Academic literature on the topic 'Virus de Hepatitis VHC'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Virus de Hepatitis VHC.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Journal articles on the topic "Virus de Hepatitis VHC"
Alhawaris. "Hepatitis C: Epidemiologi, Etiologi, dan Patogenitas." Jurnal Sains dan Kesehatan 2, no. 2 (December 31, 2019): 139–50. http://dx.doi.org/10.25026/jsk.v2i2.132.
Full textMENDOZA TICONA, Alberto, and Frine SAMALVIDES CUBA. "Transmisión de los virus de la inmunodeficiencia adquirida, hepatitis B y hepatitis C por exposiciones laborales en trabajadores de salud: Aspectos de profilaxis pre y post exposición." Revista Medica Herediana 16, no. 4 (January 3, 2013): 276. http://dx.doi.org/10.20453/rmh.v16i4.808.
Full textCalmet Schwartzmann, Fernando H., and Fernando H. Calmet Bruhn. "Hepatitis C." Diagnóstico 56, no. 1 (December 13, 2018): 24–30. http://dx.doi.org/10.33734/diagnostico.v56i1.119.
Full textRojas Rodríguez, Carlos Arturo, Angelica Tobon Guevara, Mauricio Sepulveda Copete, Nelson Rojas Rojas, and Diego Fernando Jimenez Rivera. "Hepatitis C: una aproximación clínica y epidemiológica en Cali, Colombia." Revista Colombiana de Gastroenterología 33, no. 4 (December 19, 2018): 379. http://dx.doi.org/10.22516/25007440.222.
Full textZambrano-Plata, Gloria Esperanza, and Javier Cortez. "Seroprevalencia de vih, hepatitis b, hepatitis c, chagas y sifilis en donantes de bancos de sangre de cúcuta (colombia) 1.998 - 1.999." Respuestas 6, no. 1 (June 18, 2016): 45–49. http://dx.doi.org/10.22463/0122820x.588.
Full textFouelifack, Florent Ymele, Jeanne Hortence Fouedjio, Jovanny Tsuala Fouogue, and Loic Dongmo Fouelifa. "Seroprevalences and Correlates of Hepatitis B and C Among Cameroonian Pregnant Women." Clinical Medicine Insights: Reproductive Health 12 (January 1, 2018): 117955811877067. http://dx.doi.org/10.1177/1179558118770671.
Full textLópez-Osorio, María C., Mauricio Beltrán, and María-Cristina Navas. "Epidemiología de la infección por el virus de la hepatitis C en Colombia." Revista Panamericana de Salud Pública 45 (September 16, 2021): 1. http://dx.doi.org/10.26633/rpsp.2021.96.
Full textFayos, Marina, José M. Olmos-Martínez, Remigio Mazorra, Jose D. García-Palacios, and José M. Olmos. "Sarcoidosis subcutánea en paciente con infección crónica por el virus de la hepatitis C." Revista Española de Casos Clínicos en Medicina Interna 3, no. 3 (December 2018): 110–12. http://dx.doi.org/10.32818/reccmi.a3n3a3.
Full textArroyave Ospina, Johanna Carolina, Claudia Marcela Alvarez Flórez, Gonzalo Correa Arango, Norman Balcázar Morales, María Patricia Arbeláez Montoya, and María Cristina Navas Navas. "Infección por el virus de la hepatitis C en individuos transfundidos antes de 1994 en Antioquia, Colombia." Revista Colombiana de Gastroenterología 29, no. 4 (December 30, 2014): 383–90. http://dx.doi.org/10.22516/25007440.435.
Full textSalvatierra, Karina, and Hector Florez. "Computational analysis of resistance mutations in the hepatitis C virus." Revista vínculos 15, no. 1 (May 17, 2018): 27–33. http://dx.doi.org/10.14483/2322939x.12973.
Full textDissertations / Theses on the topic "Virus de Hepatitis VHC"
Vuelvas, Galindez Silverio de Jesús. "ANÁLISIS DE LOS RESULTADOS DE LABORATORIO CLÍNICO DE PACIENTES CON PRUEBA CONFIRMATORIA A VHC DEL CENTRO ONCOLÓGICO ESTATAL EN EL PERIODO ENERO 2008 A DICIEMBRE 2017." Tesis de Licenciatura, Universidad Autónoma del Estado de México, 2019. http://hdl.handle.net/20.500.11799/104989.
Full textSantos, Márcio Bezerra. "Prevalência de marcadores sorológicos dos vírus das Hepatites B (VHB) e C (VHC) em indivíduos infectados por Schistosoma mansoni no bairro Santa Maria, Aracaju/SE." Universidade Federal de Sergipe, 2012. https://ri.ufs.br/handle/riufs/3246.
Full textThe Schistosomiasis is a parasitic disease, severe, chronic waterborne and development, whose etiologic agent is Schistosoma mansoni. It occurs in 74 countries with 207 million people infected and 700 million in risky areas. In Brazil, data indicate a prevalence of eight million. The Schistosomiasis can be exacerbated when patients are carriers of the Hepatitis B Virus (HBV) and C (HCV), resulting in simultaneous evolution of both pathologies. In Brazil, the prevalence of co-infection with HBV/HCV and S. mansoni found in studies ranged from 13.6% to 40% for HBV and 0.5% to 19.66% for the HCV. On this basis, this research aimed to identify the prevalence of serological markers of HBV and HCV and risky factors in individuals carrying the S. mansoni in the Santa Maria neighborhood, Aracaju, state of Sergipe. We conducted a cross-sectional epidemiological study. Data were collected for each patient by means of a questionnaire investigation. This questionnaire included variables identifying the subject of the research participants and variables that included the epidemiological risky factors for infection with HBV or HCV. We collected serum samples of research participants and forwarded to the laboratory testing to identify serological markers of hepatitis B and C: Total Anti-HBc IgG, Anti-HBs, HBsAg and Anti-HCV. All procedures performed using the technique of chemiluminescence immunoassay using the ARCHITECT assay for each serological marker following the protocols established by the laboratory equipment manufacturer SYSTEM ARCHITECT. In addition, we carried out the analysis of spatial distribution of co-infection in the district through the program using the TerraView Kernel intensity estimation. It was found that 16 individuals had contact with HBV (9.41%), one of these was positive for HBsAg. Only Thirty-two samples (18.82%) were positive for the marker Anti-HBs. Three samples were positive for anti-HCV (1.76%), and also a positive for Anti-HBc. The main risks of HBV and HCV infection were related to parenteral interventions of health services, as well as sexual activity without condom use in the case of HBV. Spatial analysis of cases of co-infection (Schistosomiasis and Hepatitis) allowed the visualization of areas of higher concentration of these infections, as well as those that are exposed to different degrees of risk of transmission. The survey results allow to offer, the municipal health services, a tool to facilitate the understanding of the spatial distribution of schistosomiasis and hepatitis (B and C) in Santa Maria neighborhood. Although our values are above the estimated prevalence for the Brazilian population and the Northeast, we can t infer that the individuals with Schistosomiasis are more susceptible to infection with HBV or HCV, since the risky factors were the means of risky transmission of causative agents of hepatitis and not infected with S. mansoni.
A Esquistossomose Mansônica é uma doença parasitária grave, de veiculação hídrica e evolução crônica, cujo agente etiológico é o Schistosoma mansoni. Ocorre em 74 países, com 207 milhões de pessoas infectadas e 700 milhões em áreas de risco. No Brasil, dados indicam uma prevalência de oito milhões. A Esquistossomose pode ser agravada quando os pacientes são portadores dos Vírus das Hepatites B (VHB) e C (VHC), resultando na evolução simultânea de ambas as patologias. No Brasil, As prevalências da co-infecção VHB/VHC e S. mansoni encontradas nos estudos realizados variaram de 13,6% a 40% para o HBV e de 0,5% a 19,66% para o HCV. Com base nisso, esta pesquisa objetivou identificar a prevalência de marcadores sorológicos do VHB e VHC e os fatores de risco em indivíduos portadores do S. mansoni no Bairro Santa Maria, Aracaju/SE. Foi realizado um estudo epidemiológico do tipo transversal. Coletaram-se dados de cada paciente por meio de um questionário investigativo. Este questionário contemplou variáveis de identificação do sujeito participante da pesquisa e variáveis epidemiológicas que incluíram os fatores de risco para infecção pelo HBV ou HCV. Foram coletadas alíquotas de soro dos participantes da pesquisa e encaminhadas para a realização das análises laboratoriais para identificação de marcadores sorológicos dos Vírus das Hepatites B e C: Anti-HBc Total IgG, Anti-HBs, HBsAg e Anti-HCV. Todos os procedimentos realizados utilizaram a técnica de Imunoensaio Quimioluminescente através do Ensaio ARCHITECT para cada marcador sorológico seguindo os protocolos de análises laboratoriais estabelecidos pelo fabricante do equipamento ARCHITECT SYSTEM. Além disso, realizou-se a análise espacial da distribuição da co-infecção no bairro através do programa TerraView utilizando o estimador de intensidade Kernel. Constatou-se que 16 indivíduos tiveram contato com o HBV (9,41%), desses um foi positivo para HBsAg. Apenas Trinta e duas amostras (18,82%) foram positivas para o marcador Anti-HBs. Três amostras foram positivas para Anti-HCV (1,76%), sendo uma também positiva para Anti-HBc. Os principais riscos de infecção pelo HBV e HCV foram relacionados às intervenções parenterais dos serviços de saúde, assim como à atividade sexual sem uso de preservativo, no caso do HBV. A análise espacial dos casos de co-infecção (Esquistossomose e Hepatite) permitiu a visualização de áreas de maior concentração dessas infecções, assim como as que são expostas a diferentes graus de risco de transmissão. Os resultados da pesquisa possibilitam oferecer, aos serviços municipais de saúde, um instrumento que facilite a compreensão da distribuição espacial da Esquistossomose e Hepatites (B e C) no bairro Santa Maria. Embora nossos valores sejam acima da prevalência estimada para a população brasileira e da região nordeste, não podemos inferir que os indivíduos portadores da Esquistossomose são mais susceptíveis à infecção pelo HBV ou HCV, uma vez que, os fatores de risco foram as vias de risco de transmissão de agentes causadores de hepatite e não a infecção pelo S. mansoni.
Alencar, Regiane Saraiva de Souza Melo. "Ocorrência da infecção oculta pelo vírus da hepatite B (VHB) em pacientes com cirrose hepática pelo vírus da hepatite C (VHC) com ou sem carcinoma hepatocelular (CHC)." Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/5/5147/tde-16102014-103147/.
Full textThis study evaluated serum and liver tissue samples from 50 patients with liver cirrhosis due to hepatitis C virus (HVC) that underwent liver transplant at the Hospital das Clínicas - University of São Paulo School of Medicine during the period of 1993 to 2004, divided into two groups: Group 1 (33 cirrhotic patients due to HCV) and Group 2 (17 cirrhotic patients due to HCV with hepatocellular carcinoma - HCC). Our aim was to study the occurrence of occult HBV0 infection in cirrhotic patients due to HCV with or without HCC through the molecular study of HBV DNA in the serum, tumoral liver tissue and non tumoral liver tissue by the polymerase chain reaction (PCR) techniques using in house and real time PCR. All the patients were HBsAg negative, having previous serum samples frozen at -20ºC and liver tissue explanted in paraffin, without presenting concomitant cholestatic, metabolic and autoimmune liver diseases. The following variables were collected: gender, age, biochemical and coagulation laboratory tests and HBV serology (HBsAg, anti-HBc total, anti-HBs). Among the clinical data, ascites and encephalopathy were collected for the Child and MELD prognostic indexes. In the explanted liver tissue the Ishak\'s Score, The Brazilian Society of Pathology and Hepatology Classification for chronic hepatitis, and Edmondson and Steiner Classification for HCC were applied in the liver tissue. All samples with or without tumoral liver tissue and serum were negative for HBV DNA using in house PCR technique. By the real time PCR technique only one case from Group 2 was HBV DNA positive in serum (male, 66, isolated anti-HBc total positive and HCC). In the tumoral and non-tumoral liver tissues there were two indeterminated HBV DNA cases among Group 2 patients. All samples for Group 1 patients were negative for HBV DNA using both techniques. In conclusion, our study has shown the extremely low occult hepatitis B virus infection among the HCV cirrhotic patients with or without HCC, maybe due to the low HBV past infection among the Southeastern Brazilian population
Santos, Ana Carolina de Oliveira. "Determinação do RNA-VHC no sêmen de pacientes cronicamente infectados pelo vírus da Hepatite C." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/5/5134/tde-28082009-091828/.
Full textIntroduction: Hepatitis C vírus is a huge problem for public health, and its global prevalence is estimated around 3%. Its transmission by seminal fluid is still in discussion in several fields, such as assisted reproduction and in studies about risk factors, whether the hepatitis C virus is an STD (sexually transmitted disease) or not. Twenty-three patients were investigated. Objectives: 1.Establish a technique to detect the presence or absence of the HCV in semen from chronically infected patients; 2.Compare semen samples handling techniques, in order to decrease the amount of inhibitors on the samples; 3.Compare different PCR and detection techniques for the HCV in semen samples, in order to increase the sensibility of the test. Methods: On the first phase 20 patients were selected (13 filled the inclusion criterion). Semen and serum samples were collected. The semen samples were processed with the help of Percoll® 90% and 45%. The presence of the RNA-HCV were analyzed in serum with Amplicor Roche method, qualitative test. When positive, the serum samples were genotyped and the semen samples were extracted, by the same method, and the PCR was done. On the second phase 23 patients were selected, some of them were old patients from the first phase (20 filled the inclusion criterion). Semen and serum samples were collected. The semen samples were processed through a dilution series. The presence of HCV-RNA was analised by Amplicor Roche, qualitative test and by PCR in Real-time. The epidemiological data and genotypes were analised. Resultados: From the 23 patients selected the mean age was 40,7 years, mean 45 years. The mean time of Discovery was 7,15 years. Ten patients (37,1%) didn´t present any apparent epidemiology, eight patients (29,6%) contracted HCV through injection and inhalatory drug use; six patients (22,2%) through blood transfusion; two patients (7,4%) had history of drug use and blood transfusion and one patient (3,7%) who was a health professional. Genotype 3a was found in 40,7% of the patients, followed by 1a with 26% of the patients, 1b with 14,8%, 2b with 11,1% e 1a/1b in 7,4% of the patients. The samples processed with Percoll, 86,5% presented inhibited results. Whereas on the samples that were processed with dilution series and amplified on the conventional PCR only 25,62% presented inhibited results, 65% were undetected and 9,38% were positive. On the samples processed with dilution series on the Real-time PCR 95% were undetected and only 5% were positive. Conclusion: On the attempt of decreasing the amount of inhibitors found on the semen samples, the procedure of dilution series showed us more efficient results when compared to the Percoll procedure. However, the great amount of undetected showed that the viral load might have being diluted, leading us to the necessity of a more sensitive technique. There was no significant difference between the results of the conventional PCR and the Real-time. These increase on the undetected results may be a consequence of the absence of a internal control on the PCR reactions.
Clement, Camille. "Etude de la dynamique spatiotemporelle des interactions VHC-récepteurs." Thesis, Strasbourg, 2019. http://www.theses.fr/2019STRAJ098.
Full textTo infect hepatocytes the hepatitis C virus (HCV) interacts with many entry factors and thedynamics of HCV interaction with these receptors lead to virus uptake. Among them,Claudin 1 (CLDN1) and Occludin (OCLN), major proteins composing the tight junctions(TJs). The dynamics of spatiotemporal interaction and the location of the interaction remainunclear and controversial. During my pHD I used live cell imaging to study spatiotemporaldynamics of HCV-receptors. I developed biological imaging tools and generated several celllines that endogenously expressed OCLN and CLDN1 fused to a fluorescent tag andlabeled HCV particles. Live cell imaging and tracking of single viral particles demonstratedthat the HCV-OCLN interaction occurs outside of TJs and that the OCLN seems to stabilizethe HCV-receptor complex to allow its uptake in the cell
Picelli, Natália [UNESP]. "Coinfecção pelos vírus da hepatite C (VHC) vírus da imunodificência humana (HIV): polimosrfismo dos sistemas HPA -1, -3, 3 e -5." Universidade Estadual Paulista (UNESP), 2013. http://hdl.handle.net/11449/92140.
Full textAlém de fatores virais e do hospedeiro a progressão da fibrose hepática resultante da infecção pelo Vírus da Hepatite C (VHC) tem sido relacionada a polimorfismos genéticos do hospedeiro. Nesta linha, recentemente polimorfismos dos Antígenos Plaquetários Humanos (HPA) foram associados à progressão para fibrose em pacientes monoinfectados pelo VHC. Alguns destes antígenos HPA residem em proteínas da família das integrinas, cuja expressão, também, já foi associada à progressão da fibrose hepática. No entanto, estudos relacionando polimorfismos genéticos do hospedeiro em pacientes coinfectados com o VHC e o Vírus da Imunodeficiência Humana (HIV) são raros e, não há nenhum estudo relacionando polimorfismos HPA com progressão para fibrose. Assim, o objetivo deste estudo foi avaliar possíveis associações dos polimorfismos dos sistemas HPA-1, -3 e -5, que residem em integrinas, na progressão da fibrose hepática em indivíduos coinfectados VHC/HIV. DNA Genômico de 56 pacientes coinfectados VHC/HIV foi utilizado como fonte para genotipagem dos sistemas HPA -1 e -3 por PCR-SSP, e HPA -5 por PCR-RFLP. Progressão da fibrose foi avaliada utilizando o escore de METAVIR, sendo constituídos dois grupos: Grupo 1 (G1): pacientes coinfectados VHC/HIV com baixo grau de fibrose (F1, fibrose portal sem septos ou F2, com poucos septos) e Grupo 2 (G2): pacientes coinfectados VHC/HIV com fibrose avançada (F3, numerosos septos ou F4, cirrose). Um grupo controle, do estudo de Silva e colaboradores (2012), constituído por pacientes monoinfectados pelo VHC com baixo grau de fibrose (F1 ou F2) e fibrose avançada (F3 ou F4) foi utilizado para as análises realizadas neste estudo. O Teste Exato de Fisher foi utilizado para avaliar possíveis associações entre o polimorfismo dos sistemas HPA -1, -3 e -5 e a progressão para fibrose, utilizando um nível de significância de 5%. Não houve desvio do equilíbrio...
To evaluate the associations of Human Platelet Antigen (HPA) polymorphisms -1, -3 and -5 with HIV/HCV coinfection. In this study were included 60 HIV/HCV-coinfected patients from the Sao Paulo State health service centers. Data reported by Verdichio-Moraes et al (2009) were used as the non-infected and HCV monoinfected groups to evaluate the association of HPA -1, -3 and -5 in HIV/VHC coinfected patients. HPA genotyping was performed in 60 HIV/HCV coinfected patients by PCR-SSP or PCR-RFLP. HIV subtyping and HCV genotyping was performed by RT-PCR followed sequencing. The data analyses were performed using the c2 test or Fisher’s Exact Test and the logistic regression model. HIV/HCV coinfected patients presented HCV either genotype 1 (78.3%) or non-1 (21.7%) and HIV either subtype B (85.0%) or non-B (15%). The HPA-1a/1b genotype was more frequent (p<0.05) in HIV/HCV coinfection than in HCV monoinfection and the allelic frequency of HPA-5b in the HIV/HCV coinfected patients was lower (P<0.05) than in HCV monoinfected cases and non-infected individuals. These data suggest that HIV presence may have influenced the interaction of HCV with platelets. On the other hand, HPA-5a/5b was more frequent (p<0.05) in HIV/HCV coinfected and HCV monoinfected groups than in the non-infected individuals, suggesting that this platelet genotype is related to HCV infection, regardless of HIV presence. Results suggest that the HPA profile in HIV/HCV coinfected individuals differs from the one of both HCV monoinfected and non-infected population. So, the HPA polymorphism can be a genetic marker associated with HIV/HCV coinfection
Shen, Hong. "Hepatitis C infection models." Thesis, Paris 5, 2012. http://www.theses.fr/2012PA05T016.
Full textHepatitis C virus (HCV) is one of the major causes of liver disease all over the world which has a high risk to progress to cirrhosis and hepatocellular carcinoma. Currently, the licensed standard treatment of HCV infection is Pegylated-interferon (peg-IFN) and ribavirin. Although the sustained viral response (SVR) rate of treatment has improved during these years, this therapy is not effective in all patients. In addition, several toxic side effects, complication and high cost limit the patient compliance and the efficacy of the treatment. There is no easy model of HCV infection and it is necessary to develop useful in vitro and in vivo models to study the pathobiology of HCV infection, including early events of acute infection (viral entry, immunological mechanisms, and genetic predictors) as well as the evaluation of the potency of the HCV antiviral drugs. We report here in our efforts in developing suitable models of HCV infection. In a first step, we preliminary established a small animal model to study HCV infection. Tupaia is a small, closed related to primate and cost-effective animal. In our work, we investigated the susceptibly of tupaia to HCV infection. Twelve adult tupaias were inoculated with native HCV from patient serum and full-length HCV RNA (Genotype 1a). Three young tupaias were artificially breeded for a month and then inoculated by native HCV from patient serum. HCV RNA, anti-HCV and HCV quasi species evolution were determined in the animal before and after inoculation. Transient and intermittent infection occurred in two among 3 young tupaias and HCV chronic infection occurred in four among 12 adult tupaias. Tupaia should represent a useful model for study HCV chronic infection. In a second step, an in vitro culture system of primary tupaia hepatocytes has been established in which HCV infection could be blocked neither by the soluble CD81 nor by antibodies against CD81. To understand these results, we cloned, sequenced the large extracellular loop (LEL) of tupaia CD81 and analyzed the interaction of HCV E2 with the tupaia CD81 LEL by enzyme-linked immunosorbent assay (EIA). We found that in the tupaia the amino acids sequence of HCV CD81 LEL presented in 6 different amino acid residues compared with human CD81 LEL sequence and the CD81 LEL ability to bind to HCV E2 was also decreased. The different structure of CD81 between human and tupaia could explain the alteration of the interaction between HCV E2 and CD81. This result demonstrated an important role of CD81 LEL for HCV entry. In a third step, we developed an ex vivo model of human liver slices culture and their infection with HCV. The development of human cultured HCV-replication-permissive hepatocarcinoma cell lines has provided important new virological tools to study the mechanisms of HCV infection; however this experimental model remains distantly related to physiological and pathological conditions. Here, we report the development of a new ex vivo model using human adult liver slices culture, demonstrating, for the first time, the ability of primary isolates to undergo de novo viral replication with the production of high titer infectious virus, as well as JFH-1, H77/C3, Con1/C3 (HCVcc). This experimental model was validated by demonstrating the HCV neutralization or HCV inhibition, in a dose-dependent manner, either by CD81 or E2 specific antibodies or convalescent serum from a recovered HCV patient, or by anti-viral drugs. This new ex vivo model represents a powerful tool for studying the viral life cycle, dynamics of virus spread in the liver and also for evaluating the efficacy of the new antiviral drugs. In the last step, we evaluated the efficacy of the new antiviral drugs with our ex vivo model of human adult liver slices. HCV NS3/4A protease is essential for viral replication and has been one of the most important target for developing specific antiviral drug
Matas, Crespí Marina. "Interacció VHC-hoste: Estudi genètic i clínic en pacients coinfectats amb VHC-VIH." Doctoral thesis, Universitat de les Illes Balears, 2013. http://hdl.handle.net/10803/111335.
Full textPassini, Sione Souza Santos. "Prevalência de infecção pelo vírus da hepatite C (VHC)em gestantes e transmissão materno-infantil." Centro de Pesquisas Gonçalo Moniz, 2012. https://www.arca.fiocruz.br/handle/icict/7151.
Full textMade available in DSpace on 2013-10-15T16:15:07Z (GMT). No. of bitstreams: 1 Sione Passini Prevalência de infecção... 2013.pdf: 2410664 bytes, checksum: 9fd8b1765a81738455f4e2fc95fd769a (MD5) Previous issue date: 2012
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
A transmissão materno-infantil (TMI) do vírus da hepatite C (VHC) ocorre em 4%-13% das gestações quando a mãe é infectada, e poucos estudos de prevalência foram realizados em gestantes no Brasil. O objetivo desta pesquisa foi determinar a prevalência de infecção e fatores associados à presença de infecção pelo VHC em gestantes, e determinar a taxa de TMI do VHC. O estudo foi realizado em Salvador, no período entre Maio de 2009 e Abril de 2011, na Maternidade Referência Professor José Maria Magalhães Netto. Todas as voluntárias que assinaram ao TCLE, tiveram seus prontuários revisados e tiveram amostra de soro coletada para a realização do teste rápido anti-VHC (Bioeasy), ELISA 3ª geração (Artech), e detecção do VHC-RNA Qualitativo e Quantitativo (AMPLICOR HCV TESTE, ROCHE versão 2.0). Em uma subamostra de gestantes selecionada aleatoriamente, realizouse entrevista para analisar fatores sócio-demográficos e de exposição ao VHC não disponíveis nos prontuários. A análise estatística descritiva e de associação foram realizadas utilizando o programa EPI Info 3.5.3 (CDC, Atlanta, GE, EUA). Foram incluídas no estudo 3.049 gestantes, sendo que 8 (0,26%; IC 95%: 0,12%-0,50%)foram soropositivos para o anti-VHC pelo ELISA e 6 (0,20%; IC 95%: 0,08%-0,41%) confirmaram viremia. Todos os VHC genotipados pertenceram ao genótipo 1, 1a ou 1b. Os principais fatores associados à infecção materna pelo VHC foram uso de drogas, tatuagem, e infecção por HIV (p < 0,05). Das 6 gestantes com HCV positivo, 2 (33,3%; IC 95%: 6,0%-73,8%) transmitiram o HCV para seus filhos. Em um dos casos de TMI, a mãe relatou ter feito uso de drogas injetáveis e inaláveis durante a gestação, possuía tatuagem e era portadora do HIV sob tratamento antiretroviral. O recém-nascido (RN) nasceu com idade gestacional (IG) de 38 semanas através de parto cesariano eletivo. No outro caso, a mãe relatou uso de drogas injetáveis e inaláveis, possuía piercing e tatuagem, mas não foi portadora de HIV. O RN nasceu com IG de 39 semanas, através de parto normal, com tempo de ruptura da bolsa de 15 horas. Concluímos que a prevalência de infecção pelo VHC entre gestantes é baixa quando comparada à da população em geral na mesma localidade, sendo associado a uso de drogas e tatuagem. A taxa de TMI do VHC encontrada foi maior do que o esperado. Assim, estudos mais amplos serão necessários.
The mother-to-child transmission (MTCT) of hepatitis C virus (HCV) occurs in 4%- 13% of pregnancies when the mothers are infected and very few studies were conducted to determine the HCV prevalence in pregnant women in Brazil. The aim of this work was to determine the prevalence and associated factors of HCV infection in pregnant women, and the rate of the MTCT of HCV. It was conducted in Salvador, between March 2009 and April 2011, at the maternity hospital Prof. José Maria Magalhães Netto. All volunteers signed to informed consent, their medical records were reviewed and serum samples were collect for screening anti-HCV antibody by a rapid anti-HCV testing (Bioeasy), ELISA 3rd generation (Artech), and HCV-RNA qualitative and quantitative detection (AMPLICOR HCV TEST, ROCHE version 2.0). In a randomly selected pregnant women subsample, interviews were made to evaluate socio-demographic and exposure factors for HCV, not available in the records. The descriptive and association statistical analysis were performed using Epi Info 3.5.3 (CDC, Atlanta, GE, USA). The study included 3.049 pregnant women, 8 (0.26%; 95% CI: 0.12%-0.50%) were anti-HCV positive by ELISA and 6 (0.20%; 95% CI: 0.08%-0.41%) confirmed viremia. All genotypes HCV belonged to genotype 1, 1a or 1b. Injection and inhaled drug use, tattoo and piercing were the most important associated factors for the mother infection. Out of the 6 HCV infected mothers, 2 (33.3%; 95% CI: 6.0%-73.8%) transmitted HCV to their newborns. In one of the cases of MTCT, the mother reported to injection and inhaled drug user during pregnancy, had tattoo and was HIV carrier held under antiretroviral therapy. The newborn was born at gestational age (GA) 38 weeks by elective cesarean section. In the other case, the mother was also injection and inhaled drug user, had piercing and tattooing. Her newborn was born at GA 39 weeks by normal delivery, and time of rupture of membranes was estimated to be 15 hours. We conclude that the prevalence of HCV infection among pregnant women was lower than the prevalence in the general population in the same locality, been associated to drug use and tattoo. The rate of MTCT of HCV was higher than expected. Thus, larger studies are required.
Castro, Bohórquez Francisco José. "Utilidad de la monitorización del ARN del virus de la Hepatitis C durante el tratamiento antiviral como factor predictor de respuesta mantenida." Doctoral thesis, Universitat Autònoma de Barcelona, 2001. http://hdl.handle.net/10803/4356.
Full textA) Para la evaluación de unas técnicas de RT/PCR de segunda generación en sus versiones cualitativa (Amplicor v2.0) y cuantitativa (Monitor v2.0) utilizamos tres tipos de muestras: donantes de sangre con anticuerpos Anti-VHC pero ARN no detectable por una técnica cualitativa de primera generación (n=132), pacientes con hepatitis crónica C (n=326) y diluciones de un estándar de VHC de concentración conocida. El límite inferior de detección fue de 100 copias de estándar del VHC /mL para Amplicor v2.0 y de 1000 copias/mL para Amplicor v1.0. De los 132 donantes de sangre con serología anti-VHC positiva y ARN del VHC indetectable por Amplicor v1.0, en 6 (5%) casos se detectó ARN del VHC utilizando Amplicor v2.0. La carga viral según Monitor v2.0 fue mayor que la obtenida mediante Monitor v1.0 para todos los genotipos. No hubo diferencias entre las cargas virales medias de los genotipos 1, 2 y 3 al utilizar Monitor v2.0, mientras que la carga viral del genotipo 4 fue inferior al resto. Se ha descrito que Monitor 1.0 subestima la carga viral en los genotipos 2 y 3 con respecto al genotipo 1. En cambio Monitor v2.0 cuantifica por igual los genotipos 1, 2 y 3. Además ha reducido la diferencia entre el genotipo 4 y el resto de 1.5 log a 0.5 log. En conjunto las técnicas de segunda generación son más sensibles en un logaritmo y menos genotipo dependientes que las de primer generación.
B) Fueron incluidos 184 pacientes afectos de hepatitis la crónica C que habían seguido tratamiento antiviral: 62 pacientes con interferón y 122 pacientes con interferón más ribavirina. En ambos grupos ALT y ARN de VHC se determinaron mensualmente. La respuesta mantenida ocurrió en 13 (22%) pacientes en el grupo de interferón y 21 pacientes (17%) en el grupo de terapia combinada. La persistencia de viremia cualitativa tras un mes de interferón monoterapia y tras cinco mes de terapia combinada eran los predictores más potentes de no respuesta (valor predictivo negativo de 100% y 99%, respectivamente). Las variables asociadas con la respuesta mantenida eran HCV genotipo (P=0.06), carga viral < 5.1 log/ml (P=0.005) y ARN VHC no detectable tras un mes (P<0.0001) en el grupo de interferón monoterapia; sexo femenino (P=0.04), genotipo (P=0.03), la carga viral < 5.5 log/ml (P=0.01), ALT normal (P=0.001) y descenso en la carga viral >1.2 log/ml después de 2 meses de interferón monoterapia (P<0.001) y viremia negativa tras cinco meses de terapia combinada (P<0.0001) en el grupo de tratamiento combinado. La evaluación cualitativa de ARN de VHC durante el tratamiento es el predictor más potente de respuesta mantenida de la hepatitis crónica C.
C) Se incluyeron 30 pacientes que habían seguido tratamiento con interferón-"2b más ribavirina durante 12 meses. Seis meses tras la retirada de la terapia 10 pacientes presentaron una respuesta mantenida y los otros 20 fueron considerados no respondedores. Se determinó la carga viral basal, al mes, dos meses y tres meses de tratamiento mediante una RT/PCR cuantitativa calibrada en unidades internacionales (Amplicor HCV Monitor v2.0). La carga viral no mostró variaciones significativas en los pacientes no respondedores durante los primeros meses de terapia combinada (6.3±0.7 versus 6±0.9, 5,7±1 and 5,9±0.9 log UI/mL al inicio y tras uno, dos y tres meses, respectivamente). Sin embargo la carga viral de los pacientes que presentaron respuesta mantenida disminuyó progresivamente en cada muestra mensual, llegando a ser indetectable al tercer mes en todos los pacientes. Se construyeron curvas COR referentes a la carga viral en los meses 1, 2 y 3 para predicción de respuesta mantenida. Fueron detectados los siguientes picos de sensibilidad: 5 log/mL en el mes 1, 4 log/mL en el mes 2 y 3 log/mL en el mes 3. La carga viral durante los tres primeros meses de tratamiento con interferón y ribavirina es el predictor de respuesta más potente.
The hepatitis C virus (HCV), a single-stranded RNA virus, is the etiologic agent in most cases of post-transfusion and sporadic non-A, non-B hepatitis worldwide. This infection has a high rate of persistence and progression to chronic liver disease. HCV infection is a leading cause of end-stage liver disease requiring liver transplantation, and is also associated with hepatocellular carcinoma. To evaluate the utility of monitoring RNA HCV levels during antiviral therapy as predictor of long-term response, we have done three studies.
A) HCV RNA qualitative and quantitative second generation assays (Amplicor HCV v2.0 and Amplicor HCV Monitor v2.0, respectively) have been evaluated by testing serum samples from 132 blood donors anti-HCV positive HCV RNA negative by first generation qualitative assay and 326 viremic patients. An HCV RNA transcript was synthesized and ten-fold dilutions were used to assess sensitivity. Second generation assays were one log more sensitive than their respective first generation tests (102 copies/ml vs. 103 for the qualitative tests; 103 copies/ml vs. 104 for the quantitative tests). From the 132 anti-HCV positive RNA negative subjects, 6 (5%) were positive by Amplicor v2.0. Quantification figures by Monitor v2.0 were similar in genotypes 1, 2 and 3, whereas Monitor 1.0 values were higher in genotype 1 than in genotype 2 or 3. In 114 patients, branched-DNA v2.0 obtained higher values than Monitor v2.0 and Monitor v1.0 (6.6+0.6 log RNA copies/ml, 6.4+0.6, and 5.3+0.7, respectively, P<0.001). HCV RNA qualitative and quantitative second generation assays are more sensitive and genotype independent than first generation assays.
B) One hundred and eighty-four patients with chronic hepatitis C treated with interferon alone (62 patients) or interferon plus ribavirin (122 patients) for 12 months were studied. In both groups aminotransferase and HCV RNA were tested weekly for one month, biweekly for two months and monthly thereafter. Sustained response ocurred in 13 (22%) and 21 patients (17%) in the interferon and combination group, respectively. Persistence of viremia at one month of interferon monotherapy and at five month of combination therapy were the strongest predictors of non-response (predictive value of 100% and 99%, respectively; 95% confidence interval 93.2-99.9%). Independent variables associated with sustained response were HCV genotype (P=0.06), viral load £ 5.1 logs/ml (P=0.005) and negative HCV RNA at one month (P<0.0001) in the interferon group. And female sex (P=0.04), genotype (P=0.03), viral load £ 5.5 logs/ml (P=0.01), normal ALT (P=0.001) and decline in viral load *1.2 logs/ml after 2 months of interferon monotherapy f(P<0.001) and negative viremia at five months of ribavirin onset (P<0.0001) in the combination group. Qualitative assessment of HCV RNA during treatment is the strongest predictor of sustained response during interferon or combination therapy for chronic hepatitis C.
C) The dynamics of hepatitis C virus RNA during treatment with interferon plus ribavirin are not well known. We evaluated the predictive value of HCV RNA early decline during combination therapy. Thirty chronic hepatitis C patients that had followed interferon plus ribavirin for twelve months were included. Serum HCV RNA was measured in sera obtained at baseline and at 4, 8 and 12 weeks after initiation of treatment using a second generation commercially available quantitative RT/PCR assay. After six months of postherapy follow-up 10 (33%) patients were considered sustained responders and 20 (66%) non responders. While in non responders HCV RNA levels remained stable during the first three months of treatment (6.3±0.7 versus 6±0.9, 5,7±1 and 5,9±0.9 log10 HCV RNA IU/mL at baseline and at weeks 4, 8 and 12 respectively) sustained responders showed significant declines in viral load at each subsequent sample (rHCV RNA of 3.5±1.6 log10 IU/mL, 5.1±1.7, and 6±0.9 at weeks 4,8 and 12 respectively). At week 12 all sustained responders had HCV RNA levels below 600 IU/mL, as compared to only one of 20 non responders (P<0.001). ROC curves of HCV RNA level for sustained response prediction identified sensitivity peaks (5 log at 4 weeks, 4 log at 8 weeks and 3 log at 12 weeks) with 100% negative predictive value. Our results suggest that HCV RNA levels during the first three months of combination therapy for chronic hepatitis C are the strongest predictors of response.
Books on the topic "Virus de Hepatitis VHC"
Ruggeri, Franco Maria, Ilaria Di Bartolo, Fabio Ostanello, and Marcello Trevisani. Hepatitis E Virus. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7522-4.
Full textHanda, Hiroshi, and Yuki Yamaguchi. Hepatitis Delta Virus. Boston, MA: Springer US, 2006. http://dx.doi.org/10.1007/0-387-35103-5.
Full textGuo, Haitao, and Andrea Cuconati, eds. Hepatitis B Virus. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6700-1.
Full textWang, Youchun, ed. Hepatitis E Virus. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-024-0942-0.
Full textLaw, Mansun, ed. Hepatitis C Virus Protocols. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8976-8.
Full textTang, Hong, ed. Hepatitis B Virus Infection. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-13-9151-4.
Full textJirillo, Emilio, ed. Hepatitis C Virus Disease. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-71376-2.
Full textMiyamura, Tatsuo, Stanley M. Lemon, Christopher M. Walker, and Takaji Wakita, eds. Hepatitis C Virus I. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56098-2.
Full textMiyamura, Tatsuo, Stanley M. Lemon, Christopher M. Walker, and Takaji Wakita, eds. Hepatitis C Virus II. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56101-9.
Full textBook chapters on the topic "Virus de Hepatitis VHC"
Harrison, Tim J., and Geoffrey M. Dusheiko. "Hepatitis B virus and hepatitis delta virus." In Molecular and Cell Biology of Sexually Transmitted Diseases, 203–32. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2384-6_7.
Full textStapleton, Jack T. "Hepatitis A Virus." In Viral Hepatitis, 7–33. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-702-4_2.
Full textVyas, Girish N., and T. S. Benedict Yen. "Hepatitis B Virus." In Viral Hepatitis, 35–63. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-702-4_3.
Full textBendinelli, Mauro, Maria Linda Vatteroni, Fabrizio Maggi, and Mauro Pistello. "Hepatitis C Virus." In Viral Hepatitis, 65–127. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-702-4_4.
Full textSmedile, Antonia, and Giorgio Verme. "Hepatitis D Virus." In Viral Hepatitis, 129–50. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-702-4_5.
Full textYarbough, Patrice O., and Albert W. Tam. "Hepatitis E Virus." In Viral Hepatitis, 151–74. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-702-4_6.
Full textKhuroo, Mohammad Sultan, Mehnaaz S. Khuroo, and Naira S. Khuroo. "Enteric Hepatitis Viruses: Hepatitis A Virus and Hepatitis E Virus." In Clinical Epidemiology of Chronic Liver Diseases, 171–209. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-94355-8_13.
Full textRizzetto, Mario. "Hepatitis D Virus." In Clinical Epidemiology of Chronic Liver Diseases, 135–48. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-94355-8_11.
Full textShouval, Daniel. "Hepatitis A Virus." In Viral Infections of Humans, 417–38. Boston, MA: Springer US, 2014. http://dx.doi.org/10.1007/978-1-4899-7448-8_17.
Full textMeng, Xiang-Jin. "Hepatitis E Virus." In Viral Infections of Humans, 439–54. Boston, MA: Springer US, 2014. http://dx.doi.org/10.1007/978-1-4899-7448-8_18.
Full textConference papers on the topic "Virus de Hepatitis VHC"
Garcia-Guix, Alexandra, Lina Oviedo, Rosa Sauras-Quetcuti, Gerard Mateu-Codina, Marta Nayach, Rebeca Alayon-Santana, Laura Oliva, and Marta Torrens. "Modelo de microeliminación de la Hepatitis C. Cascada de cuidados para la hepatitis C del CAS Santa Coloma - Barcelona." In 22° Congreso de la Sociedad Española de Patología Dual (SEPD) 2020. SEPD, 2020. http://dx.doi.org/10.17579/sepd2020o024.
Full textGür, A., M. Karakoç, MF Geyik, K. Nas, R. Çevik, AJ Saraç, S. Em, and F. Erdogan. "SAT0135 Association between hepatitis c virus antibody, hepatitis b virus antigen and fibromiyalgia." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.594.
Full textUsman, Z., H. Karimzadeh, U. Protzer, M. Roggendorf, and D. Frishman. "HDVdb: Hepatitis D virus database." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677295.
Full textEid, Fatma Elzahraa, Haitham Elmarakeby, Lenwood Heath, and Mahmoud ElHefnawi. "Human microRNAs targeting hepatitis C virus." In 2014 Middle East Conference on Biomedical Engineering (MECBME). IEEE, 2014. http://dx.doi.org/10.1109/mecbme.2014.6783236.
Full textPrasetyo, Afiono Agung, Yulia Sari, Ruben Dharmawan, and Marwoto. "Molecular status of human immunodeficiency virus, hepatitis B virus, and hepatitis C virus among transgender commercial sex workers in Surakarta, Indonesia." In THE 1ST INTERNATIONAL CONFERENCE ON MATHEMATICS, SCIENCE, AND COMPUTER SCIENCE (ICMSC) 2016: Sustainability and Eco Green Innovation in Tropical Studies for Global Future. Author(s), 2017. http://dx.doi.org/10.1063/1.4975949.
Full textChien, J. H., D. S. Lee, W. P. Chou, P. Y. Wang, C. R. Yang, M. H. Wu, C. Y. Tsai, et al. "Simultaneous Quantification for Hepatitis B Virus and Hepatitis C Virus Using Real-time PCR Lab-on-a-chip." In 2006 1st IEEE International Conference on Nano/Micro Engineered and Molecular Systems. IEEE, 2006. http://dx.doi.org/10.1109/nems.2006.334721.
Full textWilhelm, B., G. Trottier, J. Greig, L. Waddell, and Andrijana Rajic. "Hepatitis E virus: potential zoonosis in swine production?" In Eighth International Symposium on the Epidemiology and Control of Foodborne Pathogens in Pork. Iowa State University, Digital Press, 2009. http://dx.doi.org/10.31274/safepork-180809-841.
Full textTwu, WI, K. Tabata, D. Paul, and R. Bartenschlager. "Role of autophagy in hepatitis C virus replication." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677294.
Full textLi, Zhi, and Huan Qi. "Identification and Simulation of Hepatitis B Virus Model." In 2010 International Conference on Computational and Information Sciences (ICCIS). IEEE, 2010. http://dx.doi.org/10.1109/iccis.2010.88.
Full textArai, Eri, Ying Tian, Masahiro Gotoh, Yoriko Takahashi, Hidenori Ojima, Tomoo Kosuge, and Yae Kanai. "Abstract 1055: Genome-wide DNA methylation analysis in precancerous conditions associated with hepatitis B virus and hepatitis C virus infection." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1055.
Full textReports on the topic "Virus de Hepatitis VHC"
Sjogren, Maria H., and Kent Holtzmuller. Hepatitis C Virus Infection: Mechanism of Disease Progression. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada406083.
Full textSjogren, Maria H. Hepatitis C. Virus Infection: Mechanism of Disease Progression. Fort Belvoir, VA: Defense Technical Information Center, October 2004. http://dx.doi.org/10.21236/ada433067.
Full textSjogren, Maria H., and Brooke Huntley. Hepatitis C. Virus Infection: Mechanisms of Disease Progression. Fort Belvoir, VA: Defense Technical Information Center, October 2007. http://dx.doi.org/10.21236/ada477987.
Full textKasorndorkbua, C., P. J. Thomas, Patrick G. Halbur, D. K. Guenette, F. F. Huang, and X. J. Meng. Infection of Pigs with Avian Hepatitis E Virus (HEV). Ames (Iowa): Iowa State University, January 2005. http://dx.doi.org/10.31274/ans_air-180814-1096.
Full textKasorndorkbua, C., P. J. Thomas, Patrick G. Halbur, F. F. Huang, D. K. Guenette, and X. J. Meng. Routes of Transmission of Swine Hepatitis E virus in Pigs. Ames (Iowa): Iowa State University, January 2005. http://dx.doi.org/10.31274/ans_air-180814-1095.
Full textKoizumi, Yoshiki, Syo Nakajim, Hirofumi Ohash, Yasuhito Tanaka, Takaji Wakita, Alan S. Perelson, Shingo Iwami, and Koichi Watashi. Quantifying antiviral activity optimizes drug combinations against hepatitis C virus infection. Office of Scientific and Technical Information (OSTI), March 2016. http://dx.doi.org/10.2172/1242919.
Full textPishmisheva, Maria, Magdalena Baymakova, Elitsa Golkocheva-Markova, Todor Kundurzhiev, Roman Pepovich, Georgi T. Popov, and Ilia Tsachev. First Serological Study of Hepatitis E Virus Infection in Pigs in Bulgaria. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, July 2018. http://dx.doi.org/10.7546/crabs.2018.07.18.
Full textSobsey, Mark D. Inactivation of Hepatitis A Virus (HAV) by Chlorine and Iodine in Water. Fort Belvoir, VA: Defense Technical Information Center, November 1986. http://dx.doi.org/10.21236/ada199503.
Full textCook-Mills, Joan M., Hidayatulla G. Munshi, Robert L. Perlman, and Donald A. Chambers. Mouse Hepatitis Virus Infection Suppresses Modulation of Mouse Spleen T- Cell Activation. Fort Belvoir, VA: Defense Technical Information Center, January 1988. http://dx.doi.org/10.21236/ada237464.
Full textMartinez-Chantar, Malu. Especial Premio Nobel de Medicina 2020: La ciencia vence al virus de la hepatitis C. Sociedad Española de Bioquímica y Biología Molecular, October 2020. http://dx.doi.org/10.18567/sebbmdiv_rpc.2020.10.1.
Full text