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Relevant bibliographies by topics / Herpesvirus 6 humain

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Academic literature on the topic 'Herpesvirus 6 humain'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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Journal articles on the topic "Herpesvirus 6 humain"

1

Gautheret-Dejean, Agnès. "Actualités sur la forme intégrée du génome du sixième herpesvirus humain au génome humain (iciHHV-6)." médecine/sciences 33, no. 8-9 (August 2017): 730–31. http://dx.doi.org/10.1051/medsci/20173308014.

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Bonnafous, P., S. Nguyen-Quoc, E. Frobert, N. Weiss, C. Henquell, A. Dewilde, C. Gaudy-Graffin, and A. Gautheret-Dejean. "Algorithme d’interprétation de la charge virale sanguine du sixième herpesvirus humain (HHV-6)." Médecine et Maladies Infectieuses 47, no. 4 (June 2017): S114. http://dx.doi.org/10.1016/j.medmal.2017.03.278.

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Yamanishi, Koichi. "New human herpesviruses; human herpesvirus 6 and 7." Clinical Biochemistry 28, no. 3 (June 1995): 348. http://dx.doi.org/10.1016/0009-9120(95)91425-3.

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Morris, DavidJ, Edward Littler, Debbie Jordan, JohnR Arrand, Martin Andre, and Bertfried Matz. "ANTIBODY RESPONSES TO HUMAN HERPESVIRUS 6 AND OTHER HERPESVIRUSES." Lancet 332, no. 8625 (December 1988): 1425–26. http://dx.doi.org/10.1016/s0140-6736(88)90618-6.

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Buchbinder, A., D. V. Ablashi, C. Saxinger, S. F. Josephs, S. Z. Salahuddin, R. C. Gallo, P. Biberfeld, and A. Linde. "HUMAN HERPESVIRUS-6 AND CROSS-REACTIVITY WITH OTHER HERPESVIRUSES." Lancet 333, no. 8631 (January 1989): 217. http://dx.doi.org/10.1016/s0140-6736(89)91228-2.

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Kaufer, Benedikt B., Keith W. Jarosinski, and Nikolaus Osterrieder. "Herpesvirus telomeric repeats facilitate genomic integration into host telomeres and mobilization of viral DNA during reactivation." Journal of Experimental Medicine 208, no. 3 (March 7, 2011): 605–15. http://dx.doi.org/10.1084/jem.20101402.

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Some herpesviruses, particularly lymphotropic viruses such as Marek’s disease virus (MDV) and human herpesvirus 6 (HHV-6), integrate their DNA into host chromosomes. MDV and HHV-6, among other herpesviruses, harbor telomeric repeats (TMRs) identical to host telomeres at either end of their linear genomes. Using MDV as a natural virus-host model, we show that herpesvirus TMRs facilitate viral genome integration into host telomeres and that integration is important for establishment of latency and lymphoma formation. Integration into host telomeres also aids in reactivation from the quiescent state of infection. Our results and the presence of TMRs in many herpesviruses suggest that integration mediated by viral TMRs is a conserved mechanism, which ensures faithful virus genome maintenance in host cells during cell division and allows efficient mobilization of dormant viral genomes. This finding is of particular importance as reactivation is critical for virus spread between susceptible individuals and is necessary for continued herpesvirus evolution and survival.

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Reynaud, Joséphine M., and Branka Horvat. "Human Herpesvirus 6 and Neuroinflammation." ISRN Virology 2013 (March 14, 2013): 1–11. http://dx.doi.org/10.5402/2013/834890.

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Human herpesvirus (HHV-) 6A and HHV-6B are two distinct β-herpesviruses which have been associated with various neurological diseases, including encephalitis, meningitis, epilepsy, and multiple sclerosis. Although the reactivation of both viruses is recognized as the cause of some neurological complications in conditions of immunosuppression, their involvement in neuroinflammatory diseases in immunocompetent people is still unclear, and the mechanisms involved have not been completely elucidated. Here, we review the available data providing evidence for the capacity of HHV-6A and -6B to infect the central nervous system and to induce proinflammatory responses by infected cells. We discuss the potential role of both viruses in neuroinflammatory pathologies and the mechanisms which could explain virus-induced neuropathogenesis.

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Lacoste, Vincent, Philippe Mauclere, Guy Dubreuil, John Lewis, Marie-Claude Georges-Courbot, Jacques Rigoulet, Thierry Petit, and Antoine Gessain. "Simian Homologues of Human Gamma-2 and Betaherpesviruses in Mandrill and Drill Monkeys." Journal of Virology 74, no. 24 (December 15, 2000): 11993–99. http://dx.doi.org/10.1128/jvi.74.24.11993-11999.2000.

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ABSTRACT Recent serological and molecular surveys of different primate species allowed the characterization of several Kaposi's sarcoma-associated herpesvirus (KSHV) homologues in macaques, African green monkeys, chimpanzees, and gorillas. Identification of these new primate rhadinoviruses revealed the existence of two distinct genogroups, called RV1 and RV2. Using a degenerate consensus primer PCR method for the herpesvirus DNA polymerase gene, the presence of KSHV homologues has been investigated in two semi-free-ranging colonies of eight drill (Mandrillus leucophaeus), five mandrill (Mandrillus sphinx), and two hybrid (Mandrillus leucophaeus-Mandrillus sphinx) monkeys, living in Cameroon and Gabon, Central Africa. This search revealed the existence of not only two distinct KSHV homologues, each one belonging to one of the two rhadinovirus genogroups, but also of two new betaherpesvirus sequences, one being close to cytomegaloviruses and the other being related to human herpesviruses 6 and 7 (HHV-6 and -7). The latter viruses are the first simian HHV-6 and -7 homologues identified to date. These data show that mandrill and drill monkeys are the hosts of at least four novel distinct herpesviruses. Moreover, mandrills, like macaques and African green monkeys, harbor also two distinct gamma-2 herpesviruses, thus strongly suggesting that a second gamma-2 herpesvirus, belonging to the RV2 genogroup, may exist in humans.

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Nazaryan, R. S., Yu V. Fomenko, N. A. Scheblykina, T. A. Kolesova, N. V. Golik, and E. V. Sukhostavets. "Herpesviruses. Part 1." Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 5, no. 6 (December 12, 2020): 299–307. http://dx.doi.org/10.26693/jmbs05.06.299.

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One of the urgent problems of modern medicine is the high incidence of herpesvirus infections. The high prevalence of herpesviruses in the human population of the world allow us to consider herpes a common systemic disease of the whole organism. Doctors of any specialty are faced with the clinical manifestations of herpes infection in patients, and they themselves are a risk group of chronic herpes infections formation due to constant patient contacts and frequent professional psycho-emotional overload. Herpes infections are a group of infectious diseases caused by human herpesviruses. Now it is known 8 species of herpesvirus causing various human diseases that occur in the acute (during the initial contact with the infection) or chronic form. The herpesvirus family has a number of common properties that distinguish them from other human pathogenic viruses. There are three subfamilies in the Herpesviridae family. Alpha herpesviruses (Аlphaherpesvirinae) include the two serotypes of the herpes simplex virus (HSV-1 and HSV-2), and the varicella-zoster virus (herpes zoster). Beta herpesviruses (Betaherpesvirinae) include cytomegalovirus, human herpes viruses of types 6 and 7 (HHV-5, HHV-6, HHV-7). Gamma herpes viruses (Gammaherpesvirinae) include the Epstein-Barr virus, human herpesvirus type 8 (HHV-4, HHV-8). Clinical manifestations of herpes infection depend more on the immunity state of the infected organism than on the pathogenic properties of the pathogen itself, and develop only in conditions of immunodeficiency caused by various unfavorable factors. Herpesviruses are able to damage organs, weaken the body's immunity, creating conditions for the attachment of the other infections (fungal, bacterial), which in turn can cause organ damage. The herpesvirus ability to infect all organs and tissues of the body determines a significant clinical polymorphism of diseases, as well as the necessity to study various biological liquids. Herpesviruses can be transmitted from person to person by aerosol, contact, sexual and parenteral transmission, as well as from mother to fetus or newborn, they also can act as mutagens. The pathogenesis of herpesvirus infections is rather complex and not completely understood. For a proper understanding of the disease pathogenesis it is necessary to know the main stages of reproduction of human herpesviruses. Modern laboratory techniques are used for diagnosis of herpes infection and allow obtaining more complete information for an accurate diagnosis: virological method, electron microscopy method, the method of biological sample, the polymerase chain reaction methods for the detection of viral antigens, serological, immunological, cytological and histological methods. Conclusion. The high prevalence of diseases caused by herpes viruses, the complex, not fully understood pathogenesis and high contagiousness of diseases, as well as a variety of clinical manifestations of herpesvirus infections with the possibility of the formation of mixed forms with a blurred clinical picture dictate the need for a detailed study of herpes viruses and knowledge of methods for diagnosing herpes infections

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Prichard, Mark N., John D. Williams, Gloria Komazin-Meredith, Atiyya R. Khan, Nathan B. Price, Geraldine M. Jefferson, Emma A. Harden, Caroll B. Hartline, Norton P. Peet, and Terry L. Bowlin. "Synthesis and Antiviral Activities of Methylenecyclopropane Analogs with 6-Alkoxy and 6-Alkylthio Substitutions That Exhibit Broad-Spectrum Antiviral Activity against Human Herpesviruses." Antimicrobial Agents and Chemotherapy 57, no. 8 (May 13, 2013): 3518–27. http://dx.doi.org/10.1128/aac.00429-13.

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ABSTRACTMethylenecyclopropane nucleosides have been reported to be active against many of the human herpesviruses. The most active compound of this class is cyclopropavir (CPV), which exhibits good antiviral activity against human cytomegalovirus (HCMV), Epstein-Barr virus, both variants of human herpesvirus 6, and human herpesvirus 8. CPV has two hydroxymethyl groups on the methylenecyclopropane ring, but analogs with a single hydroxymethyl group, such as the prototypical (S)-synguanol, are also active and exhibit a broader spectrum of antiviral activity that also includes hepatitis B virus and human immunodeficiency virus. Here, a large set of monohydroxymethyl compounds with ether and thioether substituents at the 6 position of the purine was synthesized and evaluated for antiviral activity against a range of human herpesviruses. Some of these analogs had a broader spectrum of antiviral activity than CPV, in that they also inhibited the replication of herpes simplex viruses 1 and 2 and varicella-zoster virus. Interestingly, the antiviral activity of these compounds appeared to be dependent on the activity of the HCMV UL97 kinase but was relatively unaffected by the absence of thymidine kinase activity in HSV. These data taken together indicate that the mechanism of action of these analogs is distinct from that of CPV. They also suggest that they might be useful as broad-spectrum antiherpesvirus agents and may be effective in the treatment of resistant virus infections.

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Dissertations / Theses on the topic "Herpesvirus 6 humain"

1

Robert, Catherine. "Approche du diagnostic des infections à herpesvirus humain-6 (HHV-6) par des techniques immunoenzymatiques." Paris 11, 1996. http://www.theses.fr/1996PA114837.

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Herbein, Georges. "L'infection à Herpesvirus humain type 6 (HHV-6) chez les transplantés : une étude rétrospective de 32 patients." Université Louis Pasteur (Strasbourg) (1971-2008), 1991. http://www.theses.fr/1991STR1M098.

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Manichanh, Chaysavanh. "Etude phénotypique et génotypique de la résistance du sixième herpesvirus humain (HHV-6) aux antiviraux." Paris 6, 2001. http://www.theses.fr/2001PA066458.

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André-Garnier, Élisabeth Imbert-Marcille Berthe Marie. "Cytomegalovirus et Herpesvirus Humain de type 6 étude de leur réplication au sein du système hématopoïétique /." [S.l.] : [s.n.], 2003. http://theses.univ-nantes.fr/thesemed/DOCandre.pdf.

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André-Garnier, Élisabeth. "Cytomegalovirus et Herpesvirus Humain de type 6 : étude de leur réplication au sein du système hématopoi͏̈étique." Nantes, 2003. http://archive.bu.univ-nantes.fr/pollux/show.action?id=f5645905-5676-4dcd-adbc-d9cc1c12ffc6.

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Le Cytomégalovirus humain (CMVH) et l'Herpèsvirus humain de type 6 (HHV6) sont deux ?- Herpesvirinae présentant un tropisme majeur pour le système hématopoi͏̈étique. Ce travail a visé à évaluer leurs capacités de réplication au cours de la différenciation hématopoi͏̈étique. Des outils méthodologiques autorisant la mise en évidence de la réplication virale ont été développés, permettant la détection de transcrits viraux tardifs par RT-PCR. Parmi les marqueurs développés pour le CMVH, l'ARNm tardif UL22, issu d'un épissage, a montré son intérêt, en particulier dans le cadre du diagnostic de l'infection active/maladie à CMVH. Pour l'HHV6, la détection du transcrit tardif multi-épissé de la gp 82-105 (U100) et la mise en évidence en cytométrie de flux d'antigènes nucléaires tardifs ont été développés à partir de cultures de souches virales de variant B. Ces essais ont permis de préciser que la forme épissée du gène U100 est exprimée en phase tardive du cycle de réplication, alors que la forme non épissée est un marqueur de la phase précoce. La possibilité de survenue d'une réplication des deux virus au cours de l'expansion ex vivo de 10 prélèvements de cellules souches hématopoi͏̈étiques CD34+ périphériques, a ensuite été envisagée. Ces essais ont été réalisés dans le cadre d'une nouvelle approche thérapeutique, qui vise à réduire la durée d'aplasie, chez des sujets traités par hautes doses de chimiothérapie, grâce à l'injection de cellules souches différenciées in vitro. Les cultures ont été menées en milieu liquide, en présence de cytokines permettant d'engager la différenciation vers les lignées myéloi͏̈des et monocytaires. Parmi les quatre cultures de cellules provenant de patients séropositifs pour le CMVH, aucun marqueur de réactivation virale n'a été détecté. A l'inverse, dans 5/10 cultures issues de prélèvements effectués chez les patients séropositifs pour l'HHV6, le transcrit U100 a été amplifié. Ces données montrent pour la première fois et sans avoir recours à une infection préalable par une souche virale, une réplication de l'HHV6 due à une réactivation au cours de la différenciation des progéniteurs hématopoi͏̈étiques. Ces résultats originaux soulèvent le problème de la sécurité virale lors des réinjections chez des patients immunodéprimés de cellules supportant une réplication de l'HHV6
Cytomegalovirus (CMV) and Human Herpesvirus 6 (HHV6) were two ? -Herpesvirus with a major tropism for hematopoietic system. Since their interactions with hematopoiesis are still poorly understood, we evaluated their replication capacity during differenciation of hematopoietic stem cells. We first developed and evaluated tools to follow viral replication, by detection of late viral transcripts, which assess occurrence of a complete replication cycle. Among the CMV transcripts amplified by reverse transcription-PCR, the late spliced UL22 mRNA was of particular interest, notably to predict the occurrence CMV disease during active infection. For HHV6, a one-step RT-PCR amplifying the late alternatively U100 gene encoding the gp 82-105 glycoprotein and a flow cytometry method to analyse nuclear late antigens were developed from reference strains cultures. Evaluation of these methods was then realized during a sequential culture of HST strain on MT4 cells. This allows to specify that the U100 gene splicing starts at a late stage of multiplication whereas unspliced forms were detectable earlier in the cycle. We then evaluated the occurrence of viral replication during ex vivo expansion of 10 peripheral hematopoietic stem cells (CD34+) samples. Cultures were maintained in a serum free liquid medium supplemented with cytokines of myeloid-monocyte lineage. Neither CMV DNA nor CMV UL22 or UL86 mRNA were detected among the 4 cultures from CMV seropositive patients. Conversely, the late alternatively spliced U100 mRNA (HHV6) was detected at day 14 or 21 in 5/10 cultures from HHV6 seropositive patients. Our data demonstrated for the first time that HHV6 could enter in a replicative cycle during hematopoietic differenciation in the absence of in vitro infection of cells. This also raised the question of the viral safety of the infusion of ex-vivo expanded CD34-positive PBPCs

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Gautheret-Dejean, Agnès. "Etude des interactions entre les sixieme et septieme herpesvirus humains (hhv-6, hhv-7) et le virus de l'immunodeficience humaine (hiv) chez l'homme." Paris 11, 1997. http://www.theses.fr/1997PA114842.

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Jaworska, Joanna. "Role for the immediate-early 1 protein of human herpesvirus 6 in innate immune evasion." Thesis, Université Laval, 2010. http://www.theses.ulaval.ca/2010/26876/26876.pdf.

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Poirel, Laurent. "Caracterisation genetique, epidemiologie et pouvoir pathogene des nouveaux herpesvirus lymphotropes (hhv-6, hhv-7, hhv-8) (doctorat : microbiologie)." Paris 11, 1999. http://www.theses.fr/1999PA114822.

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Sifer, Christophe. "Mise au point d'un système de RT-PCR pour la mise en évidence d'un ARN messager tardif du sixième herpesvirus humain." Paris 5, 1998. http://www.theses.fr/1998PA05P189.

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Reynaud, Joséphine. "Développement d'un modèle murin transgénique d'infection par l'herpèsvirus 6A et étude des mécanismes d'induction de la neuroinflammation." Phd thesis, Ecole normale supérieure de lyon - ENS LYON, 2013. http://tel.archives-ouvertes.fr/tel-00998378.

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L'herpèsvirus humain (HHV) 6 est un betaherpèsvirus largement répandu, associé à plusieurs maladies neuroinflammatoires, telles que des encéphalites ou la sclérose en plaques (SEP). Cependant, les mécanismes impliqués dans la neuropathologie induite par les deux espèces d'HHV-6, HHV-6A et HHV-B, sont peu connus. De plus, l'absence de modèle d'infection chez le petit animal a ralenti l'étude de la pathogénèse virale. Dans ce contexte, nous avons développé un modèle d'infection par HHV-6 chez des souris transgéniques, qui expriment la protéine CD46 humaine, identifiée comme récepteur cellulaire pour HHV-6. Nous avons pu démontrer une persistance de l'ADN viral d'HHV-6A, mais pas d'HHV-6B, dans le cerveau de souris transgéniques pendant plusieurs mois. De plus nos résultats montrent qu'HHV-6A induit la sécrétion de chimiokines pro-inflammatoires par les cellules neurales murines et provoque l'infiltration de cellules immunitaires dans le cerveau de souris infectées. Enfin, HHV-6A, mais pas HHV-6B, pourrait induire des réponses cellulaires chez les cellules murines via le récepteur de l'immunité innée TLR9 (toll-like receptor 9). En collaboration avec une équipe de Grenoble, nous avons ensuite montré que l'infection par HHV-6A induit l'expression de rétrovirus endogènes humains (HERV) dans des cellules mononuclées et des lignées neurales humaines. Ces HERV, en particulier leurs protéines d'enveloppe qui présentent des propriétés pro-inflammatoires, sont associés à diverses maladies autoimmunes dont la SEP. HHV-6A pourrait donc participer au développement de pathologies inflammatoires via l'induction de ces HERV. L'ensemble de ces travaux supporte ainsi l'existence d'un lien entre l'infection par HHV-6A et la neuroinflammation, et apporte de nouvelles pistes quant aux mécanismes potentiellement impliqués.

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Books on the topic "Herpesvirus 6 humain"

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The virus within: A coming epidemic. New York: Dutton, 2000.

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Regush, Nicholas M. The virus within: A coming epidemic. New York: Dutton, 2000.

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The virus within: A coming epidemic. London: Vision, 2001.

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The virus within: A coming epidemic. Toronto: Viking, 2000.

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F, Krueger G. R., and Ablashi D. V, eds. Human herpesvirus-6: General virology, epidemiology and clinical pathology. 2nd ed. Amsterdam: Elsevier, 2006.

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V, Ablashi D., Krueger G. R. F, and Salahuddin S. Zaki, eds. Human herpesvirus-6: Epidemiology, molecular biology, and clinical pathology. Amsterdam: Elsevier, 1992.

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Ablashi, D. V., and Gerhard R. F. Krueger. Human Herpesvirus-6: Epidemiology, Molecular Biology and Clinical Pathology (Perspectives in Medical Virology, Vol. 4). Elsevier Science Pub Co, 1992.

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(Editor), Gerhard Krueger, and D. V. Ablashi (Editor), eds. Human Herpesvirus-6, Volume 12, Second Edition: General Virology, Epidemiology and Clinical Pathology (Perspectives in Medical Virology). Elsevier Science, 2006.

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Human Herpesvirus-6, Epidemiology, molecular biology and clinical pathology. Elsevier, 1992. http://dx.doi.org/10.1016/s0168-7069(08)x7003-x.

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Human Herpesvirus-6, Second Edition - General Virology, Epidemiology and Clinical Pathology. Elsevier, 2006. http://dx.doi.org/10.1016/s0168-7069(06)x1200-4.

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Book chapters on the topic "Herpesvirus 6 humain"

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Caserta, Mary T., and Caroline Breese Hall. "Human Herpesviruses: Human Herpesvirus 6." In Viral Infections of Humans, 855–66. Boston, MA: Springer US, 2014. http://dx.doi.org/10.1007/978-1-4899-7448-8_37.

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Di Luca, Dario. "Human Herpesvirus 6." In Encyclopedia of Cancer, 1753–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2850.

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Prober, Charles G. "Human Herpesvirus 6." In Advances in Experimental Medicine and Biology, 87–90. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-7185-2_7.

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Di Luca, Dario. "Human Herpesvirus 6." In Encyclopedia of Cancer, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_2850-2.

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Di Luca, Dario. "Human Herpesvirus 6." In Encyclopedia of Cancer, 2142–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_2850.

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Levine, Paul H. "Human Herpesvirus-6 and Human Herpesvirus-7." In Viral Infections of Humans, 455–71. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-0036-4_15.

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Yamanishi, Koichi, and Yasuko Mori. "Human Herpesvirus 6 and Human Herpesvirus 7." In Clinical Virology, 511–22. Washington, DC, USA: ASM Press, 2016. http://dx.doi.org/10.1128/9781555819439.ch24.

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Wood, Charles, and Charles D. Mitchell. "Human Herpesvirus 8." In Congenital and Perinatal Infections, 111–21. Totowa, NJ: Humana Press, 2006. http://dx.doi.org/10.1385/1-59259-965-6:111.

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Cone, Richard. "Human Herpesvirus 6: An Update." In Medical Virology 10, 141–63. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3738-0_7.

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Razzaque, Abdur, Koichi Yamanishi, and Donald R. Carrigan. "Pathogenicity of Human Herpesvirus-6." In Pathogenicity of Human Herpesviruses due to Specific Pathogenicity Genes, 331–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-85004-2_20.

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Conference papers on the topic "Herpesvirus 6 humain"

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Reddy, K., R. Bascom, and S. B. Goldfarb. "An Unusual Case of Young Adult Interstitial Pneumonia with Human Herpesvirus 6." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1464.

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Raposo, Jéssica, Rafaela Pinto, Amanda Lopes, Ana Silva, Tânia Mendoza, Paulo Silva, and Vanessa Paula. "Investigation of active human herpesviruses 6 and 7 infection before and after renal transplantation." In IV International Symposium on Immunobiologicals & VII Seminário Anual Científico e Tecnológico. Instituto de Tecnologia em Imunobiológicos, 2019. http://dx.doi.org/10.35259/isi.sact.2019_32830.

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Henning, Jill D., Clareann H. Bunker, Patrick Shea, Robert E. Ferrell, Alan L. Patrick, and Frank J. Jenkins. "Abstract 5726: Association between human herpesvirus 8 infection, inflammation and a polymorphism in the IL-6 signaling receptor in increased prostate cancer risk among men of African descent." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5726.

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