Submitted by Caroline Falcao (caroline.rfalcao@ufpe.br) on 2017-04-06T17:05:06Z No. of bitstreams: 2 license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) 2012-dissertação-EvônioBarrosCampeloJunior.pdf: 1895687 bytes, checksum: 45a651f79dfdcc2ce3328e3201f91911 (MD5) / Made available in DSpace on 2017-04-06T17:05:06Z (GMT). No. of bitstreams: 2 license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) 2012-dissertação-EvônioBarrosCampeloJunior.pdf: 1895687 bytes, checksum: 45a651f79dfdcc2ce3328e3201f91911 (MD5) Previous issue date: 2012-12-27 / Desde 1967, momento do seu surgimento no mundo científico, o GB vírus C (GBV-C) permanece conhecido como vírus indolente, todavia não obstante,pesquisas têm reveladoadespeito da ausência de vinculação do GBV-C com alguma doença, que a associação entre o GBV-C e HIV promove uma progressão mais lenta na doença pelo HIV em indivíduos coinfectados. Essa interaçãoteriacomo mecanismo a competição com o vírus da imunodeficiência humana (HIV) na ligação aos correceptores CCR5 e CXCR4 edessa formatem sidoobjeto de análise com intuito de promover a compreensão da dinâmica imunológica do HIV. Portanto, admitindoaimportância do GBV-C na pandemia de HIV/aids, esse trabalho determinou a prevalência da infecção pelo GBV-Cem pessoas vivendo com HIV/aids acompanhadas noServiço de Doenças Infecciosas e Parasitárias do HC-UFPE, verificou o perfil sócio-demográficoda população, identificou fatores de riscoe fez a associação entre a contagem de linfócitos TCD4 e a infecção peloGBV-C.Representou um estudode corte transversal, analisado como caso-controle, no qual a presença do GBV-C RNA foi investigada em249 pessoas vivendo com HIV/aids, de acordo com a demanda espontânea do ambulatório de Doenças Infecciosas e Parasitárias HC-UFPE,no período de junho adezembro de 2011 e que preenchiam os critérios de inclusão. Foram coletadas amostras de sangue de cada participante, os quais também assinaram um termo de consentimento livre e esclarecido e responderam questionário elaborado especificamente para a pesquisa. Adetecção do RNA do GBV-C foi realizado por PCR (Reação em CadeiadaPolimerase).O resultado da pesquisa indicou uma prevalência de 24,3%, compatível com outros estudos nacionais e internacionais,indicou o perfil sócio-demográfico, apontoua via parenteral como a mais prevalente na infecção pelo GBV-Ceassociou a contagem de linfócitos T CD4 e a infecção peloGBV-C,em pessoas vivendo com HIV/aids na fase inicial da infecção. Também a discussão apontou a necessidade de realização de trabalhos de coorte para melhor compreensão de fatores implicados na transmissão do GBV-C. / Since 1967, the time of its emergence in the scientific world, the GB virus C (GBV-C) virus remains known as indolent, but nevertheless, research has revealed despite the absence of binding of GBV-C with some disease, the association between GBV-C and HIV promotes a slower progression in HIV disease in coinfected individuals. This interaction mechanism would compete with the human immunodeficiency virus (HIV) in binding to CCR5 and CXCR4coreceptorsand thus has been the subject of analysis in order to promote understanding of the dynamics of HIV immune.Therefore, admitting the importance of GBV-C in the HIV/AIDS pandemic, this study estimated the prevalence of GBV-C infection in people living with HIV/AIDS followed in the Service of Infectious and Parasitic HC-UFPE, there the socio-demographic profile of the population, identified risk factors and made the association between CD4 count and GBV-C infection.Represented a cross-sectional study, analyzed as case-control study in which the presence of GBV-C RNA was investigated in 249 people living with HIV/AIDSat the outpatient of Infectious and Parasitic Diseases HC-UFPE, between June and December 2011 and who met the inclusion criteria. Blood samples were collected from each participant, who also signed a consent form and a questionnaire developed specifically for research. Detection of GBV-C RNA was performed by PCR (Polymerase Chain Reaction).The result of the survey indicated a prevalence of 24.3%, consistent with other national and international studies, said the socio-demographic profile, pointed the parenteral route as the most prevalent in the GBV-C infection and associated with CD4 count and GBV-C infection in people living with HIV/AIDS in the early phase of infection. Also the discussion pointed to the need to perform cohort studiesto better understand the factorsinvolvedinthe transmission of GBV-C.

This research aims to investigate how socio-economic factors influence the vulnerability of women to engage in sexual services and potential trafficking in Gauteng, South Africa. This province is South Africa’s most prosperous one with an enormous flow of migrants and is therefore of interest to investigate. Moreover, it is certainly intriguing to examine more into South Africa's measures against human trafficking; additionally, it is interesting to investigate further here because of the signature by South Africa of the Palermo protocol and look further and deeper into if this signature has helped decrease the crime. This research seeks to untangle the complex web of factors contributing to vulnerability. By examining the socio-economic and potential other dimensions of human trafficking in South Africa, the aim is to gain a deeper understanding of how these factors interact, perpetuating a cycle of victimization and further raise crucial awareness of the subject. This research has adopted a abductive qualitative content-desk study to be most appropriate for the research and in order to do at least harm as possible to the victims by using already published documents and reports. Furthermore, theories and approaches such as Radical Feminist Theory, Rational Choice Theory, Human Rights-Based Approach and V-Dem Approach have been used in order to answer the objective as successfully as possible. The conclusion of this study points at the fact that women’s lower societal position, along with patriarchal influences, cultural practices and state corruption impact human trafficking and the vulnerability for women making them fall a victim of the crime. Recommendations that have been made in the paper are further studies on the subject and an idea of universal legislation regarding human trafficking, which could be similar to Agenda 2030 and finally some urgent measures in Gauteng.

Human Pegivirus (HPgV; originally called GB virus C) is an RNA virus within the Pegivirus genus of the Flaviviridae that commonly causes persistent infection. Worldwide, approximately 750 million people are infected with HPgV. No causal association between HPgV and disease has been identified; however, several studies found an association between persistent HPgV infection and prolonged survival of HIV-infected individuals that appears to be related to a reduction in host immune activation. HPgV replicates well in vivo (>10 million genome copies/ml plasma) but grows poorly in vitro and systems to study this virus are limited. Consequently, mechanisms of viral persistence and host immune modulation remain poorly characterized, and the primary permissive cell type(s) has not yet been identified. The overall goals of my thesis were to characterize HPgV tropism, effects of HPgV infection on host immune response and mechanisms of viral persistence. Previous studies found HPgV RNA in T and B lymphocytes and ex vivo infected lymphocytes produce viral particles. To further characterize HPgV tropism, we quantified HPgV RNA in highly purified CD4+ and CD8+ T cells, including naïve, central memory, and effector memory populations, and in B cells (CD19+), NK cells (CD56+) cells and monocytes (CD14+) obtained from persistently infected humans using real time RT-PCR. Single genome sequencing was performed on virus within individual cell types to estimate genetic diversity among cell populations. HPgV RNA was present in CD4+ and CD8+ T lymphocytes (9 of 9 subjects), B lymphocytes (7 of 9), NK cells and monocytes (both 4 of 5). HPgV RNA levels were higher in naïve (CD45RA+) CD4+ cells than in central memory and effector memory cells (p<0.01). HPgV sequences were highly conserved between patients (0.117 ± 0.02 substitutions per site) and within subjects (0.006 ± 0.003 substitutions per site). The non-synonymous/synonymous substitution ratio was 0.07 suggesting low selective pressure. CFSE-labeled HPgV RNA-positive microvesicles (SEV) from serum delivered CFSE to uninfected monocytes, NK cells, T and B lymphocytes, and HPgV RNA was transferred to peripheral blood mononuclear cells (PBMCs) with evidence of subsequent viral replication. Thus, HPgV RNA-positive SEV may contribute to delivery of HPgV to PBMCs in vivo, explaining the apparent broad tropism of this persistent human RNA virus. Although HPgV infection reduces NK cell activation in HIV-infected individuals, the mechanism by which this occurs is not characterized. We studied HPgV effects on NK cell non-cytolytic function in HIV-infected people by measuring expression of IL-12 induced interferon gamma (IFNg) and cytolytic function by measuring K562 target-cell induced CD107a and granzyme B. IFNg expression was lower in HIV-HPgV co-infected subjects compared to HIV mono-infected subjects treated with combination antiretroviral therapy (p=0.02). In contrast, cytolytic NK cell functions were not affected by HPgV. Inhibition of IFNg was due to inhibition of tyrosine kinase (Tyk2) by HPgV envelope protein E2. HPgV positive human sera, extracellular vesicles containing E2 protein, recombinant E2 protein and synthetic E2 peptides containing a predicted Tyk2 interacting motif inhibited IL-12-mediated IFNg release by NK cells. Thus HPgV-E2 inhibits NK cell non-cytolytic functions. Inhibition of NK cell-induced proinflammatory/antiviral cytokines may contribute to both HPgV's ability to persist with high viral loads (>10 million genome copies/ml plasma) and reduce immune cell activation. Understanding mechanisms by which HPgV alters immune activation may contribute towards novel immunomodulatory therapies to treat HIV and inflammatory diseases.

Sexual harassment in Cairo's public spaces is a symptom of infringement upon women’s rights in Egypt. Which is ingrained in the socioeconomic context, cultural, and traditional norms of the society. This grant proposal and background research proposes the construction of an extensive anti-sexual harassment infrastructure base in Egypt. The infrastructure platform is built on an evidence-based strategy and guided by recognized best practices. The platform is geared towards alleviating the symptoms of sexual harassment in Cairo's public spaces by constructing the urgently required, but currently missing, national mechanisms which are necessary to prevent, report, prosecute, and provide survivor services for victims of sexual harassment. In addition to the immediate perceived causes and effects of sexual harassment in Egypt there is also deep-rooted ecological factors that must be considered. These ecological factors, on an individual level, both biological and personal, include the fact that approximately 97% of Egyptian girls witness female gentile mutilation (FGM) in a publicized fashion between the ages 4 & 10. The practice of FGM, may have indoctrinated little boys and little girls, from an early age, that it is socially acceptable to inflict physical and psychological pain and suffering upon the female. FGM carried out at this age, as opposed to male circumcision, which is carried out during early infancy, allows for the neurological trauma that is generated leaves a lasting imprint. On a family level, 49% of adolescent rural girls marry before the age of 16. Marriage at this age is internationally recognized as sexual abuse, yet is common practice in rural Egypt. This practice sets a negative precedence for accommodating women's voices, this precedence may last a lifetime. On a community level, based on the most recent statistically significant surveys, approximately 70% of youth, both male and female, believe women are subordinate to men. This dictates that male must exercise control of resources and decision-making. And, that a girl must do what her brother says, even if he is younger. On a society level, 86% of surveyed male respondents indicated they would do “nothing” to try and stop sexual harassment if they witnessed it happening to a stranger in public. And finally, even from the moment they are born, the large majority of women in Egypt, because of religious dictates, inherit only half of what a male sibling would. Ceteris paribus, women in Egypt, just by virtue of being female, based on inheritance, are only able to afford a living standard, for themselves and their family that is only half as high as that of their male siblings living standard, unless of course their male sibling is benevolent enough to bestow upon them his own wealth. All these factors invariable, where they apply, undermine women's status in society and negatively impact attitudes of protecting women from harm and violence, in all its forms, which includes sexual harassment in public spaces.

GB virus C (GBV-C) is a common, apathogenic virus that can inhibit human immunodeficiency virus (HIV) replication in vitro. Persistent coinfection with GBV-C has been associated with improved survival among HIV-infected adults while loss of GBV-C viremia has been associated with poor survival. If GBV-C does inhibit HIV replication, it is possible that GBV-C infection may reduce mother-to-child-transmission (MTCT) of HIV. This study investigated whether maternal or infant GBV-C infection was associated with reduced MTCT of HIV infection. The study population consisted of 1,783 pregnant women from three Bangkok perinatal HIV transmission studies (1992-94, 1996-7, 1999-2004). We tested plasma collected at delivery for GBV-C RNA, GBV-C antibody, and GBV-C viral genotype. If maternal GBV-C RNA was detected, the four- or six-month infant specimen was tested for GBV-C RNA. Rates of MTCT of HIV in GBV-C-infected and GBV-C-uninfected women and infants were compared using multiple logistic regression as were associations with MTCT of GBV-C and prevalence of GBV-C infection. The prevalence of GBV-C infection (i.e. presence of RNA or antibody) was 33% among HIV-infected women and 15% among HIV-uninfected women. Forty-one percent of GBV-C-RNA-positive women transmitted GBV-C to their infants. Only two of 101 (2.0%) GBV-C-RNA-positive infants acquired HIV infection compared to 162 (13.2%) of 1,232 of GBV-C-RNA-negative infants (RR 0.15, p<0.0001). This association remained after adjustment for maternal HIV viral load, antiretroviral prophylaxis, CD4+ count and other covariates. MTCT of HIV was not associated with presence of maternal GBV-C RNA or maternal GBV-C antibody. Maternal receipt of antiretroviral therapy was associated with increased MTCT of GBV-C, as was high GBV-C viral load, vaginal delivery and absence of infant HIV infection. GBV-C infection among women was independently associated with more than one lifetime sexual partner, intravenous drug use and HIV-infection. We observed a higher prevalence of GBV-C infection among HIV-infected compared to HIV-uninfected pregnant women in Thailand, likely due to common risk factors. Antiretroviral therapy appears to increase MTCT of GBV-C. Infant GBV-C acquisition, but not maternal GBV-C infection, was significantly associated with reduced MTCT of HIV. Mechanisms for these later two associations are unknown. / Bhanich Supapol W, Remis RS, Raboud J, Millson M, Tappero J, Kaul R, Kulkarni P, McConnell MS, Mock PA, Culnane M, McNicholl J, Roongpisuthipong A, Chotpitayasunondh T, Shaffer N, Butera S. 2008. Reduced mother-to-child transmission of HIV associated with infant but not maternal GB virus C infection. J Infect Dis 197(10):1369-1377. Bhanich Supapol W, Remis RS, Raboud J, Millson M, Tappero JW, Kaul R, Kulkarni P, McConnell MS, Mock PA, McNicholl JM, Vanprarar N, Asavapiriayanont S, Shaffer N, Butera ST. 2009. Mother-to-child transmission of GB virus C in a cohort of women coinfected with GB virus C and HIV in Bangkok, Thailand. J Infect Dis 200:227-235.

GB virus C (GBV-C) is a common, apathogenic virus that can inhibit human immunodeficiency virus (HIV) replication in vitro. Persistent coinfection with GBV-C has been associated with improved survival among HIV-infected adults while loss of GBV-C viremia has been associated with poor survival. If GBV-C does inhibit HIV replication, it is possible that GBV-C infection may reduce mother-to-child-transmission (MTCT) of HIV. This study investigated whether maternal or infant GBV-C infection was associated with reduced MTCT of HIV infection. The study population consisted of 1,783 pregnant women from three Bangkok perinatal HIV transmission studies (1992-94, 1996-7, 1999-2004). We tested plasma collected at delivery for GBV-C RNA, GBV-C antibody, and GBV-C viral genotype. If maternal GBV-C RNA was detected, the four- or six-month infant specimen was tested for GBV-C RNA. Rates of MTCT of HIV in GBV-C-infected and GBV-C-uninfected women and infants were compared using multiple logistic regression as were associations with MTCT of GBV-C and prevalence of GBV-C infection. The prevalence of GBV-C infection (i.e. presence of RNA or antibody) was 33% among HIV-infected women and 15% among HIV-uninfected women. Forty-one percent of GBV-C-RNA-positive women transmitted GBV-C to their infants. Only two of 101 (2.0%) GBV-C-RNA-positive infants acquired HIV infection compared to 162 (13.2%) of 1,232 of GBV-C-RNA-negative infants (RR 0.15, p<0.0001). This association remained after adjustment for maternal HIV viral load, antiretroviral prophylaxis, CD4+ count and other covariates. MTCT of HIV was not associated with presence of maternal GBV-C RNA or maternal GBV-C antibody. Maternal receipt of antiretroviral therapy was associated with increased MTCT of GBV-C, as was high GBV-C viral load, vaginal delivery and absence of infant HIV infection. GBV-C infection among women was independently associated with more than one lifetime sexual partner, intravenous drug use and HIV-infection. We observed a higher prevalence of GBV-C infection among HIV-infected compared to HIV-uninfected pregnant women in Thailand, likely due to common risk factors. Antiretroviral therapy appears to increase MTCT of GBV-C. Infant GBV-C acquisition, but not maternal GBV-C infection, was significantly associated with reduced MTCT of HIV. Mechanisms for these later two associations are unknown. / Bhanich Supapol W, Remis RS, Raboud J, Millson M, Tappero J, Kaul R, Kulkarni P, McConnell MS, Mock PA, Culnane M, McNicholl J, Roongpisuthipong A, Chotpitayasunondh T, Shaffer N, Butera S. 2008. Reduced mother-to-child transmission of HIV associated with infant but not maternal GB virus C infection. J Infect Dis 197(10):1369-1377. Bhanich Supapol W, Remis RS, Raboud J, Millson M, Tappero JW, Kaul R, Kulkarni P, McConnell MS, Mock PA, McNicholl JM, Vanprarar N, Asavapiriayanont S, Shaffer N, Butera ST. 2009. Mother-to-child transmission of GB virus C in a cohort of women coinfected with GB virus C and HIV in Bangkok, Thailand. J Infect Dis 200:227-235.

Made available in DSpace on 2014-12-17T14:03:41Z (GMT). No. of bitstreams: 1 MagdaFDC.pdf: 1127289 bytes, checksum: e8f867febd165499040c2d067e137209 (MD5) Previous issue date: 2005-02-23 / Coordena??o de Aperfei?oamento de Pessoal de N?vel Superior / No Brasil, a Leishmania chagasi ? a esp?cie que causa a leishmaniose visceral (LV). A Leishmania tem a capacidade de causar um estado de parasitismo intracelular nos macr?fagos. A destrui??o dos parasitas, tanto no in?cio da infec??o, como na fase tardia, depende da ativa??o de macr?fagos por citocinas. Leishmania evade da resposta imunol?gica do hospedeiro e sobrevive sem o macr?fago durante a doen?a. A infec??o por Leishmania chagasi pode induzir hepatites, independente da co-infec??o com v?rus de hepatites (A-E). A infec??o por GBV-C est? sendo associada com prote??o ? progress?o da doen?a, e aumento da sobreviv?ncia em indiv?duos HIV-1 soro positivos. Neste estudo, objetivou-se avaliar se a infec??o subcl?nica por Leishmania Chagasi depende da modula??o de outros pat?genos dentre eles o v?rus da hepatite G. Um total de 322 indiv?duos, residentes em ?reas end?micas para LV e um total de 82 pacientes de banco de sangue participaram deste estudo. Usando a t?cnica de RT-PCR seguida do sequenciamento do fragmento da PCR da regi?o 5 NTR e submetendo-se os dados obtidos a um banco de genes (BLAST) para uma an?lise comparativa de seq??ncias do Genebank obteve-se uma identidade de 98% do clone GBV1 com o isolado 34,5 da hepatite G v?rus, 5 -UTR, parcial seq??ncia (AF489995. 1). Dentre os fen?tipos avaliados, DTH+, DTH-, e LV constatou-se uma maior preval?ncia do fen?tipo DTH+ nos indiv?duos GBV-C positivos se comparados com DTH- e LV( DTH+ 57%, DTH- 10%,LV 33%).Um subgrupo de 4 indiv?duos de fen?tipo LV e positivos para GBV-C no ano de 1996 foi submetido a novas coletas em 2004. An?lises bioqu?micas de enzimas,AST,ALT , YGT,LDH, Fosfatasse Alcalina e bilirrubinas foram realizadas, bem como, dosagens de marcadores de outras hepatites.Constatou-se que as dosagens bioqu?micas n?o sofreram altera??es significativas e que os pacientes positivos no ano de 1996 para GBV-C; no ano de 2004 apresentaram HVAG positivo, com marcadores negativos, para hepatite B e C. Sugerimos uma poss?vel intera??o do v?rus da hepatite G com pacientes do fen?tipo LV e DTH+, com poss?vel ativa??o da resposta imune celular

GB virus C (GBV-C) is a lymphotropic human virus which was recently assigned to a new genus Pegivirus within the Flaviviridae family. GBV-C infection is found worldwide, and viremia prevalence is about 1% to 4% in healthy blood donors and up to 42% in HIV-infected individuals. In clinical studies, GBV-C coinfection is associated with prolonged survival of HIV-infected individuals. GBV-C infection modestly alters T cell homeostasis in vivo through various mechanisms, including modulation of chemokine and cytokine release and receptor expression, and by diminution of T cell activation, proliferation and apoptosis, all of which may contribute to improved HIV clinical outcomes. This thesis explores the interrelationship between GBV-C infection and immunoactivation and identifies potential mechanisms by which GBV-C reduces immunoactivation. Chronic HIV infection is associated with persistent immunoactivation which contributes to the immune dysfunction. In particular, T cell activation supports HIV replication and correlates with HIV viral load (VL). Persistent immunoactivation also contributes to the depletion of uninfected bystander cells by mechanisms of activation induced cell death (AICD). Although treatment with combination antiretroviral therapy (cART) reduces HIV VL, T cell activation does not return to levels found in HIVuninfected individuals. Sustained immunoactivation is also associated with lower virological response to cART suggesting therapies to reduce immunoactivation in combination with cART may benefit HIV-infected individuals. Since GBV-C infection is associated with reduced immunoactivation, understanding mechanisms by which GBV-C modulates these signaling pathways may provide insights into novel approaches to treat HIV infection and chronic immunoactivation. The effect of GBV-C infection on T cell activation and IL-2 signaling pathways were studied in a cohort of HIV-positive individuals. GBV-C viremic HIV positive individuals on cART have reduced T cell activation which was significantly associated with higher percentage of immunomodulatory CD3 +CD4-CD8-T cells. Ex vivo GBV-C infection was associated with reduced lymphocyte proliferation in response to IL-2, lower frequency of reactivation of latent HIV and protection against AICD. In vitro expression of GBV-C envelope glycoprotein E2 in CD4+ T cell lines inhibited T cell receptor (TCR) induced IL-2 secretion and inhibited IL-2 signaling pathways. This effect was mediated at least in part by reducing activation of lymphocyte specific tyrosine kinase (Lck). Through deletion mutagenesis, the inhibitory motif within the viral protein was mapped to a region that contains a predicted Lck substrate, a highly conserved tyrosine at position 87 (Y87). Lck phosphorylated GBV-C E2 protein in vitro and mutation of Y87 residue abolished the inhibitory effects of E2 protein. Synthetic peptides containing this inhibitory motif competed for Lck phosphorylation and inhibited TCR signaling in primary human T cells. The number of GBV-C infected T cells was found to be low in vivo, yet GBV-C infection reduced global TCR signaling. GBV-C RNA and E2 protein were detected in extracellular microvesicles purified from GBV-C infected human serum or the culture supernatant of E2 expressing cells, and these microvesicles inhibited TCR signaling in uninfected bystander T cells. Together, these data identify a novel mechanism by which GBV-C infection leads to global reduction in T cell activation and IL-2 signaling in the infected host, and provide a working model in which the viral envelope glycoprotein serves as a substrate for Lck and competes for Lck phosphorylation in the infected T cells and in uninfected bystander T cells.

Magister Artium (Development Studies) - MA(DVS) / Democratic South Africa was based on a constitution that is meant to have democratic values that promote human dignity and non-discrimination. Such democratic values were put in place to ensure that the human rights violations that took place in apartheid South Africa would not take place again and that everyone, especially those previously oppressed are treated with respect and dignity. Despite the guaranteed human rights that are supposed to apply to everyone, lesbians and other members of the LGBT community still face discrimination because of their sexual orientation. Nell and Shaprito (2011, p12) point out that “in stark contrast with constitutional guarantees of freedom and human rights for all, research indicates that homophobic victimization is an endemic part of the South African landscape”.

Intimate partner violence was one of the major social issues during the COVID-19 pandemic in Greece. During the pandemic, the cases of intimate partner violence seemed to increase in terms of women coming forward to report the abuse but also in media exposure. This study aims to explore the key factors for the rise in intimate partner violence numbers, as well as the effect it had on victims of intimate partner violence. PRISMA protocol was utilized to analyze the data collected. From the theoretical framework of feminist theory, three key factors for the increase of intimate partner violence in Greece were identified: lack of governmental incentives and action plans to prevent IPV and aid victims of IPV, the macho and impunity culture of Greek society, and police and legislation as patriarchal institutions.