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Artykuły w czasopismach na temat "Cytomegaloviruses – Molecular aspects"
Moulden, Jerome, Cathy Yea Won Sung, Ilija Brizic, Stipan Jonjic i William Britt. "Murine Models of Central Nervous System Disease following Congenital Human Cytomegalovirus Infections". Pathogens 10, nr 8 (21.08.2021): 1062. http://dx.doi.org/10.3390/pathogens10081062.
Pełny tekst źródłaPyzik, Michal, Eve-Marie Gendron-Pontbriand i Silvia M. Vidal. "The Impact of Ly49-NK Cell-Dependent Recognition of MCMV Infection on Innate and Adaptive Immune Responses". Journal of Biomedicine and Biotechnology 2011 (2011): 1–9. http://dx.doi.org/10.1155/2011/641702.
Pełny tekst źródłaTaher, Husam, Eisa Mahyari, Craig Kreklywich, Luke S. Uebelhoer, Matthew R. McArdle, Matilda J. Moström, Amruta Bhusari i in. "In vitro and in vivo characterization of a recombinant rhesus cytomegalovirus containing a complete genome". PLOS Pathogens 16, nr 11 (24.11.2020): e1008666. http://dx.doi.org/10.1371/journal.ppat.1008666.
Pełny tekst źródłaMach, M., T. Stamminger i G. Jahn. "Human Cytomegalovirus: Recent Aspects from Molecular Biology". Journal of General Virology 70, nr 12 (1.12.1989): 3117–46. http://dx.doi.org/10.1099/0022-1317-70-12-3117.
Pełny tekst źródłaVasilev, V. V., N. V. Rogozina i A. A. Grineva. "Molecular genetic and clinical aspects of socially relevant viruses underlying congenital diseases". Russian Journal of Infection and Immunity 11, nr 4 (20.09.2021): 635–48. http://dx.doi.org/10.15789/2220-7619-mga-1729.
Pełny tekst źródłaKoopmans, Marion. "Molecular aspects of human cytomegalovirus diseases. Frontiers of virology 2 Y". Virus Research 31, nr 2 (luty 1994): 275. http://dx.doi.org/10.1016/0168-1702(94)90010-8.
Pełny tekst źródłaGriffiths, P. D., i J. E. Grundy. "Molecular biology and immunology of cytomegalovirus". Biochemical Journal 241, nr 2 (15.01.1987): 313–24. http://dx.doi.org/10.1042/bj2410313.
Pełny tekst źródłaBoeckh, Michael, i Guy Boivin. "Quantitation of Cytomegalovirus: Methodologic Aspects and Clinical Applications". Clinical Microbiology Reviews 11, nr 3 (1.07.1998): 533–54. http://dx.doi.org/10.1128/cmr.11.3.533.
Pełny tekst źródłaYnga-Durand, Dekhtiarenko i Cicin-Sain. "Vaccine Vectors Harnessing the Power of Cytomegaloviruses". Vaccines 7, nr 4 (17.10.2019): 152. http://dx.doi.org/10.3390/vaccines7040152.
Pełny tekst źródłaTugizov, S. M., J. Y. Webster-Cyriaque, S. Syrianen, A. Chattopadyay, H. Sroussi, L. Zhang i A. Kaushal. "Mechanisms of Viral Infections Associated with HIV". Advances in Dental Research 23, nr 1 (25.03.2011): 130–36. http://dx.doi.org/10.1177/0022034511400076.
Pełny tekst źródłaRozprawy doktorskie na temat "Cytomegaloviruses – Molecular aspects"
Sumaria, Nital. "The relevance of specific molecular and cellular effectors during murine cytomegalovirus infection". University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0116.
Pełny tekst źródłaAndrews, Daniel Mark. "Effects of murine cytomegalovirus infection on dendritic cell functionality and natural killer cell responses". University of Western Australia. Centre for Ophthalmology and Visual Science, 2004. http://theses.library.uwa.edu.au/adt-WU2005.0003.
Pełny tekst źródłaKhong, Andrea. "Effect of murine cytomegalovirus infection on haematopoiesis and myeloid cell differentiation and function". University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0260.
Pełny tekst źródłaAlbuquerque, Dulcinéia Martins de. "Aspectos moleculares do citomegalovirus humano durante infecção ativa em pacientes submetidos ao transplante de medula ossea". [s.n.], 2006. http://repositorio.unicamp.br/jspui/handle/REPOSIP/311935.
Pełny tekst źródłaTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
Made available in DSpace on 2018-08-08T16:11:05Z (GMT). No. of bitstreams: 1 Albuquerque_DulcineiaMartinsde_D.pdf: 3473302 bytes, checksum: daa8d0ff76ca0850d748389f7bb2ea56 (MD5) Previous issue date: 2006
Resumo: O Citomegalovírus Humano (HCMV) continua sendo uma causa significante de morbidade em pacientes imunocomprometidos, especialmente em transplantados de medula óssea, e pode manifestar diversas complicações que incluem hepatite, doença gastrointestinal e pneumonia intersticial ou a denominada "Síndrome Viral por HCMV"caracterizada por febre, leucopenia e trombocitopenia. O HCMV pode também ter um efeito imuno-modulador, fazendo da infecção por esse vírus um fator de risco importante para o desenvolvimento de rejeição ao enxerto aguda e crônica e para co-infecção com outras herpesviroses. A detecção do genoma do HCMV pela PCR (Reação em Cadeia da Polimerase) é específica e sensível, e pode ser usada como uma poderosa ferramenta para o diagnóstico precoce da infecção causada por este vírus. Variações em regiões funcionalmente relevantes do genoma do HCMV têm sido utilizadas como marcadores genéticos em diversos estudos clínicos para diferenciar as linhagens do vírus e associá-las com a patogênese viral e com as manifestações clínicas no paciente. A glicoproteína B (gB) é a maior glicoproteína do envelope do HCMV e tem sido relacionada à entrada na célula hospedeira, transmissão célula-a-célula, e conseqüentemente à fusão das células infectadas. A amplificação do gene gB pela PCR combinada com análise de restrição por RFLP em regiões polimórficas deste gene são eficientes para a identificação dos genótipos do HCMV, tornando possível a distinção de pelo menos 4 padrões eletroforéticos. Por outro lado, a determinação da carga viral em pacientes imunologicamente afetados tem sido associada como marcador ou preditor do desenvolvimento de doença por HCMV órgão-específica. Sendo assim, a determinação da carga viral, especificamente nestes pacientes, é fundamental para a supervisão da terapia antiviral. Além disso, os valores da carga viral estão relacionados aos níveis de imunossupressão, à patogênese do HCMV e ao grupo de pacientes e/ou ao tipo de transplante e podem indicar o início da administração da terapia antiviral.O método de real-time PCR (RT-PCR) foi aplicado para a quantificação do genoma do HCMV em amostras clínicas e a detecção e posterior quantificação do DNA do HCMV em amostras de soro por esta técnica é capaz de distinguir entre pacientes com infecções sintomáticas daqueles com infecções inativas ou latente.Avanços têm sido feitos na prevenção da doença por HCMV após o transplante de medula óssea, inclusive a administração profilática, por períodos prolongados, de antivirais como o Acyclovir e o Ganciclovir e como conseqüência, pode originar linhagens resistentes relacionadas principalmente a dois genes virais: a fosfotransferase viral (UL97) e a DNA polimerase viral (UL54). Sabendo-se da importância da identificação das linhagens do HCMV em pacientes transplantados de medula óssea e da possível relação com a infecção e apresentação clínica; da relevância em determinar a carga viral como preditor de doença; e finalmente, da detecção de linhagens resistentes aos agentes antivirais disponíveis, este estudo avaliou, prospectivamente, pacientes transplantados de medula óssea em seguimento no Hemocentro/UNICAMP. Além disso, teve como principais objetivos: determinar a prevalência dos genótipos do HCMV e avaliar uma possível associação com a apresentação clínica nesses pacientes; determinar a carga viral para o monitoramento da terapia antiviral; e identificar e correlacionar mutações que conferem resistência ao Ganciclovir com carga viral e apresentação clínica. Foram incluídas na casuística, 169 amostras de DNA de sangue periférico e 187 amostras de DNA de soro de 22 pacientes transplantados de medula óssea. Dentre as 47 amostras de DNA de sangue periférico HCMV positivas, 42 foram genotipadas e observamos a prevalência do genótipo gB1 (47%) como descrito em literatura, e embora sem comprovação estatística, notamos a tendência deste genótipo com melhor prognóstico. Aplicamos a RT-PCR em 96 amostras de DNA de soro de 12 pacientes transplantados de medula óssea seguidos no Ambulatório de Hematologia, e observamos que o método é adequado para a avaliação da carga viral neste grupo de pacientes. No entanto, é necessário estabelecer um valor de corte a fim de se utilizar esta metodologia para obtenção de um valor que seja preditivo de doença e para o monitoramento do tratamento dos pacientes. Este método mostrou-se mais preciso que a ?nested?-PCR no mesmo tipo de amostra. Além disso, identificamos 8 novas mutações no gene UL97, uma delas pode estar relacionada à resistência viral ao Ganciclovir. Dentre os polimorfismos identificados, 3 parecem estar relacionados ao genótipo gB1 e possivelmente podem ser utilizadas como marcadores genéticos para a genotipagem do HCMV. Para o gene UL54 foram identificadas 5 novas mutações na região IV do gene e que geralmente é relacionada à resistência ao Ganciclovir. Nós concluímos que a determinação da carga viral é importante, mas não é o único modo de avaliar a eficiência do tratamento antiviral. Dessa forma, a avaliação de outros parâmetros moleculares, como a genotipagem e mutações relacionadas à resistência aos antivirais, são informações complementares e devem ser consideradas para o monitoramento da evolução clínica em pacientes transplantados de medula óssea
Abstract: Human Cytomegalovirus (HCMV) remains a significant cause of morbidity in immunocompromised patients, especially in bone marrow transplant recipients. It may manifest severe complications including hepatitis, gastrointestinal disease, and interstitial pneumonitis or as so-called ?HCMV viral syndrome? with fever, leukopenia, and thrombocytopenia. The HCMV may also has an immunomodulatory effect, potentially making HCMV infection an important risk factor for the development of an acute and chronic allograft rejection and for coinfection with other herpesviruses. The detection of the HCMV genome by PCR (Polymerase Chain Reaction) is specific and sensitive. Besides this, it can be used as a powerful tool for the early diagnoses of the infection caused by this virus. Variations in functionally relevant areas of the HCMV genome have been used as genetic markers in numerous clinical studies to differentiate the HCMV strains and to associate them with the viral pathogenesis further with the patients? clinical manifestations. The glycoprotein B (gB) is the major glycoprotein of HCMV?s envelope and it has been implicated in host cell entry, cell-to-cell virus transmission, consequently in the fusion of infected cells. The gB amplification by PCR combined with the restriction analysis by RFLP in polymorphic areas are effective for the identification of the HCMV genotypes, becoming possible the distinction of at least 4 electrophoretic patterns. On the other hand, the determination of the viral load in the immunologically affected patients has been associated as marker or predictor for the development of the organ specific disease by the HCMV. Hence, the determination of the viral load in these specific patients is fundamental for the management of the antiviral therapy. In addition, the viral load values are related to levels of the immune-suppression, the pathogenesis of the HCMV and the group of patients and/or the type of transplant. Furthermore, the viral load values can indicate the beginning of the antiviral therapy administration. A real-time PCR (RT-PCR) assay was applied for quantifying the HCMV genome load in clinical samples and the detection and quantification of HCMV DNA in blood serum through RT-PCR are able to distinguish patients with symptomatic infections among those with latent or inactive infections. Advances have been made in the prevention of HCMV disease after bone marrow transplantation, including prophylactic administration of antivirals such as Acyclovir and Ganciclovir. The HCMV prophylaxis with antiviral in this patients? group is administered for prolonged periods of therapy, consequently it can originate resistant viruses related mainly to two genes: the viral phosphotransferase (UL97) and the viral DNA polymerase (UL54). Ahead the importance of the identification of HCMV strains in bone marrow transplant patients, the HCMV strains performance in the patients? infection and clinical presentation, the relevance of determinating the viral load as a disease predictor, and finally, the detection of the resistant strains to the available antivirals, this study prospectively evaluated bone marrow transplant recipients followed at Hemocentro/UNICAMP. Moreover, it had as main goals: to determine the prevalence of the HCMV gB genotypes, to evaluate a possible gB genotype association with the patients? clinical presentation; to determinate the viral load for monitoring the antiviral therapy, and to correlate Ganciclovir resistant mutations in UL97 and UL54 gene with the viral load and patients? clinical presentation. From 22 bone marrow transplant recipients, DNA samples of peripheral blood (169) and DNA samples of blood serum (187) were included in this casuistic. Among 47 HCMV positive samples, 42 were genotyped. We observed the prevalence of gB1 genotype (47%), as described in the specific literature, however without statistical analysis, the raw data exhibited that gB1 genotype can be related to patients? better prognostics. From 12 followed bone marrow transplant recipients, we applied the RT-PCR in 96 DNA blood serum samples and we observed that the method was accurate for the viral load evaluation in this patients? group. However, it is necessary to establish a crucial cutoff to consider whether a specific value of viral load is a predictive value to cause HCMV disease and to monitor the patients? treatment. This method was more precise than the nested-PCR for blood serum samples. Additionally, we identified 8 new mutations in UL97 gene, one of them can be related to Ganciclovir HCMV resistance. Among all of identified polymorphisms, 3 of them can be related to gB1 genotype and may be used as genetic marker to HCMV genotyping. In the region IV of the UL54 gene, 5 new mutations were identified, and can possibly be related to Ganciclovir HCMV resistance. We concluded that the determination of the patients? viral load is crucial, even so it is not the only way to evaluate the antiviral treatment efficacy. Then, the evaluation of other molecular parameters as genotyping and mutations related to the HCMV antiviral resistance, are complementary information and must be considered to monitor the clinical evolution of bone marrow transplant recipients
Doutorado
Ciencias Basicas
Doutor em Clínica Médica
Książki na temat "Cytomegaloviruses – Molecular aspects"
Becker, Yechiel, Gholamreza Darai i Eng-Shang Huang, red. Molecular Aspects of Human Cytomegalovirus Diseases. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84850-6.
Pełny tekst źródła(Editor), Niels Lemmermann, red. Cytomegaloviruses: Molecular Biology And Immunology. Caister Academic Press, 2006.
Znajdź pełny tekst źródłaReddehase, Matthias J. Cytomegaloviruses: From Molecular Pathogenesis to Intervention. Caister Academic Press, 2013.
Znajdź pełny tekst źródłaYechiel, Becker, Darai Gholamreza i Huang E. -S, red. Molecular aspects of human cytomegalovirus diseases. Berlin: Springer-Verlag, 1993.
Znajdź pełny tekst źródłaBecker, Yechiel. Molecular Aspects of Human Cytomegalovirus Diseases. Springer, 2012.
Znajdź pełny tekst źródłaCzęści książek na temat "Cytomegaloviruses – Molecular aspects"
Gibson, Wade. "Molecular Biology of Human Cytomegalovirus". W Molecular Aspects of Human Cytomegalovirus Diseases, 303–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84850-6_16.
Pełny tekst źródłaMelnick, Joseph L., Ervin Adam i Michael E. DeBakey. "Human Cytomegalovirus and Atherogenesis". W Molecular Aspects of Human Cytomegalovirus Diseases, 80–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84850-6_4.
Pełny tekst źródłaHaskill, Stephen, Lindsay Dudding i Eng-Shang Huang. "Cytomegalovirus and Macrophage Interaction". W Molecular Aspects of Human Cytomegalovirus Diseases, 101–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84850-6_6.
Pełny tekst źródłaHamilton, John D. "Cytomegalovirus and Blood Transfusion". W Molecular Aspects of Human Cytomegalovirus Diseases, 150–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84850-6_9.
Pełny tekst źródłaHuang, Eng-Shang, i Timothy F. Kowalik. "The Pathogenicity of Human Cytomegalovirus: An Overview". W Molecular Aspects of Human Cytomegalovirus Diseases, 3–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84850-6_1.
Pełny tekst źródłaHo, M. "Cytomegalovirus Infection After Solid Organ Transplantation". W Molecular Aspects of Human Cytomegalovirus Diseases, 162–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84850-6_10.
Pełny tekst źródłaWinston, Drew J. "Cytomegalovirus Infection in Bone Marrow Transplantation". W Molecular Aspects of Human Cytomegalovirus Diseases, 183–204. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84850-6_11.
Pełny tekst źródłaSmyth, R. L., T. W. Higenbottam, J. P. Scott i J. Wallwork. "The Management of Cytomegalovirus Infection in Heart-Lung Transplant Recipients". W Molecular Aspects of Human Cytomegalovirus Diseases, 205–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84850-6_12.
Pełny tekst źródłaHuang, Eng-Shang, i Timothy F. Kowalik. "Diagnosis of Human Cytomegalovirus Infection: Laboratory Approaches". W Molecular Aspects of Human Cytomegalovirus Diseases, 225–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84850-6_13.
Pełny tekst źródłaSerody, Jonathan S., i Charles M. van der Horst. "The Control of Cytomegalovirus Infection: Chemotherapy". W Molecular Aspects of Human Cytomegalovirus Diseases, 256–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84850-6_14.
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