Instituto de Medicina Tropical - IMT
URI Permanente desta comunidade
O Instituto de Medicina Tropical de São Paulo (IMTSP) foi criado em 1959 para desenvolver pesquisas e fornecer subsídio científico e tecnológico para o diagnóstico, tratamento, controle e prevenção das doenças tropicais e grandes endemias do nosso país. Durante 40 anos o IMTSP esteve ligado à Faculdade de Medicina da Universidade de São Paulo, mas, a partir de dezembro de 2000, tornou-se uma unidade autônoma, um Instituto Especializado da USP.
As pesquisas no IMTSP abrangem diversos aspectos da ciência médica nessa área, como o diagnóstico, a patogenia e o tratamento, voltando-se também para as questões epidemiológicas e de prevenção. O IMTSP, além de instituição de pesquisa, também é um centro de formação, de aperfeiçoamento e de prestação de serviços especializados na área: possui um curso regular de extensão sobre saúde dos viajantes, para a comunidade externa e no 2º semestre de 2007 teve o curso de Pós-Graduação em Medicina Tropical e Saúde Internacional aprovado pela Capes.
Site oficial: http://www.imt.usp.br/
As pesquisas no IMTSP abrangem diversos aspectos da ciência médica nessa área, como o diagnóstico, a patogenia e o tratamento, voltando-se também para as questões epidemiológicas e de prevenção. O IMTSP, além de instituição de pesquisa, também é um centro de formação, de aperfeiçoamento e de prestação de serviços especializados na área: possui um curso regular de extensão sobre saúde dos viajantes, para a comunidade externa e no 2º semestre de 2007 teve o curso de Pós-Graduação em Medicina Tropical e Saúde Internacional aprovado pela Capes.
Site oficial: http://www.imt.usp.br/
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- Instituto de Medicina Tropical - IMT
- Instituto de Medicina Tropical - IMT
- Instituto de Medicina Tropical - IMT
Submissões Recentes
Core Promoter and Pre-Core Variants of the Hepatitis B Virus (HBV) Are Frequent in Chronic Hepatitis B HBeAg-Negative Patients Infected by Genotypes A and D
(2023) REUTER, Tania; GOMES-GOUVEA, Michele Soares; CHUFFI, Samira; DUQUE, Ulisses Horst; PERINI, Waltesia; AZEVEDO, Raymundo Soares; PINHO, Joao Renato Rebello; LEWIS-XIMENEZ, Lia L.; VILLAR, Livia Melo; ESPUL, Carlos Alberto; PUJOL, Flor H.; ROMAN, Sonia
In Brazil, hepatitis B virus endemicity is low, moderate, or high in some areas, such as Espirito Santo State in the southeast region. In this study, we intend to characterize the basal core promoter (BCP) and pre-core region (PC) variants and their association with clinical/epidemiological disease patterns in patients infected with genotypes A and D. The study included 116 chronic hepatitis B patients from Espirito Santo State, Southeast Brazil, infected with genotypes A and D. Basal core promoter (BCP) and pre-core mutations were analyzed in these patients. The frequency of BCP and PC mutations was compared with age, HBeAg status, HBV genotype and subgenotype, HBV-DNA level, clinical classification, and transmission route. HBeAg-negative status was found in 101 (87.1%) patients: 87 (75.0%) were infected with genotype A (A1 = 85; A2 = 2) and 29 (25.0%) were infected with genotype D (D3 = 24; D4 = 3; D2 = 2). BCP + PC variants altogether were more frequent (48.1%) in genotype D than in genotype A strains (6.0%) (p < 0.001). When this evaluation was performed considering the cases that presented only the A1762T and/or G1764A (BCP) mutations, it was observed that the frequency was higher in genotype A (67.5%) compared to genotype D (7.4%) (p < 0.001). On the other hand, considering the samples with mutations only in positions G1896A and/or G1899A (PC), the frequency was higher in genotype D (75.8%) than in genotype A (6.9%) (p < 0.001). Interestingly, HBV DNA was lower than 2000 IU/mL especially when both BCP/PC mutations were present (p < 0.001) or when only PC mutations were detected (p = 0.047), reinforcing their role in viral replication.
Intranasal Liposomal Formulation of Spike Protein Adjuvanted with CpG Protects and Boosts Heterologous Immunity of hACE2 Transgenic Mice to SARS-CoV-2 Infection
(2023) RUSSO, Momtchilo; MENDES-CORREA, Maria Cassia; LINS, Bruna B.; KERSTEN, Victor; PERNAMBUCO, Paulo C. A.; MARTINS, Toni Ricardo; TOZETTO-MENDOZA, Tania Regina; BOAS, Lucy Santos Vilas; GOMES, Brisa Moreira; DATI, Livia Mendonca Munhoz; DUARTE-NETO, Amaro Nunes; REIGADO, Gustavo Roncoli; FREDERICO, Ana Beatriz T.; CUNHA, Danielle R. de A.; PAULA, Anderson Vicente de; SILVA, Jose Igor G. da; VASCONCELOS, Carlos F. Moreira; CHAMBERGO, Felipe S.; NUNES, Viviane Abreu; BOM, Ana Paula Dinis Ano; CASTILHO, Leda R.; MARTINS, Rodrigo A. P.; HIRATA, Mario Hiroyuki; MIROTTI, Luciana; TRIPP, Ralph A.
Mucosal vaccination appears to be suitable to protect against SARS-CoV-2 infection. In this study, we tested an intranasal mucosal vaccine candidate for COVID-19 that consisted of a cationic liposome containing a trimeric SARS-CoV-2 spike protein and CpG-ODNs, a Toll-like receptor 9 agonist, as an adjuvant. In vitro and in vivo experiments indicated the absence of toxicity following the intranasal administration of this vaccine formulation. First, we found that subcutaneous or intranasal vaccination protected hACE-2 transgenic mice from infection with the wild-type (Wuhan) SARS-CoV-2 strain, as shown by weight loss and mortality indicators. However, when compared with subcutaneous administration, the intranasal route was more effective in the pulmonary clearance of the virus and induced higher neutralizing antibodies and anti-S IgA titers. In addition, the intranasal vaccination afforded protection against gamma, delta, and omicron virus variants of concern. Furthermore, the intranasal vaccine formulation was superior to intramuscular vaccination with a recombinant, replication-deficient chimpanzee adenovirus vector encoding the SARS-CoV-2 spike glycoprotein (Oxford/AstraZeneca) in terms of virus lung clearance and production of neutralizing antibodies in serum and bronchial alveolar lavage (BAL). Finally, the intranasal liposomal formulation boosted heterologous immunity induced by previous intramuscular vaccination with the Oxford/AstraZeneca vaccine, which was more robust than homologous immunity.
Encephalopathy Caused by Human Parvovirus B19 Genotype 1 Associated with Haemophilus influenzae Meningitis in a Newborn
(2023) FERREIRA, Noely Evangelista; COSTA, Antonio C. da; KALLAS, Esper G.; SILVEIRA, Cassia G. T.; OLIVEIRA, Ana Carolina S. de; HONORATO, Layla; PAIAO, Heuder G. O.; LIMA, Silvia H.; VASCONCELOS, Dewton de M.; CORTES, Marina F.; COSTA, Silvia F.; MENDOZA, Tania R. T.; GOMES, Helio R.; WITKIN, Steven S.; MENDES-CORREA, Maria C.
Parvovirus B19 infection is associated with a wide range of clinical manifestations, from asymptomatic to severe neurological disorders. Its major clinical symptoms, fever and rash, are common to multiple viruses, and laboratory tests to detect B19 are frequently not available. Thus, the impact of B19 on public health remains unclear. We report the case of a 38-day old girl admitted to Sao Paulo Clinical Hospital, Brazil, with an initial diagnosis of bacterial meningitis, seizures, and acute hydrocephalus. Antibiotic therapy was maintained for one week after admission and discontinued after negative laboratory results were obtained. Nine days after symptoms onset, a cerebral spinal fluid (CSF) sample revealed persistent pleocytosis. The complete B19 complete genome was subsequently identified in her CSF by a metagenomic next-generation sequencing approach. This report highlights the possible involvement of B19 in the occurrence of acute neurological manifestations and emphasizes that its possible involvement might be better revealed by the use of metagenomic technology to detect viral agents in clinical situations of unknown or uncertain etiology.
Imiquimod chemoprophylaxis for field cancerization in xeroderma pigmentosum patients-A prospective study
(2023) ROCHA, Lilian Kelly Faria Licariao; FERREIRA, Paula; GIANOTTI, Marcelo A.; AVANCINI, Joao; MENCK, Carlos F. M.; CASTRO, Ligia P.; OLIVEIRA, Zilda Najjar Prado de; RIVITTI, Maria C.; SAMORANO, Luciana P.; PEREIRA, Naiura Vieira; FESTA NETO, Cyro
Coronary Inflammation by Computed Tomography Pericoronary Fat Attenuation and Increased Cytokines in Young Male Anabolic Androgenic Steroid Users
(2023) SOUZA, Francis Ribeiro de; ROCHITTE, Carlos E.; SILVA, Douglas Carli; SAMPAIO, Barbara; PASSARELLI, Marisa; SANTOS, Marcelo R. dos; FONSECA, Guilherme W.; BATTAGLIA-FILHO, Antonio Carlos; CORREA, Kelly; VAL, Renata Margarida do; YONAMINE, Mauricio; PEREIRA, Rosa Maria R.; NEGRAO, Carlos Eduardo; KALIL-FILHO, Roberto; ALVES, Maria Janieire de Nazare Nunes
Background: Anabolic androgenic steroid (AAS) abuse has been associated with coronary artery disease (CAD). Pericoronary fat attenuation (pFA) is a marker of coronary inflammation, which is key in the atherosclerotic process.Objective: To evaluate pFA and inflammatory profile in AAS users.Methods: Twenty strength-trained AAS users (AASU), 20 AAS nonusers (AASNU), and 10 sedentary controls (SC) were evaluated. Coronary inflammation was evaluated by mean pericoronary fat attenuation (mPFA) in the right coronary artery (RCA), left anterior descending coronary artery (LAD), and left circumflex (LCx). Interleukin (IL)-1 (IL-1), IL-6, IL-10, and TNF-alpha were evaluated by optical density (OD) in a spectrophotometer with a 450 nm filter. P<0.05 indicated statistical significance.Results: AASU had higher mPFA in the RCA (-65.87 [70.51-60.70] vs.-78.07 [83.66-72.87] vs.-78.46 [85.41-71.99] Hounsfield Units (HU), respectively, p<0.001) and mPFA in the LAD (-71.47 [76.40-66.61] vs.-79.32 [84.37-74.59] vs.-82.52 [88.44-75.81] HU, respectively, p=0.006) compared with AASNU and SC. mPFA in the LCx was not different between AASU, AASNU, and SC (-72.41 [77.17-70.37] vs.-80.13 [86.22-72.23] vs.-78.29 [80.63-72.29] HU, respectively, p=0.163). AASU compared with AASNU and SC, had higher IL-1, (0.975 [0.847-1.250] vs. 0.437 [0.311-0.565] vs. 0.530 [0.402-0.780] OD, respectively, p=0.002), IL-6 (1.195 [0.947-1.405] vs. 0.427 [0.377-0.577] vs. 0.605 [0.332-0.950] OD, p=0.005) and IL-10 (1.145 [0.920-1.292] vs. 0.477 [0.382-0.591] vs. 0.340 [0.316-0.560] OD, p<0.001). TNF-alpha was not different between the AASU, AASNU, and SC groups (0.520 [0.250-0.610] vs. 0.377 [0.261-0.548] vs. 0.350 [0.182-430]), respectively.Conclusion: Compared with ASSNU and controls, AASU have higher mPFA and higher systemic inflammatory cytokines profile suggesting that AAS may induce coronary atherosclerosis through coronary and systemic inflammation.