RESUMO
The discovery of the Australia Antigen in the mid-1960s led, in a few years, to the identification of the virus of Hepatitis B [...].
Assuntos
Hepatite D/diagnóstico , Hepatite D/virologia , Vírus Delta da Hepatite/isolamento & purificação , Antivirais/uso terapêutico , Hepatite D/tratamento farmacológico , Hepatite D/história , Vírus Delta da Hepatite/genética , Vírus Delta da Hepatite/imunologia , História do Século XX , HumanosRESUMO
Hepatitis delta virus (HDV) increases morbidity in Hepatitis B virus (HBV)-infected patients. In the mid-eighties, an outbreak of HDV fulminant hepatitis (FH) in the Central African Republic (CAR) killed 88% of patients hospitalized in Bangui. We evaluated infections with HBV and HDV among students and pregnant women, 25 years after the fulminant hepatitis (FH) outbreak to determine (i) the prevalence of HBV and HDV infection in this population, (ii) the clinical risk factors for HBV and/or HDV infections, and (iii) to characterize and compare the strains from the FH outbreak in the 1980s to the 2010 HBV-HDV strains. We performed a cross sectional study with historical comparison on FH-stored samples (n = 179) from 159 patients and dried blood-spots from volunteer students and pregnant women groups (n = 2172). We analyzed risk factors potentially associated with HBV and HDV. Previous HBV infection (presence of anti-HBc) occurred in 345/1290 students (26.7%) and 186/870 pregnant women (21.4%)(p = 0.005), including 110 students (8.8%) and 71 pregnant women (8.2%), who were also HBsAg-positive (p = 0.824). HDV infection occurred more frequently in pregnant women (n = 13; 18.8%) than students (n = 6; 5.4%) (p = 0.010). Infection in childhood was probably the main HBV risk factor. The risk factors for HDV infection were age (p = 0.040), transfusion (p = 0.039), and a tendency for tattooing (p = 0.055) and absence of condom use (p = 0.049). HBV-E and HDV-1 were highly prevalent during both the FH outbreak and the 2010 screening project. For historical samples, due to storage conditions and despite several attempts, we could only obtain partial HDV amplification representing 25% of the full-length genome. The HDV-1 mid-eighties FH-strains did not form a specific clade and were affiliated to two different HDV-1 African subgenotypes, one of which also includes the 2010 HDV-1 strains. In the Central African Republic, these findings indicate a high prevalence of previous and current HBV-E and HDV-1 infections both in the mid-eighties fulminant hepatitis outbreak and among asymptomatic young adults in 2010, and reinforce the need for universal HBV vaccination and the prevention of HDV transmission among HBsAg-positive patients through blood or sexual routes.
Assuntos
Vírus da Hepatite B/isolamento & purificação , Hepatite B/virologia , Hepatite D/virologia , Vírus Delta da Hepatite/isolamento & purificação , Adolescente , Adulto , República Centro-Africana/epidemiologia , Estudos Transversais , Surtos de Doenças/história , Feminino , Genótipo , Hepatite B/epidemiologia , Hepatite B/história , Hepatite B/transmissão , Vírus da Hepatite B/classificação , Vírus da Hepatite B/genética , Vírus da Hepatite B/fisiologia , Hepatite D/epidemiologia , Hepatite D/história , Hepatite D/transmissão , Vírus Delta da Hepatite/classificação , Vírus Delta da Hepatite/genética , Vírus Delta da Hepatite/fisiologia , História do Século XX , História do Século XXI , Humanos , Masculino , Filogenia , Gravidez , Complicações na Gravidez/epidemiologia , Complicações na Gravidez/virologia , Adulto JovemRESUMO
Hepatitis has gone along with human history since its origins, due to its prompt identifiability linked to jaundice as a symptom. Written evidence of outbreaks of epidemic jaundice can be tracked back a few millenniums before Christ. Unavoidable confusion arises due to the overlap of different sources possibly linked to different aetiologies, identified over time as epidemic jaundice (HAV or HEV hepatitis?) and serum hepatitis (HBV or HCV hepatitis?). The journey that brought to recognize viruses as the main cause of jaundice was long and started midway during the last century, when the infectious hypothesis, which had taken place step by step, was finally confirmed by epidemiological investigations of an outbreak occurring in the US army in 1942, after a yellow fever immunization campaign. Further research identified two clinically different types of hepatitis, called for the first time hepatitis A and hepatitis B.
Assuntos
Hepatite Viral Humana/história , Surtos de Doenças/história , Hepatite A/história , Hepatite B/história , Antígenos de Superfície da Hepatite B/história , Hepatite C/história , Hepatite D/história , Hepatite E/história , Hepatite Viral Humana/diagnóstico , Hepatite Viral Humana/epidemiologia , História do Século XVII , História do Século XVIII , História do Século XX , História do Século XXI , História Antiga , História Medieval , Humanos , SicíliaRESUMO
Esta análise morfológica e imuno-histoquímica de hepatopatias fulminantes da Amazônia incluindo a série histórica original de Hepatite de Lábrea (HL) e casos de Febre Amarela (FA) concentrou-se em padrões de lesão . Mostraram-se características da FA: morte celular por apoptose medio-zonal, balonização hepatocelular, elevado índice de proliferação celular avaliado pelo PCNA e flebite portal. Os casos de HL mostraram extensa necrose hepatocelular lítica, células em mórula, regeneração hepatocelular com multinucleações e transformação pseudo-acinar, flebite portal e centro-lobular, com extinção parenquimatosa, depósitos portais de fibras elásticas e colágeno tipo I e depósitos lobulares de colágeno III / This morphologic and immunohistochemical analysis of fulminant hepatic failure from Amazon Basin, including the original historical series of Labrea Hepatitis (LH) and of Yellow fever (YF) cases was concentrated on lesion patterns. Midzonal apoptotic cellular death, hepatocellular ballooning degeneration, high cellular proliferation index assessed by PCNA and portal phlebitis were shown to be characteristics of YF. LH cases showed extensive lytic hepatocellular necrosis, morula cells, hepatocellular regeneration with multinucleation and pseudo-acinar transformation, portal and hepatic vein phlebitis, with parenchymal extinction, portal elastic fibers and type I collagen fibers and lobular type III collagen fiber deposition...