According to the UNAIDS global report 2013, an estimated 6.1 million people are living with human immunodeficiency virus (HIV) in South Africa. The incidence of Kaposi sarcoma (KS) has increased dramatically since the Acquired Immunodeficiency Syndrome (AIDS) epidemic. Of the estimated 66 200 cases of KS worldwide, 58 800 are thought to have occurred in SSA (Parkin 2002). However, there remains a paucity of published data about KS from South Africa. This retrospective study was conducted to describe the epidemiology of KS at Chris Hani Baragwanath Academic Hospital (CHBAH) and to determine possible links among the CD4 counts, intensity and distribution of human herpes virus 8 latency- associated nuclear antigen 1 (HHV8 LNA-1) immunohistochemical staining and the stage of KS. Nine hundred and thirty eight histopathology reports of KS diagnosed in 901 patients at CHBAH between 2005 and 2009 were reviewed and demographic data (age, gender, topographic site, CD4 count, HIV status, KS stage, HHV8 LNA-1 staining, concomitant pathology) were recorded. The H&E stained sections and HHV8 LNA-1 immunostains of a cohort of 127 cases were subsequently reviewed and categorised with regard to intensity and distribution of staining. The male:female ratio was 1,2:1. The mean age was 36,8 years (standard deviation {SD} 10,2 years) and the median CD4 count 127,5 cells/mm3 (quartile range {QR} 184,5 cells/mm3). Lower limb skin biopsies accounted for 49,6% of cases. Concomitant pathology was seen in 4,6% of cases. Infections and inflammatory dermatoses were the most frequently diagnosed concomitant pathology in cutaneous biopsies. Paediatric, visceral and endemic KS accounted for only limited proportions of cases (1,44% of patients; 1,4% and 1,3% respectively). There was a significant difference in the distribution of HHV8 LNA-1 staining in patch versus nodular KS (p = 0,011). The CD4 counts were not predictive of KS Page | v stage (p = 0,701) or the intensity (p = 0,877) and distribution (p = 0,846) of HHV8 LNA-1 immunohistochemical staining. This study highlights the epidemiology of KS and the variability in HHV8 LNA-1 immunohistochemical staining across CD4 counts and stages of KS.

Thesis (Ph. D.)--Cornell University, January, 2007. / Vita. Includes bibliographical references (leaves 146-195).

Thesis (Ph. D.)--University of Washington, 2002. / Vita. Includes bibliographical references (leaves 163-232).

Orientador: Jose Vassallo / Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas / Made available in DSpace on 2018-08-06T13:44:11Z (GMT). No. of bitstreams: 1 Chagas_CristianoAparecido_D.pdf: 2698514 bytes, checksum: 839362fd3abba979b5a2b1472c7865a6 (MD5) Previous issue date: 2006 / Resumo: Contexto: o herpesvírus humano tipo 8 (HHV8) foi recentemente associado a neoplasias humanas, como o sarcoma de Kaposi e o linfoma não Hodgkin de células B das cavidades serosas em pacientes infectados pelo vírus da imunodeficiência humana (HIV), além da doença de Castleman multicêntrica. Estudos epidemiológicos mostraram soropositividade em porcentagens variáveis da população, inclusive em crianças. Acredita-se que a forma de transmissão seja predominantemente sexual nos adultos, mas existem formas de infecção não relacionadas à atividade sexual que explicam a soropositividade em crianças e em indivíduos que não apresentaram contato sexual prévio. O vírus foi demonstrado em células epiteliais orais descamadas, mas há apenas um raro relato sobre sua presença no anel de Waldeyer em um individuo HIV positivo. Objetivos: detectar a presença do antígeno nuclear latente (LNA-1) e de RNAm do HHV8 em tecidos amidalianos e adenoideanos de indivíduos de até 20 anos de idade; em caso de reatividade, verificar quais tipos celulares albergam o vírus (linfóides, endoteliais, estromais, epiteliais); verificar se existe preferência por um dos dois órgãos estudados, amídalas ou adenóides; verificar em que idade a freqüência de positividade, se existir, se concentra (menor que 2 anos; 2 a 5; 6 a 10; maior que 10 anos); comparar a reatividade dos dois métodos. Métodos: estudo retrospectivo em amídalas e adenóides previamente fixadas em formalina e incluídas em parafina. Um total de 343 tecidos do anel de Waldeyer foi analisado (181 amídalas e 162 adenóides), de 293 pacientes (174 do sexo masculino e 119 do feminino; média de idade 6,05 anos, desvio padrão 3,80; mediana de idade 5 anos). A detecção de antígenos proteicos do vírus foi feita por imunoístoquímica (IQ), utilizando um anticorpo anti-LNAl, revelando-se a reação pelo método do LSAB+. A detecção do RNAm viral foi feita por hibridização in situ (HIS), utilizando-se um coquetel de sondas T1-1. Resultados/Conclusões: em 20 casos (6,83%) houve reatividade para o HHV8 em células morfologicamente caracterizadas como linfóides. Em 3 destes casos células epiteliais foram também positivas. Em todos os 20 casos houve reatividade à HIS, porém em apenas 2 casos houve reatividade concomitante à IQ. Em 19 casos houve reatividade nas tonsilas e em apenas um na adenóide. Houve percentual decrescente de positividade nas faixas etárias de pacientes menores de 2 anos, até 5, até 7 e maiores de 10 anos, embora sem diferenças significativas. Nossos dados reforçam a teoria da contaminação pelo HHV8 peia saliva já na faixa etária pediátrica. O método de hibridização molecular in situ mostrou-se muito superior à imunoistoquímica, provavelmente devido à pequena quantidade de material proteico nas células infectadas / Abstract: Objective: Human herpesvirus 8 (HHV8) has been associated with multicentric Castieman's disease, Kaposi's sarcoma and effusion non-Hodgkin's lymphoma. Epidemiological studies have shown seropositivity in variable proportions of populations. It seems to be sexually transmitted among adults and through oral contact among children. The virus has been demonstrated in desquamating oral epithelial cells, but there was only a rare report on its presence in the Waldeyer's ring in an HIV positive subject. The purpose of the present study is to detect HHV8 in tonsils and adenoids from children up to 20 years of age in which these organs had been surgically removed due to hypertrophy, using immunohistochemistry and in situ hybridization. Methods: Paraffin wax-embedded sections consisting of 181 tonsils and 162 adenoids from 293 patients were analyzed. HHV8 was detected by immunohistochemistry (IHC) using the anti-LNAl antibody (Novocastra) and the LSAB+ detection system (Dako). For the in situ hybridization (ISH), the Tl-1 probe for the viral mRNA and the detection system used were provided by Novocastra. Results: In 20 cases (6.83%), HHV8 was detected in cells morphologically characterized as lymphoid. In three of them epithelial cells were also positive. In 19 cases, the virus was detected in tonsils and in just 1 case in an adenoid. In all 20 cases detection was possible by ISH, whereas in only 2 of them there was a concomitant positivity by IHC. Discussion/Conclusion: Our data support the oral route of contamination by HHV8 in children, in whom tonsils and adenoids may harbor the virus. It is found especially in tonsils and only rarely in adenoids. In these organs ISH is the method of choice to detect this virus, probably due to the small amount of viral proteins / Doutorado / Ciencias Biomedicas / Doutor em Ciências Médicas

Thesis (Ph. D.)--University of Washington, 2003. / Vita. Includes bibliographical references (leaves 77-89).

Thesis (Ph. D.)--University of Washington, 2006. / Vita. Includes bibliographical references (leaves 84-104).

O HHV-8 (herpesvírus 8 humano) é o agente etiológico do sarcoma de Kaposi (SK). Diferentemente dos outros herpesvírus, o HHV-8 é distribuído de modo não ubíquo ao redor do mundo. São sete os principais genótipos de HHV-8, de acordo com o padrão de variabilidade da ORF K1: A, B, C, D, E, F e Z. Estudos da variabilidade genética do HHV-8 poderão trazer melhores interpretações sobre o potencial patogênico dos genótipos de HHV-8 e das variações genotípicas funcionais. Dados sobre a variabilidade genética do HHV-8 no Brasil, em que o SK é associado ao HIV, permanecem escassos. Pelo nosso conhecimento, esse é o primeiro estudo que compara a variabilidade genética de HHV-8 em indivíduos infectados por HIV com SK e sem SK no Brasil. Objetivo. O estudo visou analisar a variabilidade genética do HHV-8 entre indivíduos infectados por HIV com SK e sem histórico de SK. Métodos. Sequências de DNA de HHV-8 foram investigadas em amostras criopreservadas de células mononucleares do sangue periférico a partir de 37 indivíduos infectados por HIV com SK (grupo 1); e de amostras de saliva de indivíduos sem SK (grupo 2), as quais foram selecionadas por meio da detecção positiva de DNA/ORF73/HHV-8 a partir de um total de 751 indivíduos. Dados demográficos e clínicos do estadio e evolução do SK, assim como parâmetros laboratoriais foram caracterizados. As análises moleculares e reconstruções filogenéticas foram baseadas nas ORFs K1 e K12 do HHV-8. Resultados. Foram obtidas sequências de DNA dos loci K1 e/ou K12 de 75 indivíduos, 34 indivíduos do grupo 1 e 41 do grupo 2. O sistema de primers empregado foi capaz de detectar os genótipos A, B, C, F e amplo perfil de subgenótipos de K1/HHV-8. Os dados não mostraram associação de genótipos de HHV-8 com a presença de SK ou estadio de SK. Todavia, o subgenótipo B1 predominou naqueles em que não houve registro de piora de SK (p=0,04). Os subgenótipos B1 e C3 foram igualmente predominantes em ambos os grupos. As frequências do genótipos A foram de 24% e 12,2% e dos genótipos B e C foram de 34,1 e 35,3%, nos grupos 1 e 2, respectivamente. O genótipo F foi descrito pela primeira no Brasil, um caso de cada grupo. Um amplo perfil de subgenótipos de C no grupo 2 sem SK foi encontrado (C1, C2, C3, C5 e C7). Subgenótipos K1 C5 e C7, exclusivos do grupo 2 (7%), foram confirmados como recombinantes. Não houve variabilidade genotípica de HHV-8 em amostras biológicas diferentes do mesmo indivíduo em oito casos estudados. Sítios polimórficos (6/59) em regiões codificadoras de miRNA do locus K12 foram observados, sendo 70% presentes exclusivamente em sequências de HHV-8 do grupo com SK e protótipos de SK. Conclusão. Embora não houvesse associação entre genótipos de HHV-8 e presença ou estadio de SK, o subgenótipo B1 foi significativamente relacionado ao melhor prognóstico de SK. Alguns recombinantes foram observados no locus K1 de HHV-8 em indivíduos do grupo 2 sem SK. A presença de SNPs em regiões codificadoras de miR12-12 e miR12-10 predominou em sequências de HHV-8 de indivíduos com SK, grupo 1, e protótipos de SK epidêmico, endêmico e clássico. A escoha de primers foi importante para garantir a amplificação de todos os genótipos e amplo perfil de subgenotipos de HHV-8. / HHV-8 (Human Herpes Virus 8) is the etiological agent of Kaposi\'s sarcoma (KS). Unlike other herpesviruses, the distribution of HHV-8 is not so ubiquitous around the world. There are seven major HHV-8 genotypes, according to the variability pattern of the ORF K1: A, B, C, D, E, F and Z. Studies on the genetic variability of HHV-8 may help to better understand the pathogenic potential of HHV-8 genotypes and their functional genotypic variations. Data on the genetic variability of HHV-8 in Brazil, where KS is associated with HIV infected people, remain scarce. To our knowledge, this is the first study comparing the genetic variability of HHV-8 among HIV-infected individuals with KS and without KS in Brazil. Objective. The study aimed to analyze the genetic variability of HHV-8 among HIV-infected individuals with and without KS. Casuistry and Methods. HHV-8 DNA sequences were obtained from samples of cryopreserved peripheral blood mononuclear cells from 37 individuals infected with HIV-KS (group 1); and saliva from individuals without KS (group 2) who were selected by means of detection of positive DNA/ORF73/HHV-8 from a total of 751 individuals. Demographic and clinical data (stage and progression of KS), as well as laboratory parameters were characterized. Molecular analysis and phylogenetic reconstructions were based on sequences of the ORFs K1 and/or K12 of HHV-8. Results. K1 and/or K12 DNA sequences of HHV-8 were obtained from 75 subjects, 34 from group 1 and 41 from group 2. The primer system used was able to detect the genotypes A, B, C, F and a wide profile of HHV- 8 K1 subgenotypes. Data showed no association of genotypes with the occurrence of KS or with visceral KS either. However, subgenotype B1 predominated in individuals who did not report any progression of KS (p=0.04). Subgenotypes B1 and C3 were equally prevalent in both groups. Genotype A frequencies were 24 % and 12.2% and genotypes B and C were 34.1 and 35.3 % in groups 1 and 2, respectively. We also described here for the first time the genotype F of HHV-8 in Brazil. A wide profile of subgenotypes C (C1, C2, C3, C5 and C7) in the group without KS was found. HHV-8 K1 DNA sequences of group 2 (7%) belonging to subgenotypes C5 and C7 were confirmed as recombinants. Our findings did not show virus variability in the same patient in samples collected at different times or from different biological material in the eight cases studied here. There was no statistical difference regarding the presence/absence of a given SNP from locus K12 between groups with and without KS. However, there were a total of 6/59 polymorphic sites in coding regions of miRNA, 70% of which present only in the HHV-8 DNA sequence of group with KS and KS prototypes. Conclusion. Although there was no association between HHV-8 genotypes and the presence of KS and KS clinical stage, subgenotype B1 was significantly related to the absence of progression of KS. Some recombinants in K1/HHV-8 locus were observed in the group without KS. The presence of SNPs in coding regions of miR12-12 and miR12- 10 predominated in sequences of HHV- 8 of SK cases (group 1) and of epidemic, endemic and classic KS prototypes. The choice of primers was essential to ensure amplification of all HHV- 8 genotypes and wide profile de subgenotypes.

Thesis (Ph. D.)--University of Virginia, 2007. / Title from title page. Includes bibliographical references. Also available online through Digital Dissertations.

O HHV-8 (herpesvírus 8 humano) é o agente etiológico do sarcoma de Kaposi (SK). Diferentemente dos outros herpesvírus, o HHV-8 é distribuído de modo não ubíquo ao redor do mundo. São sete os principais genótipos de HHV-8, de acordo com o padrão de variabilidade da ORF K1: A, B, C, D, E, F e Z. Estudos da variabilidade genética do HHV-8 poderão trazer melhores interpretações sobre o potencial patogênico dos genótipos de HHV-8 e das variações genotípicas funcionais. Dados sobre a variabilidade genética do HHV-8 no Brasil, em que o SK é associado ao HIV, permanecem escassos. Pelo nosso conhecimento, esse é o primeiro estudo que compara a variabilidade genética de HHV-8 em indivíduos infectados por HIV com SK e sem SK no Brasil. Objetivo. O estudo visou analisar a variabilidade genética do HHV-8 entre indivíduos infectados por HIV com SK e sem histórico de SK. Métodos. Sequências de DNA de HHV-8 foram investigadas em amostras criopreservadas de células mononucleares do sangue periférico a partir de 37 indivíduos infectados por HIV com SK (grupo 1); e de amostras de saliva de indivíduos sem SK (grupo 2), as quais foram selecionadas por meio da detecção positiva de DNA/ORF73/HHV-8 a partir de um total de 751 indivíduos. Dados demográficos e clínicos do estadio e evolução do SK, assim como parâmetros laboratoriais foram caracterizados. As análises moleculares e reconstruções filogenéticas foram baseadas nas ORFs K1 e K12 do HHV-8. Resultados. Foram obtidas sequências de DNA dos loci K1 e/ou K12 de 75 indivíduos, 34 indivíduos do grupo 1 e 41 do grupo 2. O sistema de primers empregado foi capaz de detectar os genótipos A, B, C, F e amplo perfil de subgenótipos de K1/HHV-8. Os dados não mostraram associação de genótipos de HHV-8 com a presença de SK ou estadio de SK. Todavia, o subgenótipo B1 predominou naqueles em que não houve registro de piora de SK (p=0,04). Os subgenótipos B1 e C3 foram igualmente predominantes em ambos os grupos. As frequências do genótipos A foram de 24% e 12,2% e dos genótipos B e C foram de 34,1 e 35,3%, nos grupos 1 e 2, respectivamente. O genótipo F foi descrito pela primeira no Brasil, um caso de cada grupo. Um amplo perfil de subgenótipos de C no grupo 2 sem SK foi encontrado (C1, C2, C3, C5 e C7). Subgenótipos K1 C5 e C7, exclusivos do grupo 2 (7%), foram confirmados como recombinantes. Não houve variabilidade genotípica de HHV-8 em amostras biológicas diferentes do mesmo indivíduo em oito casos estudados. Sítios polimórficos (6/59) em regiões codificadoras de miRNA do locus K12 foram observados, sendo 70% presentes exclusivamente em sequências de HHV-8 do grupo com SK e protótipos de SK. Conclusão. Embora não houvesse associação entre genótipos de HHV-8 e presença ou estadio de SK, o subgenótipo B1 foi significativamente relacionado ao melhor prognóstico de SK. Alguns recombinantes foram observados no locus K1 de HHV-8 em indivíduos do grupo 2 sem SK. A presença de SNPs em regiões codificadoras de miR12-12 e miR12-10 predominou em sequências de HHV-8 de indivíduos com SK, grupo 1, e protótipos de SK epidêmico, endêmico e clássico. A escoha de primers foi importante para garantir a amplificação de todos os genótipos e amplo perfil de subgenotipos de HHV-8. / HHV-8 (Human Herpes Virus 8) is the etiological agent of Kaposi\'s sarcoma (KS). Unlike other herpesviruses, the distribution of HHV-8 is not so ubiquitous around the world. There are seven major HHV-8 genotypes, according to the variability pattern of the ORF K1: A, B, C, D, E, F and Z. Studies on the genetic variability of HHV-8 may help to better understand the pathogenic potential of HHV-8 genotypes and their functional genotypic variations. Data on the genetic variability of HHV-8 in Brazil, where KS is associated with HIV infected people, remain scarce. To our knowledge, this is the first study comparing the genetic variability of HHV-8 among HIV-infected individuals with KS and without KS in Brazil. Objective. The study aimed to analyze the genetic variability of HHV-8 among HIV-infected individuals with and without KS. Casuistry and Methods. HHV-8 DNA sequences were obtained from samples of cryopreserved peripheral blood mononuclear cells from 37 individuals infected with HIV-KS (group 1); and saliva from individuals without KS (group 2) who were selected by means of detection of positive DNA/ORF73/HHV-8 from a total of 751 individuals. Demographic and clinical data (stage and progression of KS), as well as laboratory parameters were characterized. Molecular analysis and phylogenetic reconstructions were based on sequences of the ORFs K1 and/or K12 of HHV-8. Results. K1 and/or K12 DNA sequences of HHV-8 were obtained from 75 subjects, 34 from group 1 and 41 from group 2. The primer system used was able to detect the genotypes A, B, C, F and a wide profile of HHV- 8 K1 subgenotypes. Data showed no association of genotypes with the occurrence of KS or with visceral KS either. However, subgenotype B1 predominated in individuals who did not report any progression of KS (p=0.04). Subgenotypes B1 and C3 were equally prevalent in both groups. Genotype A frequencies were 24 % and 12.2% and genotypes B and C were 34.1 and 35.3 % in groups 1 and 2, respectively. We also described here for the first time the genotype F of HHV-8 in Brazil. A wide profile of subgenotypes C (C1, C2, C3, C5 and C7) in the group without KS was found. HHV-8 K1 DNA sequences of group 2 (7%) belonging to subgenotypes C5 and C7 were confirmed as recombinants. Our findings did not show virus variability in the same patient in samples collected at different times or from different biological material in the eight cases studied here. There was no statistical difference regarding the presence/absence of a given SNP from locus K12 between groups with and without KS. However, there were a total of 6/59 polymorphic sites in coding regions of miRNA, 70% of which present only in the HHV-8 DNA sequence of group with KS and KS prototypes. Conclusion. Although there was no association between HHV-8 genotypes and the presence of KS and KS clinical stage, subgenotype B1 was significantly related to the absence of progression of KS. Some recombinants in K1/HHV-8 locus were observed in the group without KS. The presence of SNPs in coding regions of miR12-12 and miR12- 10 predominated in sequences of HHV- 8 of SK cases (group 1) and of epidemic, endemic and classic KS prototypes. The choice of primers was essential to ensure amplification of all HHV- 8 genotypes and wide profile de subgenotypes.

Xiao Wei. / Thesis submitted in: December 2002. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references (leaves 95-109). / Abstracts in English and Chinese. / ABSTRACT --- p.i / ABSTRACT (CHINESE VERSION) --- p.iii / ACKNOWLEDGEMENTS --- p.v / TABLE OF CONTENTS --- p.vii / LIST OF TABLES --- p.ix / LIST OF FIGURES --- p.x / LIST OF ABBREVIATIONS --- p.xii / Chapter Chapter One --- Introduction --- p.1 / Chapter 1.1 --- Discovery of HHV8 --- p.2 / Chapter 1.2 --- Biology of HHV8 --- p.3 / Chapter 1.2.1 --- Morphology --- p.3 / Chapter 1.2.2 --- Classification --- p.3 / Chapter 1.2.3 --- Cell culture --- p.4 / Chapter 1.2.4 --- Latent and lytic life cycle --- p.4 / Chapter 1.2.5 --- Genome organisation --- p.5 / Chapter 1.2.6 --- Strain variability --- p.6 / Chapter 1.3 --- Disease association of HHV8 --- p.8 / Chapter 1.3.1 --- Kaposi's sarcoma --- p.8 / Chapter 1.3.2 --- Other associated diseases --- p.10 / Chapter 1.4 --- Tropism of HHV8 --- p.11 / Chapter 1.5 --- Epidemiology of HHV8 --- p.13 / Chapter 1.5.1 --- Geographic distribution --- p.13 / Chapter 1.5.2 --- Age distribution --- p.15 / Chapter 1.5.3 --- HIV-infected individuals without Kaposi's sarcoma --- p.16 / Chapter 1.5.4 --- Bone marrow transplant and blood transfusion recipients --- p.19 / Chapter 1.5.5 --- Sexually transmitted disease clinic attendees --- p.18 / Chapter 1.5.6 --- HIV-negative intravenous drug users --- p.19 / Chapter 1.6 --- Transmission of HHV8 --- p.20 / Chapter 1.7 --- Methods for HHV8 antibody detection --- p.23 / Chapter 1.7.1 --- Antibodies against latent antigens --- p.23 / Chapter 1.7.2 --- Antibodies against lytic antigens --- p.24 / Chapter 1.7.3 --- Comparison between assays --- p.25 / Chapter 1.8 --- Project design --- p.26 / Chapter Chapter Two --- Methods and Materials --- p.29 / Chapter 2.1 --- Study I. Seroprevalence of HHV8 in Hong Kong --- p.30 / Chapter 2.1.1 --- Study population --- p.30 / Chapter 2.1.2 --- Source of HHV8 antigens --- p.32 / Chapter 2.1.3 --- Positive and negative controls --- p.34 / Chapter 2.1.4 --- Procedures for immunofluorescence assay --- p.34 / Chapter 2.1.5 --- Statistical methods --- p.36 / Chapter 2.2 --- Study II. Prevalence of HHV8 DNA in cervical scrapes --- p.36 / Chapter 2.2.1 --- Study population --- p.36 / Chapter 2.2.2 --- Preparation of cell lysate --- p.38 / Chapter 2.2.3 --- PCR amplification for human beta-actin gene --- p.38 / Chapter 2.2.4 --- PCR for HHV8 DNA --- p.41 / Chapter 2.2.5 --- Statistical methods --- p.45 / Chapter 2.3 --- Study III. HHV8 ORF 26 nucleotide sequence determination --- p.45 / Chapter 2.3.1 --- Study samples --- p.45 / Chapter 2.3.2 --- Sequencing method --- p.46 / Chapter 2.3.3 --- Nucleotide sequence data analysis --- p.49 / Chapter Chapter Three --- Result --- p.51 / Chapter 3.1 --- Study I. Seroprevalence of HHV8 in Hong Kong populations --- p.52 / Chapter 3.1.1 --- Seroprevalence of HHV8 in reference group --- p.52 / Chapter 3.1.2 --- HIV-negative intravenous drug users --- p.55 / Chapter 3.1.3 --- HIV-positive individuals without Kaposi's sarcoma --- p.57 / Chapter 3.1.4 --- Transfusion-dependent patients --- p.59 / Chapter 3.2 --- Study II. Prevalence of HHV8 DNA in cervical samples --- p.61 / Chapter 3.2.1 --- Optimisation of beta-actin PCR --- p.61 / Chapter 3.2.2 --- Optimisation of HHV8 ORF 26 PCR --- p.61 / Chapter 3.2.3 --- Analytical sensitivity of HHV8 nested PCR --- p.67 / Chapter 3.2.4 --- General female population --- p.67 / Chapter 3.2.5 --- Sexually transmitted disease clinic attendees --- p.73 / Chapter 3.3 --- Study III. Sequence variation of HHV8 ORF 26 fragment --- p.76 / Chapter Chapter Four --- Discussion --- p.84 / Chapter 4.1 --- Study I. Seroprevalence of HHV8 in Hong Kong populations --- p.85 / Chapter 4.1.1 --- Distribution of HHV8 in reference group --- p.86 / Chapter 4.1.2 --- HIV-positive individuals without Kaposi's sarcoma --- p.87 / Chapter 4.1.3 --- HIV-negative intravenous drug users --- p.88 / Chapter 4.1.4 --- Transfusion dependent patients --- p.88 / Chapter 4.2 --- Study II. Prevalence of HHV8 DNA in cervical samples --- p.89 / Chapter 4.2.1 --- General female population --- p.90 / Chapter 4.2.2 --- Sexual transmitted disease clinic attendees --- p.90 / Chapter 4.3 --- Study III. HHV8 ORF 26 nucleotide sequence variation --- p.91 / Chapter 4.3.1 --- Sequence variability --- p.91 / Chapter 4.3.2 --- HHV8 ORF26 genotyping --- p.91 / Chapter 4.3.3 --- Comparison with HHV8 isolates from other populations --- p.92 / Chapter 4.4 --- Conclusions --- p.93 / REFERENCES --- p.95