry, 159–68. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-71229-7_9.

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Kleiman, A., N. Senyuta, A. Trjakin, T. Vinogradova, A. Karseladze, V. Gurtsrvitch, and S. Tjulandin. "Expression of Human Endogenous Retroviruses HERV-K/HTDV in Germ Cell Tumours: Possible Biological Role and Clinical Application." In Germ Cell Tumours V, 43–44. London: Springer London, 2002. http://dx.doi.org/10.1007/978-1-4471-3281-3_7.

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Conference papers on the topic "Human endogenous retroviruse"

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Jones, Peter A. "Abstract IA14: Targeting human endogenous retroviruses for epigenetic therapy." In Abstracts: AACR International Conference: New Frontiers in Cancer Research; January 18-22, 2017; Cape Town, South Africa. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.newfront17-ia14.

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Giménez, Karen, and Elisa Oltra. "Human endogenous retrovirus and clinical treatments of neurological disease." In 6th International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/ecmc2020-07296.

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Pollock, Remy, Rohan Machhar, Laila Zaman, Dafna D. Gladman, and Vinod Chandran. "FRI0356 DIFFERENTIAL EXPRESSION OF HUMAN ENDOGENOUS RETROVIRUSES IN PSORIATIC DISEASE." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.6288.

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Engel, K., A. Krüger, V. Vandrey, J. Schneider, I. Volkmer, A. Emmer, and M. S. Staege. "Expression of human endogenous retroviruses and associated transcripts in Hodgkin lymphoma cells." In ISCAYAHL 2020. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1701848.

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Cutts, Zachary, Sarah Patterson, Lenka Maliskova, Chun Jimmie Ye, Maria Dall’Era, Jinoos Yazdany, Lindsey A. Criswell, Chaz Langelier, Marina Sirota, and Cristina Lanata. "606 Cell-specific human endogenous retrovirus expression, host gene expression and SLE phenotypes." In LUPUS 21ST CENTURY 2022 CONFERENCE, Abstracts of Sixth Scientific Meeting of North American and European Lupus Community, Tucson, AZ, USA – September 20–23, 2022. Lupus Foundation of America, 2022. http://dx.doi.org/10.1136/lupus-2022-lupus21century.27.

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Chung, Woo-Keun, Hyong-Jun Kim, and Hwan-Gue Cho. "A web-based comparative visualization system for human endogenous RetroVirus(HERV) on whole genomes." In Proceeding of the third international workshop. New York, New York, USA: ACM Press, 2009. http://dx.doi.org/10.1145/1651318.1651333.

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Bermejo, AV, J. Daradoumis, P. Azcoaga, E. Ragonnaud, L. Neukrich, KN Nielsen, AC Andersoon, et al. "P03.05 Vaccine immunotherapy against human endogenous retrovirus: a focus on anti-herv-k antibodies." In iTOC9 – 9th Immunotherapy of Cancer Conference, September 22–24, 2022 – Munich, Germany. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-itoc9.33.

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Yuan, Zihao, Ningyan Zhang, Zhiqiang An, and Wenjin Zheng. "Abstract B37: Analysis of the differential expression of human endogenous retrovirus in glioblastoma multiforme." In Abstracts: AACR Special Conference on the Microbiome, Viruses, and Cancer; February 21-24, 2020; Orlando, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.mvc2020-b37.

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Saini, Sunil Kumar, Anne-Mette Bjerregaard, Andreas D. Ørskov, Ashwin Unnikrishnan, Staffan Holmberg, Govardhan Anande, Amalie Kai Bentzen, et al. "Abstract B129: Human endogenous retroviruses as a potential reservoir for T-cell mediated cancer immunotherapy." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-b129.

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Ohtani, Hitoshi, Minmin Liu, Wanding Zhou, Gangning Liang, and Peter A. Jones. "Abstract 2993: A switch in epigenetic silencing mechanisms of endogenous retroviruses during human genome evolution." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2993.

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Reports on the topic "Human endogenous retroviruse"

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Garry, Robert F. Involvement of a Human Endogenous Retrovirus in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada396835.

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Garry, Robert F. Involvement of a Human Endogenous Retrovirus in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada409400.

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