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Journal articles on the topic "Herpes virus 8"

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Landy, Helain J., and John H. Grossman. "Herpes Simplex Virus." Obstetrics and Gynecology Clinics of North America 16, no. 3 (September 1989): 495–515. http://dx.doi.org/10.1016/s0889-8545(21)00405-8.

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Meignin, Véronique, and Lionel Galicier. "Hémopathies lymphoïdes et HHV-8 (human herpes virus 8)." Annales de Pathologie 29, no. 5 (October 2009): 376–82. http://dx.doi.org/10.1016/j.annpat.2009.09.006.

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Porter, S. R., L. Di Alberti, and N. Kumar. "Human herpes virus 8 (Kaposi’s sarcoma herpesvirus)." Oral Oncology 34, no. 1 (January 1998): 5–14. http://dx.doi.org/10.1016/s1368-8375(97)00038-9.

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Rodríguez Arrieta, Luis Antonio, Gener Mahaht Rada, Luis Antonio Salazar, and Rita Magola Sierra. "Sarcoma de Kaposi y enfermedad de Castleman multicéntrica VHH-8 positivo - VIH Negativo." Acta Médica Colombiana 43, no. 1S (May 20, 2019): 30–32. http://dx.doi.org/10.36104/amc.2018.1357.

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El sarcoma de Kaposi y la enfermedad de Castleman multicéntrica/virus herpes humano-8 positivo/virus de la inmunodeficiencia humana negativo representan un subgrupo etiológico dentro del espectro clínico de las enfermedades asociadas al virus herpes humano-8 positivo, inicialmente fueron consideradas dos entidades aisladas. El virus tiene un papel protagónico por su tropismo por el tejido linfoide y su potencial oncogénico. La presencia de sarcoma de Kaposi y enfermedad de Castleman multicéntrica/virus herpes humano-8 (VHH-8) positivo/virus de la inmunodeficiencia humana (VIH) negativo sugiere la posibilidad de una deficiencia inmunológica subyacente. Se presenta un caso de una mujer de 67 años de edad con dermatosis en extremidades de curso indolente y aparición posterior de múltiples adenomegalias, esplenomegalia además síntomas sistémicos. Se destaca el abordaje diagnóstico, la coexistencia de dos enfermedades etiológicamente ligadas al virus herpes humano-8, sin asociación de inmunosupresión
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Cathomas, G. "Human herpes virus 8: a new virus discloses its face." Virchows Archiv 436, no. 3 (March 10, 2000): 195–206. http://dx.doi.org/10.1007/s004280050031.

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Díaz-García, Juan Daniel, Juan Pablo Venzor-Castellanos, Karen Hopf-Estandia, and Eunice Rojas-Zaldívar. "PLasmablastic lymphoma with coinfection by Epstein Barr Virus and Herpes Human Virus 8: a case report." ACTUALIDAD MEDICA 104, no. 808 (December 31, 2019): 188–90. http://dx.doi.org/10.15568/am.2019.808.cc03.

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Marlina, Erni, Ali Yusran, and Zohra Nazaruddin. "Diagnosis dan tatalaksana nyeri pada rongga mulut yang disebabkan oleh infeksi virus herpes Diagnosis and management of pain in oral cavity caused by herpes virus infection." Journal of Dentomaxillofacial Science 11, no. 1 (February 28, 2012): 33. http://dx.doi.org/10.15562/jdmfs.v11i1.291.

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There are 80 types of known herpes virus, 8 of them can cause infection on humans. They are herpes simplex virus(HSV) 1 and 2, varicella zoster virus (VZV), cytomegalovirus, Epstein-Barr virus, human herpes virus (HHV6) Aand B, and paramyxovirus. HSV1, HSV2, and VZV are the virus known to cause oral mucosal diseases. This paperaims to review and discuss orofacial pain caused by herpes virus infection. Detail anamnesis about prodromal signand symptom with clinical features that vesicles, labial and intraoral lesions, and unilateral distribution of lesionsare characterized oral herpes virus infections. It can be concluded that detailed anamnesis and an understandingabout oral clinical sign and symptom may confirm diagnosis of herpes virus infections.
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Ariza-Heredia, Ella J., and Raymund R. Razonable. "Human Herpes Virus 8 in Solid Organ Transplantation." Transplantation 92, no. 8 (October 2011): 837–44. http://dx.doi.org/10.1097/tp.0b013e31823104ec.

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Bernit, Emmanuelle, Véronique Veit, Christine Zandotti, Julie Gachon, Nicolas Schleinitz, and Jean Robert Harlé. "Chronic Lymphadenopathies and Human Herpes Virus Type 8." Scandinavian Journal of Infectious Diseases 34, no. 8 (January 2002): 625–26. http://dx.doi.org/10.1080/00365540210147552.

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Leao, Jair Carneiro, Andreza Barkokebas Santos de Faria, Déborah Daniela Diniz Fonseca, Luiz Alcino Monteiro Gueiros, Igor Henrique Morais Silva, and Stephen R. Porter. "Intrahost genetic variability of human herpes virus-8." Journal of Medical Virology 85, no. 4 (February 15, 2013): 636–45. http://dx.doi.org/10.1002/jmv.23491.

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Dissertations / Theses on the topic "Herpes virus 8"

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O'Leary, John James. "Molecular analysis of Kaposi's sarcoma associated herpes virus (KSHV) in immunocompromised patients." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360468.

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Couty, Jean-Pierre. "Aspects moléculaires de l'infection par l'herpèsvirus humain de type 8 (hhv-8/kshv)." Limoges, 1999. http://www.theses.fr/1999LIMO104A.

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Hong, Angela Manyin. "Cell cycle protein expression in AIDS-related and classical Kaposi's sarcoma." Thesis, The University of Sydney, 2004. http://hdl.handle.net/2123/583.

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Kaposi�s sarcoma (KS) is a peculiar vascular neoplasm that occurs mainly in elderly Mediterranean men and patients with acquired immunodeficiency syndrome (AIDS). The current literature indicates that KS is initiated by the human herpes virus 8 (HHV8) as a reactive polyclonal process but with deregulation of oncogene and tumour suppressor genes, it can progress to a true malignancy with monoclonality. Clinically, classical KS often presents as an indolent disease affecting mainly the lower extremities whereas AIDS-related KS has no site predilection and can progress rapidly with systemic involvement. Histologically, KS can be classified into patch, plaque and nodular stages. Interestingly, classical and AIDS-related KS are indistinguishable histologically and this suggests that AIDS-related KS and classical KS might be initiated by a common aetiology but given their different clinical courses, they may progress through different mechanisms. In view of the importance of the cell cycle proteins in the development and progression of many human malignancies, this thesis aims to examine the role of these proteins in the progression of the two main clinical subtypes of KS. The cell cycle protein expressions in a cohort of 47 patients with KS with welldocumented clinical and histological features were studied. Using a monclonal antibody against the latent nuclear antigen-1 molecule of HHV8, HHV8 was detected in 78% of the cases. The more advanced nodular lesions were found to have a higher level of proliferative activity as measured by the proliferation x marker, Ki-67. This suggests it is valid to use the histological specimens as a tumour progression model of KS. The role of the Rb/cyclin D1/p16 pathway was examined. The more advanced nodular stage KS lesions were more likely to be positive for cyclin D1, suggesting that cyclin D1 is important in the progression from patch stage to nodular stage. p16 acts as a tumour suppressor and it has an inhibitory effect on cyclin D1. The p16 expression rate was low in early stage KS but high in the more advanced lesions. It seems that reduced p16 expression occurs early in KS and may be important in its development. The rate of Rb expression, on the other hand, did not differ significantly among the histological subtypes. The results revealed the significant role of the Rb/cyclin D1/p16 pathway in the progression of KS. Of the mitotic cyclins examined, cyclin A expression was correlated with the advanced tumor stage. The rate of p34cdc2 expression was high in the lesions and there was no correlation with histological stage. This suggests that p34cdc2 is important in the early development of the tumour but not necessarily in its progression. Along the p53-apoptotic pathway, mutant p53 expression was significantly more common in the nodular stage. The cyclin G1 (a protooncogene, one of the target genes of p53) expression also paralleled that of mutant p53 with the majority of the KS lesions showing cyclin G1 expression and significant xi correlation between advanced histological stage and increasing rate of cyclin G1 expression. These findings suggest that progression along the p53 pathway may be important in the advanced stage development of KS. On the other hand, expression of the CDK inhibitor, p27, a protein that normally negatively regulates cyclin G1, was reduced in nodular KS. These findings suggest that some KS lesions may progress through a deregulated or abnormal p53 pathway. There were correlations between cyclin D1, cyclin A, cyclin G1, mutant p53 and negative HIV status. The findings suggest that components of both the Rb/cyclin D1/p16 and p53-apoptotic pathways are important in the progression of classical KS. Rb protein was the only cell cycle protein whose rate of expression correlated significantly with HHV8 status in KS. The majority of HHV8 positive lesions were also positive for Rb protein, unlike HHV8 negative lesions. This suggests that some of the HHV8 negative lesions can progress through a defective Rb pathway whereas the role of Rb in the progression may not be as important in the HHV8 positive lesions. This was an unexpected finding given that one of the postulated mechanisms of tumour initiation by the HHV8 virus is via the viral cyclin it produces. The viral cyclin produced by HHV8 acts through the Rb pathway much the same as cyclin D1 and one would have expected that HHV8 positive cases are less likely to be positive for the Rb protein. In summary, the majority of the KS lesions examined in this thesis show HHV8 infection. The Rb/cyclin D1/p16 pathway appears to be important in the progression of the different stages of KS and expression of the proteins involved in the p53 pathway were found to be important in the advanced stages of the development of KS. There were differential expressions of cell cycle proteins between AIDS-related and classical KS, and between HHV8 positive and HHV8 negative lesions. The findings also provided some clues to the possible mechanisms of development in KS lesions that were not initiated by HHV8.
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4

Hong, Angela Manyin. "Cell cycle protein expression in AIDS-related and classical Kaposi's sarcoma." University of Sydney. Pathology, 2004. http://hdl.handle.net/2123/583.

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Kaposi�s sarcoma (KS) is a peculiar vascular neoplasm that occurs mainly in elderly Mediterranean men and patients with acquired immunodeficiency syndrome (AIDS). The current literature indicates that KS is initiated by the human herpes virus 8 (HHV8) as a reactive polyclonal process but with deregulation of oncogene and tumour suppressor genes, it can progress to a true malignancy with monoclonality. Clinically, classical KS often presents as an indolent disease affecting mainly the lower extremities whereas AIDS-related KS has no site predilection and can progress rapidly with systemic involvement. Histologically, KS can be classified into patch, plaque and nodular stages. Interestingly, classical and AIDS-related KS are indistinguishable histologically and this suggests that AIDS-related KS and classical KS might be initiated by a common aetiology but given their different clinical courses, they may progress through different mechanisms. In view of the importance of the cell cycle proteins in the development and progression of many human malignancies, this thesis aims to examine the role of these proteins in the progression of the two main clinical subtypes of KS. The cell cycle protein expressions in a cohort of 47 patients with KS with welldocumented clinical and histological features were studied. Using a monclonal antibody against the latent nuclear antigen-1 molecule of HHV8, HHV8 was detected in 78% of the cases. The more advanced nodular lesions were found to have a higher level of proliferative activity as measured by the proliferation x marker, Ki-67. This suggests it is valid to use the histological specimens as a tumour progression model of KS. The role of the Rb/cyclin D1/p16 pathway was examined. The more advanced nodular stage KS lesions were more likely to be positive for cyclin D1, suggesting that cyclin D1 is important in the progression from patch stage to nodular stage. p16 acts as a tumour suppressor and it has an inhibitory effect on cyclin D1. The p16 expression rate was low in early stage KS but high in the more advanced lesions. It seems that reduced p16 expression occurs early in KS and may be important in its development. The rate of Rb expression, on the other hand, did not differ significantly among the histological subtypes. The results revealed the significant role of the Rb/cyclin D1/p16 pathway in the progression of KS. Of the mitotic cyclins examined, cyclin A expression was correlated with the advanced tumor stage. The rate of p34cdc2 expression was high in the lesions and there was no correlation with histological stage. This suggests that p34cdc2 is important in the early development of the tumour but not necessarily in its progression. Along the p53-apoptotic pathway, mutant p53 expression was significantly more common in the nodular stage. The cyclin G1 (a protooncogene, one of the target genes of p53) expression also paralleled that of mutant p53 with the majority of the KS lesions showing cyclin G1 expression and significant xi correlation between advanced histological stage and increasing rate of cyclin G1 expression. These findings suggest that progression along the p53 pathway may be important in the advanced stage development of KS. On the other hand, expression of the CDK inhibitor, p27, a protein that normally negatively regulates cyclin G1, was reduced in nodular KS. These findings suggest that some KS lesions may progress through a deregulated or abnormal p53 pathway. There were correlations between cyclin D1, cyclin A, cyclin G1, mutant p53 and negative HIV status. The findings suggest that components of both the Rb/cyclin D1/p16 and p53-apoptotic pathways are important in the progression of classical KS. Rb protein was the only cell cycle protein whose rate of expression correlated significantly with HHV8 status in KS. The majority of HHV8 positive lesions were also positive for Rb protein, unlike HHV8 negative lesions. This suggests that some of the HHV8 negative lesions can progress through a defective Rb pathway whereas the role of Rb in the progression may not be as important in the HHV8 positive lesions. This was an unexpected finding given that one of the postulated mechanisms of tumour initiation by the HHV8 virus is via the viral cyclin it produces. The viral cyclin produced by HHV8 acts through the Rb pathway much the same as cyclin D1 and one would have expected that HHV8 positive cases are less likely to be positive for the Rb protein. In summary, the majority of the KS lesions examined in this thesis show HHV8 infection. The Rb/cyclin D1/p16 pathway appears to be important in the progression of the different stages of KS and expression of the proteins involved in the p53 pathway were found to be important in the advanced stages of the development of KS. There were differential expressions of cell cycle proteins between AIDS-related and classical KS, and between HHV8 positive and HHV8 negative lesions. The findings also provided some clues to the possible mechanisms of development in KS lesions that were not initiated by HHV8.
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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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Marcelin, Anne-Geneviève. "Apport de la sérologie dans l'épidémiologie du 8ème Herpesvirus humain." Paris 5, 1997. http://www.theses.fr/1997PA05P197.

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7

Boralevi, Franck. "Huitième virus herpès humain (HHV-8) et maladie de Kaposi : une étude d'épidémiologie moléculaire menée sur 48 cas." Bordeaux 2, 1999. http://www.theses.fr/1999BOR23075.

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8

Squiavinato, Annie Cristhine Moraes Sousa [UNESP]. "Produção de vetores recombinantes para análise das propriedades biológicas e cancerígenas da proteína K1 do herpesvírus associado ao sarcoma de Kaposi (KSHV/HHV-8)." Universidade Estadual Paulista (UNESP), 2014. http://hdl.handle.net/11449/113889.

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O herpesvírus associado ao sarcoma de Kaposi (KSHV) é um gammaherpesvírus associado ao sarcoma de Kaposi (SK). A proteína K1 do KSHV é conhecida por aumentar a sobrevivência e proliferação celular em células infectadas. A ORF-K1 viral apresenta elevada variabilidade, de modo a discriminar diferentes genótipos do KSHV. Até o momento não se sabe se diferentes genótipos virais apresentam características biológicas próprias. Assim, vetores recombinantes contendo a ORF-K1 de genótipos virais A e B foram gerados. A ORF-K1 foi obtida a partir do DNA de linhagens de linfoma de efusão primária (PEL) constitutivamente infectadas pelo KSHV. O amplicon da ORF-K1 e vetor comercial foram digeridos, ligados e clonados em bactéria E. coli DH5α. Clones selecionados foram então submetidos à sequenciamento automatizado de DNA. As sequências geradas dos vetores recombinantes foram alinhadas e comparadas com sequências-protótipo de ORF-K1 do KSHV. Sequência de aminoácidos dos vetores recombinantes foram geradas e analisadas quanto a região codificadora do ITAM de K1. Um clone validado de cada vetor recombinante foi transfectado estavelmente em células HEK293 e a expressão de K1 foi avaliada por Western blot (WB) O sequenciamento de DNA demonstrou que a ORF-K1 dos vetores recombinantes de genótipo A, B e C corresponde a de sequências-protótipo depositadas de linhagens de PEL. A presença de K1 no lisado de células HEK293 transfectadas foi demonstrada por WB. A análise da sequência de aminoácidos de K1 codificada nos vetores recombinantes revelou que o domínio ITAM de K1 do genótipo B apresenta aminoácidos distintos em relação ao ITAM de K1 de genótipos A e C. Portanto, vetores recombinantes de ORF-K1 foram produzidos e validados, e serão úteis para se estabelecer modelo experimental para análises das propriedades biológicas da proteína K1 do KSHV
Kaposi's sarcoma-associated herpesvirus (KSHV) is a gammaherpesvirus associated with the development of Kaposi's sarcoma. The K1 protein of KSHV has been shown to induce increases the survival and proliferation of infected cells. The viral ORF-K1 shows high variability, so it is possible to distinguish different KSHV genotypes (genotypes A, B, C, D). So far, it is unclear whether different viral genotypes have their own biological characteristics. To this intent, recombinant vectors were generated containing the ORFK1 genotypes A and B. ORF-K1 was obtained from the DNA of primary effusion lymphoma (PEL) cell lines. The amplicon generated and the commercial vector were digested, bonded and cloned in E.coli DH5α. Selected clones underwent automated DNA sequencing. The generated sequences were compared with prototype sequences of ORF-K1. The amino acid sequences from vectors were generated and analyzed in the K1 ITAM-coding region. Validated clones were stably transfected into HEK293 cells and K1 expression was evaluated using Western blot (WB). DNA sequencing showed that the ORF-K1 recombinant vectors corresponds to the prototype sequences deposited from PEL cell lines. WB demonstrated the presence of K1 in the lysate of HEK293 transfected cells. Analysis of the K1 amino acid sequence encoded in the vectors revealed that ITAM domain of K1 (genotype B) has distinct amino acids from the ones in the ITAM domain of K1 (genotypes A and C). Therefore ORF-K1 recombinant vectors were produced and validated, and will be useful to establish an experimental model for analysis of the biological properties of the K1 protein
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Al-Otaibi, Luba M. "Studies into the disparity in extent of human herpes virus 8 infection in Saudi Arabian general population, chronic renal failure patients and renal allograft recipients." Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1444092/.

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Transplantation-associated Kaposi's sarcoma (KS), causatively associated with human herpes virus 8 (HHV-8), is particularly prevalent in Saudi Arabia, although the prevalence rate of HHV-8 infection in the general population there is comparable to that in other geographical regions. The serologic and genomic prevalences of HHV-8 in samples representing the general population (n=238), patients with end-stage renal disease (n=78), and renal allograft recipients (n=66) were investigated. To evaluate if oral shedding of HHV-8 might play a role in transplantation KS, the extent of HHV-8 shedding in the mouth compared to other anatomical compartments, and the presence of multiple HHV-8 infection were also studied. PCR protocols were applied to amplify 3 fragments of the viral genome (from open reading frames 26 and K1) from whole-mouth saliva, parotid saliva, buccal and palatal exfoliates, plasma, sub sets of peripheral blood cells, and KS lesional tissue, and to quantify the salivary viral load. Demographic and clinical data were analysed to identify risk factors for HHV-8 infection. A higher HHV-8 seroprevalence was observed in patients with renal disease compared to the general population, but no significant difference in HHV-8 DNA detection rates in CD45+ cells was found. The oral cavity was identified as a major site of HHV-8 shedding in renal disease patients regardless of a previous history of KS. In patients with end-stage renal disease, HHV-8 DNA was more frequently detectable in oral samples than in blood. They and renal allograft recipients showed evidence of being multiply infected by HHV-8. These findings suggest that iatrogenic, salivary HHV-8 transmission between patients with renal disease prior to transplantation accounts for the relatively high prevalence of HHV-8 infection. Implementation of measures to minimise contamination of oral fluid between renal disease patients may play a role in controlling HHV-8 transmission and reduce the incidence of transplantation-associated KS.
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Lontchi, Yimagou Eric. "Infection par le virus de l'herpès humain de type 8 (HHV8) et inflammation : implications dans le diabète de type 2 cétonurique." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066207/document.

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Le Ketosis-Prone Diabetes (KPD) est un phénotype de diabète intermédiaire entre le diabète de type 1 et le diabète de type 2, fréquemment rencontré chez le sujet d’origine noire africaine. Cette forme de diabète suscite un intérêt certain de par son évolution clinique marquée notamment par la restauration de l’insulinosécrétion initialement altérée. Sobngwi et coll. en 2008 ont établi une association entre le virus HHV8 et le KPD chez des sujets Africains vivant en France. Nulle part ailleurs l’étude n’a été reproduite. L’objectif de cette thèse était de rechercher la potentielle association entre l’infection à HHV8 et le KPD ; puis d’évaluer l’impact de l’infection à HHV8 sur le profil inflammatoire des phénotypes du diabète de type 2. L’étude s’appuie sur une population de patients Africains vivant en Afrique admis consécutivement pour une décompensation hyperglycémique (glycémie à jeun≥2,5g/l) au Centre National d’Obésité de l’Hôpital Central de Yaoundé. Plus spécifiquement, il était question de :• étudier la fréquence du diabète non auto-immun à tendance cétosique (KPD); • étudier l’association entre le virus HHV8 et le KPD;• rechercher si l’infection à HHV8 est associée à un profil inflammatoire pouvant participer aux phénotypes de diabète. Etait inclus dans l’étude tout patient diabétique âgé de plus de 18 ans présentant un diabète aigu avec syndrome cardinal et cétonurie (KPD1), ceux ayant présenté un diabète inaugural aigu avec syndrome cardinal et cétonurie et en rémission depuis plus de trois mois et sans cétonurie à l’inclusion (KPD2), et ceux présentant un diabète de type 2 connu sans cétonurie (DT2). Etait exclu de l’étude tout patient présentant des stigmates d’auto-immunité du diabète de type 1 A, un diabète « MODY », une endocrinopathie, une maladie du pancréas, ou un diabète de type auto-immun. Chez l’ensemble des participants admis, nous avons collecté les données cliniques (le poids, la taille, l’IMC, le rapport tour de taille sur tour de hanche, la pression artérielle, et le pourcentage de graisse) et des prélèvements à jeun ont été effectués (sérum et cellules mononuclées du sang périphérique) pour les analyses biologiques : la glycémie par glucose oxydase, l’HbA1c par HPLC, les paramètres du profil lipidique par des methodes enzymatiques, les concentrations d’insuline et de peptide-C par électrochimiluminescence, les anticorps anti-HHV8 par immunofluorescence, l’ADN viral HHV8 par PCR en temps réel, et les marqueurs de l’inflammation par le Luminex. Les indices HOMA-β et HOMA-IR ont été utilisés pour évaluer l’insulinosécrétion et la sensibilité à l’insuline respectivement. Les marqueurs sérologiques de l’inflammation recherchés étaient : TNF-α, MCP-1, IL-8, MIP-1β, VEGF et MIP-1α
Ketosis-Prone Diabetes (KPD) is a diabetes phenotype intermediate between type 1 and type 2 diabetes, frequently encountered in populations of African origin. This form of diabetes arouses some interest because of its clinical course marked in particular by restoring the initial impaired insulin secretion. Sobngwi et al. in 2008 established an association between HHV-8 virus and KPD in African population living in France. Nowhere else has the study been replicated. The objective of this thesis was to investigate the potential association between HHV-8 infection and KPD; then evaluate the impact of HHV-8 infection on the inflammatory profile of type 2 diabetes phenotypes. The study is based on African patients living in Africa consecutively admitted for hyperglycemic decompensation (Fasting blood glucose≥2,5g/l) at the National Obesity Centre of the Yaounde Central Hospital. More specifically, the issue was:• study the frequency of non-immune ketosis-prone diabetes (KPD);• investigate the association between HHV8 and KPD;• investigate whether HHV-8 infection is associated with an inflammatory profile that may participate in diabetes phenotypes.Was included in this study all diabetic patients old more than 18 years with acute diabetes with syndrome cardinal and ketonuria (KPD1), those who presented with an acute inaugural cardinal syndrome and diabetes ketonuria and in remission for more than three months and without ketonuria at baseline (KPD2), and those with type 2 diabetes experienced without ketonuria (T2D). Was excluded from the study all patient with stigmata of autoimmunity of type 1 A diabetes, diabetes "MODY", endocrinopathy, pancreatic disease or an autoimmune diabetes.Among all participants admitted, we collected clinical data (weight, height, BMI, waist to hip ratio, blood pressure, and the percentage of fat) and levies fasting were made (serum and peripheral blood mononuclear cells) for biological testing: glyceamia by glucose oxidase, HbA1c by HPLC, lipid profile by enzymatic methods, the insulin and C-peptide concentrations by electrochemiluminescence, anti-HHV8 antibodies by immunofluorescence, HHV8 viral DNA by real-time PCR, and markers of inflammation by Luminex. HOMA-β and HOMA-IR indices were used to assess insulinsecretion and insulinsensitivity respectively. Serological markers of inflammation investigated were : TNF-α, MCP-1, IL-8, MIP-1β, MIP-1α and VEGF
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Books on the topic "Herpes virus 8"

1

(Contributor), WHO, ed. Epstein-Barr Virus and Kaposi's Sarcoma Herpes Virus/Human Herpesvirus 8 (IARC Monographs on Eval of Carcinogenic Risk to Humans). World Health Organisation, 1997.

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Ajithkumar, Thankamma, Ann Barrett, Helen Hatcher, and Natalie Cook. HIV related tumours. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235636.003.0016.

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Kaposi's sarcoma (KS) is a low-grade multifocal vascular tumour associated with human herpesvirus 8 (HHV8)/Kaposi's sarcoma herpes virus (KSHV) infection.KS lesions of all epidemiological forms are similarly comprised of HHV8-positive (LNA-1 immunoreactive) spindle-shaped tumour cells, vessels, and chronic inflammatory cells. Lesions evolve from early patch, to plaque, and later tumour nodules....
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Johansen, Bruce, and Adebowale Akande, eds. Nationalism: Past as Prologue. Nova Science Publishers, Inc., 2021. http://dx.doi.org/10.52305/aief3847.

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Nationalism: Past as Prologue began as a single volume being compiled by Ad Akande, a scholar from South Africa, who proposed it to me as co-author about two years ago. The original idea was to examine how the damaging roots of nationalism have been corroding political systems around the world, and creating dangerous obstacles for necessary international cooperation. Since I (Bruce E. Johansen) has written profusely about climate change (global warming, a.k.a. infrared forcing), I suggested a concerted effort in that direction. This is a worldwide existential threat that affects every living thing on Earth. It often compounds upon itself, so delays in reducing emissions of fossil fuels are shortening the amount of time remaining to eliminate the use of fossil fuels to preserve a livable planet. Nationalism often impedes solutions to this problem (among many others), as nations place their singular needs above the common good. Our initial proposal got around, and abstracts on many subjects arrived. Within a few weeks, we had enough good material for a 100,000-word book. The book then fattened to two moderate volumes and then to four two very hefty tomes. We tried several different titles as good submissions swelled. We also discovered that our best contributors were experts in their fields, which ranged the world. We settled on three stand-alone books:” 1/ nationalism and racial justice. Our first volume grew as the growth of Black Lives Matter following the brutal killing of George Floyd ignited protests over police brutality and other issues during 2020, following the police assassination of Floyd in Minneapolis. It is estimated that more people took part in protests of police brutality during the summer of 2020 than any other series of marches in United States history. This includes upheavals during the 1960s over racial issues and against the war in Southeast Asia (notably Vietnam). We choose a volume on racism because it is one of nationalism’s main motive forces. This volume provides a worldwide array of work on nationalism’s growth in various countries, usually by authors residing in them, or in the United States with ethnic ties to the nation being examined, often recent immigrants to the United States from them. Our roster of contributors comprises a small United Nations of insightful, well-written research and commentary from Indonesia, New Zealand, Australia, China, India, South Africa, France, Portugal, Estonia, Hungary, Russia, Poland, Kazakhstan, Georgia, and the United States. Volume 2 (this one) describes and analyzes nationalism, by country, around the world, except for the United States; and 3/material directly related to President Donald Trump, and the United States. The first volume is under consideration at the Texas A & M University Press. The other two are under contract to Nova Science Publishers (which includes social sciences). These three volumes may be used individually or as a set. Environmental material is taken up in appropriate places in each of the three books. * * * * * What became the United States of America has been strongly nationalist since the English of present-day Massachusetts and Jamestown first hit North America’s eastern shores. The country propelled itself across North America with the self-serving ideology of “manifest destiny” for four centuries before Donald Trump came along. Anyone who believes that a Trumpian affection for deportation of “illegals” is a new thing ought to take a look at immigration and deportation statistics in Adam Goodman’s The Deportation Machine: America’s Long History of Deporting Immigrants (Princeton University Press, 2020). Between 1920 and 2018, the United States deported 56.3 million people, compared with 51.7 million who were granted legal immigration status during the same dates. Nearly nine of ten deportees were Mexican (Nolan, 2020, 83). This kind of nationalism, has become an assassin of democracy as well as an impediment to solving global problems. Paul Krugman wrote in the New York Times (2019:A-25): that “In their 2018 book, How Democracies Die, the political scientists Steven Levitsky and Daniel Ziblatt documented how this process has played out in many countries, from Vladimir Putin’s Russia, to Recep Erdogan’s Turkey, to Viktor Orban’s Hungary. Add to these India’s Narendra Modi, China’s Xi Jinping, and the United States’ Donald Trump, among others. Bit by bit, the guardrails of democracy have been torn down, as institutions meant to serve the public became tools of ruling parties and self-serving ideologies, weaponized to punish and intimidate opposition parties’ opponents. On paper, these countries are still democracies; in practice, they have become one-party regimes….And it’s happening here [the United States] as we speak. If you are not worried about the future of American democracy, you aren’t paying attention” (Krugmam, 2019, A-25). We are reminded continuously that the late Carl Sagan, one of our most insightful scientific public intellectuals, had an interesting theory about highly developed civilizations. Given the number of stars and planets that must exist in the vast reaches of the universe, he said, there must be other highly developed and organized forms of life. Distance may keep us from making physical contact, but Sagan said that another reason we may never be on speaking terms with another intelligent race is (judging from our own example) could be their penchant for destroying themselves in relatively short order after reaching technological complexity. This book’s chapters, introduction, and conclusion examine the worldwide rise of partisan nationalism and the damage it has wrought on the worldwide pursuit of solutions for issues requiring worldwide scope, such scientific co-operation public health and others, mixing analysis of both. We use both historical description and analysis. This analysis concludes with a description of why we must avoid the isolating nature of nationalism that isolates people and encourages separation if we are to deal with issues of world-wide concern, and to maintain a sustainable, survivable Earth, placing the dominant political movement of our time against the Earth’s existential crises. Our contributors, all experts in their fields, each have assumed responsibility for a country, or two if they are related. This work entwines themes of worldwide concern with the political growth of nationalism because leaders with such a worldview are disinclined to co-operate internationally at a time when nations must find ways to solve common problems, such as the climate crisis. Inability to cooperate at this stage may doom everyone, eventually, to an overheated, stormy future plagued by droughts and deluges portending shortages of food and other essential commodities, meanwhile destroying large coastal urban areas because of rising sea levels. Future historians may look back at our time and wonder why as well as how our world succumbed to isolating nationalism at a time when time was so short for cooperative intervention which is crucial for survival of a sustainable earth. Pride in language and culture is salubrious to individuals’ sense of history and identity. Excess nationalism that prevents international co-operation on harmful worldwide maladies is quite another. As Pope Francis has pointed out: For all of our connectivity due to expansion of social media, ability to communicate can breed contempt as well as mutual trust. “For all our hyper-connectivity,” said Francis, “We witnessed a fragmentation that made it more difficult to resolve problems that affect us all” (Horowitz, 2020, A-12). The pope’s encyclical, titled “Brothers All,” also said: “The forces of myopic, extremist, resentful, and aggressive nationalism are on the rise.” The pope’s document also advocates support for migrants, as well as resistance to nationalist and tribal populism. Francis broadened his critique to the role of market capitalism, as well as nationalism has failed the peoples of the world when they need co-operation and solidarity in the face of the world-wide corona virus pandemic. Humankind needs to unite into “a new sense of the human family [Fratelli Tutti, “Brothers All”], that rejects war at all costs” (Pope, 2020, 6-A). Our journey takes us first to Russia, with the able eye and honed expertise of Richard D. Anderson, Jr. who teaches as UCLA and publishes on the subject of his chapter: “Putin, Russian identity, and Russia’s conduct at home and abroad.” Readers should find Dr. Anderson’s analysis fascinating because Vladimir Putin, the singular leader of Russian foreign and domestic policy these days (and perhaps for the rest of his life, given how malleable Russia’s Constitution has become) may be a short man physically, but has high ambitions. One of these involves restoring the old Russian (and Soviet) empire, which would involve re-subjugating a number of nations that broke off as the old order dissolved about 30 years ago. President (shall we say czar?) Putin also has international ambitions, notably by destabilizing the United States, where election meddling has become a specialty. The sight of Putin and U.S. president Donald Trump, two very rich men (Putin $70-$200 billion; Trump $2.5 billion), nuzzling in friendship would probably set Thomas Jefferson and Vladimir Lenin spinning in their graves. The road of history can take some unanticipated twists and turns. Consider Poland, from which we have an expert native analysis in chapter 2, Bartosz Hlebowicz, who is a Polish anthropologist and journalist. His piece is titled “Lawless and Unjust: How to Quickly Make Your Own Country a Puppet State Run by a Group of Hoodlums – the Hopeless Case of Poland (2015–2020).” When I visited Poland to teach and lecture twice between 2006 and 2008, most people seemed to be walking on air induced by freedom to conduct their own affairs to an unusual degree for a state usually squeezed between nationalists in Germany and Russia. What did the Poles then do in a couple of decades? Read Hlebowicz’ chapter and decide. It certainly isn’t soft-bellied liberalism. In Chapter 3, with Bruce E. Johansen, we visit China’s western provinces, the lands of Tibet as well as the Uighurs and other Muslims in the Xinjiang region, who would most assuredly resent being characterized as being possessed by the Chinese of the Han to the east. As a student of Native American history, I had never before thought of the Tibetans and Uighurs as Native peoples struggling against the Independence-minded peoples of a land that is called an adjunct of China on most of our maps. The random act of sitting next to a young woman on an Air India flight out of Hyderabad, bound for New Delhi taught me that the Tibetans had something to share with the Lakota, the Iroquois, and hundreds of other Native American states and nations in North America. Active resistance to Chinese rule lasted into the mid-nineteenth century, and continues today in a subversive manner, even in song, as I learned in 2018 when I acted as a foreign adjudicator on a Ph.D. dissertation by a Tibetan student at the University of Madras (in what is now in a city called Chennai), in southwestern India on resistance in song during Tibet’s recent history. Tibet is one of very few places on Earth where a young dissident can get shot to death for singing a song that troubles China’s Quest for Lebensraum. The situation in Xinjiang region, where close to a million Muslims have been interned in “reeducation” camps surrounded with brick walls and barbed wire. They sing, too. Come with us and hear the music. Back to Europe now, in Chapter 4, to Portugal and Spain, we find a break in the general pattern of nationalism. Portugal has been more progressive governmentally than most. Spain varies from a liberal majority to military coups, a pattern which has been exported to Latin America. A situation such as this can make use of the term “populism” problematic, because general usage in our time usually ties the word into a right-wing connotative straightjacket. “Populism” can be used to describe progressive (left-wing) insurgencies as well. José Pinto, who is native to Portugal and also researches and writes in Spanish as well as English, in “Populism in Portugal and Spain: a Real Neighbourhood?” provides insight into these historical paradoxes. Hungary shares some historical inclinations with Poland (above). Both emerged from Soviet dominance in an air of developing freedom and multicultural diversity after the Berlin Wall fell and the Soviet Union collapsed. Then, gradually at first, right wing-forces began to tighten up, stripping structures supporting popular freedom, from the courts, mass media, and other institutions. In Chapter 5, Bernard Tamas, in “From Youth Movement to Right-Liberal Wing Authoritarianism: The Rise of Fidesz and the Decline of Hungarian Democracy” puts the renewed growth of political and social repression into a context of worldwide nationalism. Tamas, an associate professor of political science at Valdosta State University, has been a postdoctoral fellow at Harvard University and a Fulbright scholar at the Central European University in Budapest, Hungary. His books include From Dissident to Party Politics: The Struggle for Democracy in Post-Communist Hungary (2007). Bear in mind that not everyone shares Orbán’s vision of what will make this nation great, again. On graffiti-covered walls in Budapest, Runes (traditional Hungarian script) has been found that read “Orbán is a motherfucker” (Mikanowski, 2019, 58). Also in Europe, in Chapter 6, Professor Ronan Le Coadic, of the University of Rennes, Rennes, France, in “Is There a Revival of French Nationalism?” Stating this title in the form of a question is quite appropriate because France’s nationalistic shift has built and ebbed several times during the last few decades. For a time after 2000, it came close to assuming the role of a substantial minority, only to ebb after that. In 2017, the candidate of the National Front reached the second round of the French presidential election. This was the second time this nationalist party reached the second round of the presidential election in the history of the Fifth Republic. In 2002, however, Jean-Marie Le Pen had only obtained 17.79% of the votes, while fifteen years later his daughter, Marine Le Pen, almost doubled her father's record, reaching 33.90% of the votes cast. Moreover, in the 2019 European elections, re-named Rassemblement National obtained the largest number of votes of all French political formations and can therefore boast of being "the leading party in France.” The brutality of oppressive nationalism may be expressed in personal relationships, such as child abuse. While Indonesia and Aotearoa [the Maoris’ name for New Zealand] hold very different ranks in the United Nations Human Development Programme assessments, where Indonesia is classified as a medium development country and Aotearoa New Zealand as a very high development country. In Chapter 7, “Domestic Violence Against Women in Indonesia and Aotearoa New Zealand: Making Sense of Differences and Similarities” co-authors, in Chapter 8, Mandy Morgan and Dr. Elli N. Hayati, from New Zealand and Indonesia respectively, found that despite their socio-economic differences, one in three women in each country experience physical or sexual intimate partner violence over their lifetime. In this chapter ther authors aim to deepen understandings of domestic violence through discussion of the socio-economic and demographic characteristics of theit countries to address domestic violence alongside studies of women’s attitudes to gender norms and experiences of intimate partner violence. One of the most surprising and upsetting scholarly journeys that a North American student may take involves Adolf Hitler’s comments on oppression of American Indians and Blacks as he imagined the construction of the Nazi state, a genesis of nationalism that is all but unknown in the United States of America, traced in this volume (Chapter 8) by co-editor Johansen. Beginning in Mein Kampf, during the 1920s, Hitler explicitly used the westward expansion of the United States across North America as a model and justification for Nazi conquest and anticipated colonization by Germans of what the Nazis called the “wild East” – the Slavic nations of Poland, the Baltic states, Ukraine, and Russia, most of which were under control of the Soviet Union. The Volga River (in Russia) was styled by Hitler as the Germans’ Mississippi, and covered wagons were readied for the German “manifest destiny” of imprisoning, eradicating, and replacing peoples the Nazis deemed inferior, all with direct references to events in North America during the previous century. At the same time, with no sense of contradiction, the Nazis partook of a long-standing German romanticism of Native Americans. One of Goebbels’ less propitious schemes was to confer honorary Aryan status on Native American tribes, in the hope that they would rise up against their oppressors. U.S. racial attitudes were “evidence [to the Nazis] that America was evolving in the right direction, despite its specious rhetoric about equality.” Ming Xie, originally from Beijing, in the People’s Republic of China, in Chapter 9, “News Coverage and Public Perceptions of the Social Credit System in China,” writes that The State Council of China in 2014 announced “that a nationwide social credit system would be established” in China. “Under this system, individuals, private companies, social organizations, and governmental agencies are assigned a score which will be calculated based on their trustworthiness and daily actions such as transaction history, professional conduct, obedience to law, corruption, tax evasion, and academic plagiarism.” The “nationalism” in this case is that of the state over the individual. China has 1.4 billion people; this system takes their measure for the purpose of state control. Once fully operational, control will be more subtle. People who are subject to it, through modern technology (most often smart phones) will prompt many people to self-censor. Orwell, modernized, might write: “Your smart phone is watching you.” Ming Xie holds two Ph.Ds, one in Public Administration from University of Nebraska at Omaha and another in Cultural Anthropology from the Chinese Academy of Social Sciences, Beijing, where she also worked for more than 10 years at a national think tank in the same institution. While there she summarized news from non-Chinese sources for senior members of the Chinese Communist Party. Ming is presently an assistant professor at the Department of Political Science and Criminal Justice, West Texas A&M University. In Chapter 10, analyzing native peoples and nationhood, Barbara Alice Mann, Professor of Honours at the University of Toledo, in “Divide, et Impera: The Self-Genocide Game” details ways in which European-American invaders deprive the conquered of their sense of nationhood as part of a subjugation system that amounts to genocide, rubbing out their languages and cultures -- and ultimately forcing the native peoples to assimilate on their own, for survival in a culture that is foreign to them. Mann is one of Native American Studies’ most acute critics of conquests’ contradictions, and an author who retrieves Native history with a powerful sense of voice and purpose, having authored roughly a dozen books and numerous book chapters, among many other works, who has traveled around the world lecturing and publishing on many subjects. Nalanda Roy and S. Mae Pedron in Chapter 11, “Understanding the Face of Humanity: The Rohingya Genocide.” describe one of the largest forced migrations in the history of the human race, the removal of 700,000 to 800,000 Muslims from Buddhist Myanmar to Bangladesh, which itself is already one of the most crowded and impoverished nations on Earth. With about 150 million people packed into an area the size of Nebraska and Iowa (population less than a tenth that of Bangladesh, a country that is losing land steadily to rising sea levels and erosion of the Ganges river delta. The Rohingyas’ refugee camp has been squeezed onto a gigantic, eroding, muddy slope that contains nearly no vegetation. However, Bangladesh is majority Muslim, so while the Rohingya may starve, they won’t be shot to death by marauding armies. Both authors of this exquisite (and excruciating) account teach at Georgia Southern University in Savannah, Georgia, Roy as an associate professor of International Studies and Asian politics, and Pedron as a graduate student; Roy originally hails from very eastern India, close to both Myanmar and Bangladesh, so he has special insight into the context of one of the most brutal genocides of our time, or any other. This is our case describing the problems that nationalism has and will pose for the sustainability of the Earth as our little blue-and-green orb becomes more crowded over time. The old ways, in which national arguments often end in devastating wars, are obsolete, given that the Earth and all the people, plants, and other animals that it sustains are faced with the existential threat of a climate crisis that within two centuries, more or less, will flood large parts of coastal cities, and endanger many species of plants and animals. To survive, we must listen to the Earth, and observe her travails, because they are increasingly our own.
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Book chapters on the topic "Herpes virus 8"

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Warford, Ann L., and Evan Steinberg. "Newer Approaches to Perinatal Herpes Simplex Virus Testing." In Medical Virology 8, 1–21. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-0891-9_1.

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Kamboj, Mini, and David M. Weinstock. "Epstein-Barr Virus, Varicella Zoster Virus, and Human Herpes Viruses-6 and -8." In Principles and Practice of Cancer Infectious Diseases, 359–70. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60761-644-3_31.

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Arvin, Ann M., Wayne M. Sullender, Francois Boucher, Pamela S. Diaz, Paul A. Hensleigh, and Charles G. Prober. "The Analysis of Immunity to Specific Proteins of Herpes Simplex and Varicella Zoster Virus and Its Clinical Applications." In Medical Virology 8, 41–71. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-0891-9_3.

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Razonable, Raymund R. "Herpes Simplex Viruses 1 and 2, Varicella Zoster Virus, and Human Herpes Viruses 6, 7, and 8 in Transplant Recipients." In Principles and Practice of Transplant Infectious Diseases, 667–77. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9034-4_39.

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"Virus del herpes humano 8." In Red Book (2012) - Spanish, 416–18. 29th ed. American Academy of Pediatrics, 2013. http://dx.doi.org/10.1542/9781581108026-part03-virus3.

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"Herpes Simplex Virus." In Viral Infections and Treatment, 181–208. CRC Press, 2003. http://dx.doi.org/10.1201/b14823-8.

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Kimberlin, David W., and Charles G. Prober. "Herpes Simplex Virus." In Principles and Practice of Pediatric Infectious Diseases, 1056–65. Elsevier, 2018. http://dx.doi.org/10.1016/b978-0-323-40181-4.00204-8.

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Prober, Charles G. "Herpes Simplex Virus." In Principles and Practice of Pediatric Infectious Disease, 1012–21. Elsevier, 2008. http://dx.doi.org/10.1016/b978-0-7020-3468-8.50210-8.

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Pattman, Richard, Michael Snow, Pauline Handy, K. Nathan Sankar, and Babiker Elawad. "Human herpes virus-8 (HHV-8)." In Oxford Handbook of Genitourinary Medicine, HIV and AIDS. Oxford University Press, 2005. http://dx.doi.org/10.1093/med/1.1.med-9780198520771-div1-167.

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Caserta, Mary T. "Herpes Simplex Virus Infections." In Pediatric Clinical Advisor, 268–69. Elsevier, 2007. http://dx.doi.org/10.1016/b978-032303506-4.10151-8.

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Conference papers on the topic "Herpes virus 8"

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Gandhiraj, D., A. C. Miller, C. Zhang, J. K. Mwangi, D. Picker, E. Charbek, and D. Stoeckel. "Human Herpes Virus-8 Negative Primary Effusion Lymphoma." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6971.

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Liu, R., J. Wang, R. Liu, and S. Rabkin. "Abstract P2-18-01: Treatment of Human Breast Tumors by Oncolytic Herpes Simplex Virus." In Abstracts: Thirty-Third Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 8‐12, 2010; San Antonio, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/0008-5472.sabcs10-p2-18-01.

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Ghatol, Abhijeet, and Nikhil Barot. "A Case Of Human Herpes Virus 8 (HHV 8)-Associated Extracavitary Lymphoma In A Patient With Disseminated Kaposi Sarcoma And HIV." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2970.

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Henning, Jill D., Kathrine Kercher, Clareann H. Bunker, Robert E. Ferrel, Alan L. Patrick, and Frank J. Jenkins. "Abstract B006: Analysis of the interaction of human herpes virus 8 and gp130 in prostate cancer risk." In Abstracts: AACR Special Conference: Prostate Cancer: Advances in Basic, Translational, and Clinical Research; December 2-5, 2017; Orlando, Florida. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.prca2017-b006.

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Liu, R., W. Zeng, P. Hu, J. Wu, J. Li, J. Wang, and L. Lei. "Abstract P4-05-01: Oncolytic Herpes Simplex Virus Vector G47Δ Effectively Targets Breast Cancer Stem Cells." In Abstracts: Thirty-Fifth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 4‐8, 2012; San Antonio, TX. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/0008-5472.sabcs12-p4-05-01.

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Taveira, Elisa Borges, Marco Fidel Guevara-Vega, Igor Andrade Santos, Douglas Carvalho Caixeta, Victoria Riquena Grosche, Thulio Marquez Cunha, Murillo Guimarães Carneiro, Ana Carolina Gomes Jardim, and Robinson Sabino-Silva. "SARS-CoV-2 structures detection in artificial saliva using ATR-FTIR associated with Linear Discriminant Analysis." In Latin America Optics and Photonics Conference. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/laop.2022.tu1c.8.

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Here, we used ATR-FTIR platform supported by artificial intelligence algorithms to identify unique infrared vibrational modes of a pseudotyped human immunodeficiency virus type-1 (HIV-1) coupled to Spike (S) protein of SARS-CoV-2 (HIV/NanoLuc-SARS-CoV-2 pseudotype virus).
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Al Khatib, Hebah A., Fatiha M. Benslimane, Israa El Bashir, Asmaa A. Al Thani, and Hadi M. Yassine. "Within-Host Diversity of SARS-Cov-2 in COVID-19 Patients with Variable Disease Severities." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0280.

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Background: The ongoing pandemic of SARS-COV-2 has already infected more than eight million people worldwide. The majority of COVID-19 patients are either asymptomatic or have mild symptoms. Yet, about 15% of the cases experience severe complications and require intensive care. Factors determining disease severity are not yet fully characterized. Aim: Here, we investigated the within-host virus diversity in COVID-19 patients with different clinical manifestations. Methods: We compared SARS-COV-2 genetic diversity in 19 mild and 27 severe cases. Viral RNA was extracted from nasopharyngeal samples and sequenced using Illumina MiSeq platform. This was followed by deep-sequencing analyses of SARS-CoV-2 genomes at both consensus and sub-consensus sequence levels. Results: Consensus sequences of all viruses were very similar, showing more than 99·8% sequence identity regardless of the disease severity. However, the sub-consensus analysis revealed significant differences in within-host diversity between mild and severe cases. Patients with severe symptoms exhibited a significantly (p-value 0.001) higher number of variants in coding and non-coding regions compared to mild cases. Analysis also revealed higher prevalence of some variants among severe cases. Most importantly, severe cases exhibited significantly higher within-host diversity (mean= 13) compared to mild cases (mean=6). Further, higher within-host diversity was observed in patients above the age of 60 compared to the younger age group. Conclusion: These observations provided evidence that within-host diversity might play a role in the development of severe disease outcomes in COVID19 patients; however, further investigations is required to elucidate this association.
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