Tierärztl. Hochsch., Diss., 2004--Hannover.

Made available in DSpace on 2014-06-11T19:33:26Z (GMT). No. of bitstreams: 0 Previous issue date: 2008-07-04Bitstream added on 2014-06-13T18:45:08Z : No. of bitstreams: 1 silva_sb_dr_botfmvz.pdf: 1670441 bytes, checksum: a3ebab095a955dd5ab0d977a8cafe405 (MD5) / Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) / O tumor venéreo transmissível (TVT) caracteriza-se por ser uma neoplasia de origem controversa. Baseado nos resultados obtidos anteriormente por nosso grupo de pesquisa, dos três tipos morfológicos do TVT, os de morfologia plasmocitóide são mais agressivos. De acordo com as características morfológicas do TVT, a resposta à terapia é variável e sabendo-se que a utilização da survivina, bem como da caspase-3, do Bcl-6, do Bcl-2, do Ki-67 e da COX-2 são importantes para auxiliar no prognóstico, no manejo do paciente e na monitoração da doença durante e após a terapia, este projeto visou, além de estudos citogenéticos, observar se há diferenças na expressão dos imunomarcadores acima citados, nos TVTs plasmocitóides e linfocitóides. Para tal, foram utilizados 30 cães atendidos no Hospital Veterinário da FMVZ-UNESP, Campus de Botucatu. Devido baixa incidência de TVT linfocitóide no HV-UNESP-Botucatu, não foi possível fazer correlações entre os tipos plasmocitóide e linfocitóide. A positividade da survivina variou de 96,15 a 100% em 200 células contadas e, em dois casos, a marcação da survivina foi citoplasmática e nuclear, nos outros casos a marcação foi apenas citoplasmática. A marcação pelo anticorpo anti-caspase-3 nos 30 casos de TVT foi baixa, variando de 0 a 6,5% de positividade em 200 células contadas, o que sugere um comportamento agressivo do TVT. Neste estudo, o TVT não expressou Bcl-2 nem Bcl-6 nas tentativas de imunomarcação. Dos 30 casos de TVT que foi realizado marcação pelo Ki-67, em 21 casos foi possível a contagem de células e houve uma média de positividade de 15,57%. Houve expressão de COX-2 em todos os casos e os valores variaram de 90,66 a 100% de positividade em 200 células contadas, exceto por um caso que apresentou 24,50% de positividade. A distribuição... / The characterization of transmissible venereal tumor (TVT) as neoplastic in origin is controversial. Based on results obtained previously by our research group, of the three TVT morphological types, those of plasmocytoid morphology are most aggressive. According to morphological characteristics of TVT, response to therapy is variable; and given that using survivin, caspase-3, Bcl-6, Bcl-2, Ki-67 and COX-2 to aid in prognosis, patient management and the monitoring of this disease during and after therapy, this project aimed, besides cytogenetic studies, to observe whether there are differences in expression of the aforementioned immunomarkers, in plasmocytoid TVTs and lymphocytoids. For this, 30 dogs, treated at the Veterinary Hospital of FMVZ-UNESP, Campus at Botucatu, were utilized without restriction as to sex, breed or age, with cytological diagnosis of transmissible venereal tumor. There was prevalence of males; age varied from 1 to 14 years, the majority were SRD dogs and localization was preferentially genital. Due to low lymphocytoid TVT incidence (5.91%) at HV-UNESP–Botucatu, it was not possible to make correlations between plasmocytoid and lymphcytoid types. Positivity of survivin varied from 96.15 to 100% in the 200 cells counted and, in two cases, marking for survivin was cytoplasmic and nuclear, while in other cases marking was only cytoplasmic. Survivin is associated with more aggressive behavior and shorter lifespan in the majority of tumors. In men, highly aggressive neoplasias present lower cytoplasmic expression of caspase-3 than low-grade neoplasias. Marking by anti-caspase-3 antibody in 30 TVT cases was low, varying from 0 to 6.5% positiviity in 200 cells counted, which suggests aggressive TVT behavior. In our study, TVT did not express Bcl-2 or Bcl-6... (Complete abstract click electronic access below)

Orientador: Noeme Sousa Rocha / Banca: Alessandre Hataka / Banca: Ana Maria Barros Soares / Banca: Mirela Tinucci Costa / Banca: Julio Lopes Sequeira / Resumo: Foram analisados 132 casos de tumor venéreo transmissível (TVT) de ocorrência natural, atendidos no Hospital Veterinário de Botucatu, considerando aspectos clínicos e epidemiológicos. Os pacientes eram, em sua maioria, sem raça definida e com idade variando entre um e 18 anos, com maior freqüência na idade de quatro anos. A localização mais freqüente foi a genital, seguida pela nasal; 25% dos pacientes apresentavam metástases. Estas ocorreram mais freqüentemente na pele (31% das metástases), seguida pela localização mamária, em fêmeas, e em linfonodos, nos machos. Foram colhidas amostras de 188 tumores para avaliação citológica por microscopia ótica, microscopia eletrônica de transmissão, imunofenotipagem e estimação de danos no DNA pelo teste do cometa. As massas foram avaliadas de acordo com a localização, em genitais ou extragenitais, com o comportamento biológico, em primárias e não primárias (metastáticas ou recorrentes) e, ainda, de acordo com o tamanho e tempo de evolução clínica. A avaliação citológica incluiu a classificação de acordo com o padrão morfológico predominante, em linfocitóide (18,4%), plasmocitóide (52,5%) ou misto (29,1%). As amostras extragenitais e não primárias foram predominantemente do padrão plasmocitóide. Foram observadas as características de malignidade gerais, citoplasmáticas, nucleares e nucleolares apresentadas. Anisocitose, anisocariose e macrocariose foram observadas em todos os padrões citomorfológicos, assim como a presença de vacúolos citoplasmáticos, basofilia e eosinofilia citoplasmáticas e corpúsculos linfoglandulares. As características citoplasmáticas de malignidade observadas com maior freqüência foram projeções citoplasmáticas e espessamento... (Resumo completo, clicar acesso eletrônico abaixo) / Abstract: A hundred and thirty-two dogs with naturally transplanted transmissible venereal tumor (TVT) from ambulatory service of the Veterinary Hospital UNESP, Botucatu, were analyzed for epidemiological and clinical aspects. The animals were predominantly mongrel dogs, with age range between one and eighteen years, and mean of four years. The most usual location was genital, followed by nasal; 25% presents metastasis, the cutaneous location being the most frequent, followed by lymph nodes, in males, and mammary, in females. A sample of 188 tumors were collected for cytologic evaluation in optical microscopy, transmission electron microscopy, immunophenotyping and measure of DNA damage by the Comet test. The masses were classified by location as genital or extragenital, by biological behavior as primary or non-primary (metastastatic or recurrent), and by size and time of clinical evolution. The cytologic evaluation included cytomorphological classification in lymphocyte-like (18.4%), plasma-cell-like (52.5%) and mixed pattern (29.1%). Extragenital and non-primary tumors were essentially plasma cell-like. Malignancy features were noted as general, cytoplasmatic, nuclear and nucleolar. Anisocytosis, anisocariosis and macrocariosis were present in all cytomorphological patterns, as well as cytoplasmatic vacuoles, basophilic and eosinophilic tintorial properties, and lymphoglandular bodies. Cytoplasmatic malignancy criteria most frequently observed were cytoplasmatic projections and cellular membrane thickness. Cells resembling a racket were related to lymphocyte-like pattern. Nuclear buds, perinuclear halos, hyperchromatic nuclei, pseudoinclusions, nuclear membrane thickness and mitosis (normal and abnormal), binucleation, and nuclear lobulations (pleomorphic nuclei) were the most frequents nuclear malignancy criteria. The lymphocyte-like pattern was less related... (Complete abstract click electronic address below) / Doutor

Orientador: Konradin Metze / Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas / Made available in DSpace on 2018-08-11T22:07:37Z (GMT). No. of bitstreams: 1 Scarpelli_KarimeCury_M.pdf: 4019689 bytes, checksum: 327500d1e9eaf9d7ba789fda03cc4064 (MD5) Previous issue date: 2008 / Mestrado / Ciencias Biomedicas / Mestre em Ciências Médicas

Les similitudes entre les mécanismes neurotoxiques responsables des encéphalopathies spongiformes Transmissibles (EST) et des synucléinoapthies, ainsi que la présence concomitante des formes pathologiques de la protéine prion et de l’α-synucléine au sein d’une même maladie neurodégénérative sont deux observations qui nous ont conduits à étudier les relations existant potentiellement entre les altérations moléculaires de l’α-synucléine et les maladies à prion. Après avoir développé des anticorps monoclonaux en immunisant avec de l’α-synucléine recombinante humaine des souris n’exprimant pas de façon endogène cet immunogène, nous avons caractérisé les altérations moléculaires de l’α-synucléine apparaissant conjointement à une symptomatologie motrice sévère lors du vieillissement de souris transgéniques (TgM83) surexprimant l’α-synucléine humaine mutée en A53T. Les essais d’inoculation intracérébrale de souris TgM83 par différentes souches de prion ont mis en évidence que la transmission de l’encéphalopathie spongiforme bovine de type H permet de déclencher chez ces animaux une maladie à prion de façon concomitante au développement d’altérations moléculaires de l’α-synucléine. Enfin, l’importante accélération de la pathologie liée a l’α-synucléine observée chez des souris TgM83 ayant été inoculées par des tissus contenant des formes altérées de l’α-synucléine, constitue un résultat soutenant le fait que la pathologie liée a l’α-synucléine serait capable de se propager expérimentalement de proche en proche, comme la protéine prion pathologique au cours des EST / The overlap of neurotoxic mecanisms involved in prion diseases and synucleinopathies, and the concomitant detection of pathological forms of prion and α-synuclein in a same neurodegenerative disease, raise questions about the existence of potential relationship between α‐synuclein molecular alteration and prion diseases. First, we developed monoclonal antibodies by immunizing mice presenting a spontaneous deletion of the α-synuclein gene with human recombinant α‐synuclein. Then, we characterized the molecular alterations appearing jointly to clinical signs during the aging of a transgenic mouse model of synucleinopathies (TgM83), overexpressing human A53T α‐synuclein. Then, an approach routinely done in the field of prion was used to trigger a synucleinopathy alongside a prion disease. For this purpose, TgM83 mice were inoculated intracerebrally by three different prion strains : transmission of H-type bovine spongiform encephalopathy allows the onset of a prion disease concomitantly to the α‐synuclein pathology developed by the TgM83 mouse model. Finally, intracerebral inoculation of TgM83 mice with brain homogenates from symptomatic mice affected by a synucleinopathy triggers an important acceleration of the α‐synuclein pathology, resulting in the early onset of motor clinical signs associated with molecular alterations of α-synuclein. These data suggest that α-synuclein alterations can be experimentally transmitted from one mouse to another, supporting the idea that, far from being confined to the transmissible spongiform encephalopathies, the « prion-like » propagation of misfolded neuronal proteins might occur in synucleinopathies

Transmissible spongiform encephalopathies (TSEs) are a group of fatal neurodegenerative diseases that are characterised by long incubation periods, protein aggregation and vacuolation. During TSE pathogenesis the normal, cellular prion protein, (PrPC), which is encoded by the gene PRNP, misfolds and accumulates as abnormal disease associated prion protein, (PrPSc) within the central nervous system. Variants of the Prion protein gene are associated with susceptibility to TSE disease. For example sheep scrapie disease is modulated by several PRNP alleles, with certain alleles carried by susceptible animals being different from those carried by resistant animals. The mechanisms linking PRNP genetics and disease is poorly understood but may involve protein sequence, PrPC expression levels, and possibly differences in protein processing. Post-translational modification of PrPC leads to specific cleavage (alpha cleavage) between amino acids 115/116 of ovine PrP, producing two fragments C1 and N1. Cleavage of PrP may occur as a protective mechanism, as a response to changes in the cellular environment or as a feature of an as yet unknown biological function. In the context of TSEs, alpha cleavage may inadvertently provide a protective role by reducing available PrPC protein for conversion into PrPSc, assuming that the C1 fragment would be an inefficient substrate for conversion, the opposite theory was also proposed. The former hypothesis became the focus of this present study, with the idea that total full-length PrPC, total C1 or the ratio between full-length PrPC and C1 may be linked to differences in scrapie susceptibility. To investigate these aims the C1 fragment was measured as a percentage of total PrPC in different PRNP genotypes with varying degrees of susceptibility to scrapie and in different brain regions. This study found that PrPC alpha cleavage increased during development from the new born lamb to the adult sheep, which may have consequences for the susceptibility differences related to age. There are also variations in the amount of alpha cleavage between brain regions such as cortex and medulla that may influence scrapie strain targeting. Overall the amount of the C1 fragment in the different brain areas varied as much as 10x (range 5% to 60%). There was a significant difference in the ratio of C1 to the other PrPC forms between two PRNP genotype groups carrying the VRQ and ARQ allele but there was no correlation between C1 level and scrapie susceptibility or scrapie incubation period in our scrapie models. Alpha cleavage of PrPC also occurs in various transgenic mouse models expressing different ruminant PrP sequences. In PrPC over-expressing transgenic mouse models a higher ratio of C1 was observed, this may suggest a link between PrPC expression levels and alpha cleavage. Transgenic mice are therefore important models to further investigate the link between PrPC biology and scrapie disease phenotype. In conclusion, this thesis has shown for the first time that certain ovine PRNP alleles can influence alpha cleavage of the PrPC protein; however it appears not to be a significant indicator of TSE disease susceptibility in sheep.

Transmissible spongiform encephalopathies (TSEs), such as scrapie and variant Creutzfeldt-Jakob disease are infectious, fatal, neurodegenerative diseases. Following peripheral infection TSE agents usually accumulate in lymhoid tissues before spreading to the central nervous system. In mice, follicular dendritic cells (FDCs) expressing the host prion protein (PrPC) are essential for scrapie agent accumulation in lymphoid tissues. The accumulation of the scrapie agent on FDCs is critical for the efficient spread of infection to the brain. However, it is unknown whether FDCs themselves actively replicate the scrapie agent, or simply accumulate it following production by other cells types such as neurones, lymphocytes or other stromal cell populations. To definitively address this issue a transgenic mouse model was created in which PrPC is switched on or off exclusively on FDCs. Expression of cre-recombinase (Cre) under the action of cell-specific gene promoters can be used to induce or delete the expression of a target gene in specific cell populations. In this model, Cre expression is driven by the complement receptor type 2 gene (Cr2/CD21) which is expressed by FDCs and mature B lymphocytes. Characterisation of the CD21-cre mouse line was achieved by crossing with a ROSA26 reporter strain. The CD21-cre mouse line was subsequently crossed with floxed-PrP mouse lines to produce compound transgenic mouse lines in which PrPC expression was switched on or off, only in FDCs. Cre expression by B lymphocytes was eliminated by γ-irradiation and grafting recipient mice with Cre-deficient bone marrow. Immunohistochemical analysis confirmed the expression PrPC had been switched on or off exclusively on FDCs. Subsequently, the mice were challenged with scrapie by intra-peritoneal injection to determine the precise role of FDCs in the accumulation of scrapie in lymphoid tissues. Switching off PrPC expression exclusively on FDCs prevented the accumulation of TSE agent specific disease-associated PrPSc in the spleen after i.p inoculation. Conversely, in mice in which PrPC was expressed only on FDC, successful replication of the agent occurred on the FDC network in the spleen. Taken together, these data show PrPC-expressing FDCs alone are sufficient to support the accumulation of the scrapie agent within lymphoid tissues. Furthermore, these data suggest FDC replicate the TSE agent and do not simply accumulate it following synthesis by other cell types.

Transmissible spongiform encephalopathies (TSEs) are a group of fatal, neurodegenerative diseases that can affect both humans and animals. TSEs can be sporadic, familial, or acquired diseases. The prion hypothesis states that a misfolded form of the host glycoprotein, PrPC, acts as the infectious agent in TSE disease. The misfolded form, PrPSc, is increased in β-sheet content, detergent insoluble and partially resistant to proteinase K (PK) digestion. Based on the prion hypothesis, most current post-mortem diagnostic tests rely on the presence of PrPSc as indicative of TSE disease. However, recently experimental cases of TSE disease have been identified where no PrPSc deposition is evident. One example of this is a murine transgenic model of Gerstmann Sträussler Scheinker (GSS) disease. GSS is a familial TSE disease, caused by a number of different mutations in human PrP including a point mutation from proline to leucine at residue 102. A murine model of GSS disease, produced through gene-targeting, contains the same point mutation at the equivalent residue, 101, in murine PrP. These mice do not develop spontaneous disease during their lifespan, but when inoculated intra-cerebrally with either human P102L GSS (101LL/GSS) or hamster 263K scrapie (101LL/263K); develop a clinical disease and vacuolar TSE-related pathology. Upon biochemical and immunohistochemical analysis, the brain tissues of these clinically ill mice contain little or no detectable PrPSc. However titration experiments have previously shown infectivity titres of 107-109IU/g of brain tissue. Standard PK digestion (at 37°C), NaPTA precipitation and isolation of PrPSc through detergent insolubility and differential centrifugation all confirmed the observation of little or no detectable PK-resistant PrP (PrP-res) in the 101LL/GSS and 101LL/263K brain tissues, despite the high levels of TSE infectivity. The presence of PrPSc and/or TSE infectivity in the spleen during disease pathogenesis is dependent upon TSE agent strain and host species. Previous studies utilising wild-type mice infected with ME7, have shown that the levels of infectivity observed in spleen tissue are 2- 3log10 lower than those observed in the brain tissue of the same mice. However, experiments conducted as part of this thesis showed that sub-passage of both the brain and spleen tissue from clinically ill 101LL/GSS and 101LL/263K mice into 101LL mice by intra-cerebral inoculation result in short incubation periods, indicating that infectivity levels were similarly high in both tissues. Biochemical analysis of the primary spleen tissue identified the presence of PrP-res, albeit at lower levels than those observed in wild-type spleens infected with a standard laboratory TSE strain, ME7 or 79A. However, the presence of PrP-res indicates that the spleen has a role in disease pathogenesis, which will require further investigation. Additionally, the spleen tissue maintains the discrepancy between PrP-res and TSE infectivity that is observed in the brain tissue of these models and further questions the prion hypothesis. As little or no PrP-res was detectable in the brain tissues of 101LL/GSS and 101LL/263K mice by standard biochemical and immunohistochemical techniques, it was hypothesised that an in vitro amplification technique, protein misfolding cyclic amplification (PMCA) could amplify PrPSc to detectable levels. A series of optimisation experiments were performed to produce a reliable positive control for amplification of mouse PrPSc from a standard laboratory mouse TSE strain, 79A or ME7, with a normal wild-type mouse brain homogenate substrate. While a wide range of technical and experimental conditions were investigated, consistent and reproducible amplification of mouse PrPSc was not achieved and therefore amplification of PrPSc from 101LL/GSS and 101LL/263K tissues could not be performed as interpretation of results would be complicated without the presence of a positive control. Previous research has shown that while other commercial assays, e.g. TeSeE (BioRad), identified tissues from these models as borderline positive or negative for TSE disease, one TSE diagnostic assay, the IDEXX HerdChek kit, that utilises the Seprion ligand, identified both the brain and spleen tissue from 101LL/GSS and 101LL/263K clinical mice as positive for TSE disease. In order to identify if TSE infectivity is associated with the target of the Seprion ligand, brain tissue homogenates from 101LL/GSS, 101LL/263K and a positive control wild-type/79A homogenate were depleted of the Seprion ligand target utilising a PAD-beads kit (Microsens Biotechnologies), which incorporates the Seprion ligand as the capture agent, in combination with magnetic beads. Upon inoculation, a single depletion of the homogenates produced no significant reduction in incubation period to clinical disease in either the depleted homogenates or the wash buffers produced, in comparison to a non-depleted brain homogenate. This result indicates that a single depletion with the Seprion ligand, did not remove enough of the aggregated protein to significantly alter the level of infectivity in the depleted homogenate and that any infectious agent, which was initially bound to the Seprion ligand due to non-specific interactions, was then released during the wash steps of the procedure. Proteomic differences between all components produced during a single depletion of an infected brain homogenate, wild-type/79A, or a normal uninfected brain homogenate were assessed to potentially identify the target of the Seprion ligand. In conclusion, these murine models of TSE disease, 101LL/GSS and 101LL/263K, which contain both high infectivity levels with little or no PrP-res in the brain tissue and similar high levels of infectivity with low levels of PrP-res in the spleen, questions the accepted correlation between levels of infectivity and PrP-res or PrPSc as proposed by the prion hypothesis. It is hypothesised that either an alternative form of PrP, which has not yet been identified is the infectious agent in these disease models, or that the TSE infectious agent is a component which associates with PrPSc rather than being PrPSc itself. The eventual identification of the infectious agent present in these unusual disease models will increase our understanding of these diseases, potentially offer improved diagnostics for infectivity, and perhaps identify novel therapeutic targets.

The Transmissible Spongiform Encephalopathies (TSEs) or “prion” diseases are a group of fatal neurodegenerative diseases the aetiology of which is not fully understood. These diseases are characterised by a number of pathological changes in the central nervous system (CNS) including; vacuolation of the neuropil, gliosis and deposition of PrPSc; the abnormal form of the host glycoprotein PrP. Although the major pathology in these diseases is associated with the CNS the immune system is central to the pathogenesis of many natural and experimental TSEs including natural scrapie in sheep, chronic wasting disease in free ranging and captive deer and variant CJD (vCJD) in humans. Unlike many infectious diseases where deficiencies in immune function are opportunistic for the invading pathogen a competent immune system is required for efficient TSE infection via peripheral routes. As infection of the lymphoid tissues in many TSEs can occur many months before the detection of infectivity in the CNS, the determination of those cells in the lymphoid system has been the focus of much research and a number of studies now point towards the importance of the follicular dendritic cell (FDC), a long-lived radio resistant cell, in TSE pathogenesis. The involvement of FDCs in peripheral TSE pathogenesis relates to the inability of ionising radiation to influence pathogenesis, the association of PrP protein with FDCs in both uninfected and infected lymphoid tissues, and the demonstration that TSE pathogenesis is severely impaired in mice devoid of these cells. The aims of this thesis were to further understand the role of FDCs in the pathogenesis of a range of mouse-adapted experimental TSE strains and to determine if peripherally acquired TSE infections are influenced by host age or by stimulation of the immune system. Using chimaeric mouse models where a mismatch in the expression of PrP protein between FDCs and lymphoid/myeloid cells was produced, further evidence for a critical role for in the pathogenesis of the ME7 TSE strain was produced. Although these findings produced strong evidence that FDCs were important for the ME7 strain the possibility that different TSE strains may target different cell types in the peripheral lymphoid system was explored using a range of mice with specific immunological defects. Infection of these mice with several experimental TSE strains showed that the presence of mature FDCs was also important for the pathogenesis of the strains tested. Clinical cases of vCJD have been confined almost exclusively to young adults, although the reasons behind this apparent age-related susceptibility are not fully understood. The capacity of the immune system to mediate immune responses to pathogens declines with age as a result of impaired lymphocyte and FDC function. As FDCs are critically involved in the pathogenesis of many TSEs, including vCJD, it was hypothesised that an aging immune system may impair disease pathogenesis. Peripheral infection of senescent mice failed to produce clinical disease during lifespan, although evidence of disease transmission, was detected in a proportion of aged mice. These findings demonstrate that this inefficient disease transmission, as a consequence of age, may lead to considerable levels of sub-clinical disease within the population. Finally the influence of immune system stimulation, by the generation of a humoral immune response, on peripheral TSE pathogenesis was investigated. These findings demonstrated that immunisation can influence pathogenesis, but only during the early stages of infection prior to spread to the CNS. These data imply that modulation of the immune system does not alter TSE pathogenesis once disease has been initiated in the CNS. Finally, these studies have found some preliminary evidence that TSE infection may induce FDC activation suggesting that TSE infection may influence the immune response. Together, these data show that a functional immune system and specifically, the presence of mature FDCs, are central to the pathogenesis of peripherally acquired TSE infections.

Vivenciando no dia-dia que o número de casos das infecções sexualmente transmitidas (IST) e da aids vem aumentando em todo mundo e na África, principalmente na população jovem, é imprescindível a tomada de medidas preventivas para seu controle. Assim, desenvolvemos este estudo do tipo descritivo transversal com o objetivo de identificar os conhecimentos e risco para IST e aids entre estudantes de nível médio. O referencial teórico foi o “o Modelo de Crenças em Saúde" que compõe as dimensões de susceptibilidade percebida, severidade percebida, benefícios percebidos e barreiras percebidas. A população estudada constituiu-se de 385 estudantes, pertencente a três escolas de ensino médio. A coleta dos dados ocorreu no período de maio a junho de 2004 e os dados analisados quali-quantitativamente. Para análise quantitativa, os dados foram codificados e registrados numa base de dados e tratados em estatística descritiva. Quanto aos dados qualitativos foram tratados com base no Método de BARDIN (1977), sendo analisados e interpretados utilizando o referencial teórico do Modelo de Crenças em saúde de Rosenstock (1974a). Quanto às características demográficas, 59,9% dos estudantes eram do sexo feminino, 49,1% do sexo masculino, a idade variou entre 13 e 45 anos, 83,9% referiram ser solteiros. Com relação às práticas sexuais, 77,4% dos alunos investigados eram sexualmente ativos, sendo que 51,6% mencionaram nunca terem usado ou usado algumas vezes o preservativo; 66,7% referiram nunca terem usado e ou usado algumas vezes o preservativo com o parceiro fixo; 55,3% perceberam o risco de adquirir as IST/ aids. Quanto as informações acerca das IST /aids 95,8% dos respondentes já ouviram falar da aids, 95,3% de sífilis, 92,9% de gonorréia, 58,1% de hepatite B, sendo que 90,1% dos informantes tiveram como fonte de informação a televisão, 85,4% o radio, 78,4% os amigos, 74,5% os livros, 65,9% o jornal. Quanto à susceptibilidade, através dos enunciados dos participantes referiram perceber a sua vulnerabilidade e risco em adquirir IST/ aids. No tocante à severidade percebida, os estudantes associaram a aids a doença sem cura e à morte. Os informantes demonstram terem tido conhecimentos sobre os modos de transmissão e medidas preventivas das principais IST, porém bastante limitados. Sobre benefícios percebidos, foram mencionados pelos investigados alguns fatores facilitadores do uso do preservativo, como meio de prevenção e método contraceptivo, para além da citação de algumas barreiras percebidas como, a dificuldade no uso do preservativo. Diante destas situações, é imprescindível a implementação de programas educativos de prevenção com vistas à promoção da saúde. / Experiencing in everyday life that the number of cases with sexually transmissible infections (STI) and aids is increasing all over the world and in Africa, mainly in the juvenile population, preventive measures are essential for their control. Thus, this escriptive and cross-sectional study aimed to identify knowledge and risk of STI and aids among secondary students. The theoretical reference framework was the “Health Belief Model", which covers the dimensions of perceived susceptibility, perceived severity, perceived benefits and perceived barriers. The study population consisted of 385 students from three secondary schools. Data were collected in May and June and subject to qualitative and quantitative analysis. With a view to quantitative analysis, data were coded, registered in a database and treated by means of descriptive statistics. In qualitative analysis, data were treated on the basis of BARDIN’s method (1977) and analyzed and interpreted through the theoretical reference framework of ROSENSTOCK’s (1974 a) Health Belief Model. With respect to demographic characteristics, 59.9% of the students were women and 49.1% men, ages ranged from 13 to 45 years and 83.9% mentioned they were single. What sexual practices is concerned, 77.4% of the investigated students were sexually active; 51.6% indicated they had used the condom never or a few times; 66.7% mentioned they had used the condom never or a few times with their fixed partner; 55.3% perceived the risk of acquiring STI/aids. As to information about STI/aids, 95.8% of the respondents had already heard about aids, 95.3% about syphilis, 92.9% about gonorrhea and 58.1% about hepatitis B. 90.1% of the informants obtained their information from television, 85.4% from radio, 78.4% from friends, 74.5% from books and 65.9% from newspapers. With respect to susceptibility, the participants’ discourse indicated they perceived their vulnerability and risk of acquiring STI/aids. What perceived severity is concerned, students associated aids to an incurable disease and to death. The informants demonstrated their knowledge about transmission modes and measures to prevent the main STI, although quite limited. As to perceived benefits, the participants mentioned some facilitating factors of condom use as a means of prevention and contraceptive method. Furthermore, they indicated some perceived barriers as difficulties for condom use. In light of these situations, educational prevention programs have to be implemented with a view to health promotion.