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1.
Trop Doct ; 49(4): 271-273, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31248318

RESUMO

The course of acute hepatitis A (AHA) in childhood is most often benign. There are relatively few reports of gallbladder involvement during such infection and its consequences. We discuss the cases of 75 children (mean age = 4.5 years) with confirmed AHA. Clinical and laboratory evaluation upon admission were classical for AHA. Only two children had normal bilirubin levels and 38.7% had visible involvement of the gallbladder with wall thickening of >3 mm, while six met criteria for acute acalculous cholecystitis. There appears to be no clear relationship between thickening of the gallbladder wall and transaminase levels, but a significant relationship with total and direct bilirubin levels (P < 0.05). Ultrasonographic examination should therefore be carried out in each case of AHA and follow-up should be performed with greater caution, if there are changes in the gallbladder wall.


Assuntos
Vesícula Biliar/patologia , Hepatite A/patologia , Doença Aguda , Bilirrubina/sangue , Criança , Pré-Escolar , Feminino , Vesícula Biliar/diagnóstico por imagem , Hepatite A/sangue , Hepatite A/diagnóstico por imagem , Humanos , Masculino , Ultrassonografia
2.
Vet Microbiol ; 221: 33-37, 2018 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-29981705

RESUMO

Generally, duck hepatitis A virus type 1 (DHAV-1) only infects young ducklings. Since December 2016, severe outbreaks of duck viral infection with egg drop, feed consumption decline, and ovary-oviduct disease have occurred in some laying duck flocks in Shandong Province of China. DHAV-1 isolated from the affected ducks was confirmed as the causative pathogen of the egg drop. Compared with other DHAV-1 strains, the novel isolate has three special amino acid mutation points in the most variable regions at the C-terminus of VP1. The experimental infection in laying ducks indicated that successful immunization with DHAV-1 vaccine could protect laying duck from infection. To the best of our knowledge, this is the first reported incidence of a severe duck disease outbreak involving egg drop syndrome caused by DHAV-1.


Assuntos
Surtos de Doenças/veterinária , Patos , Vírus da Hepatite A/classificação , Hepatite A/veterinária , Doenças das Aves Domésticas/virologia , Animais , China/epidemiologia , Feminino , Hepatite A/patologia , Hepatite A/virologia , Oviductos/patologia , Oviductos/virologia , Oviposição , Filogenia , Doenças das Aves Domésticas/epidemiologia , Doenças das Aves Domésticas/patologia
3.
BMC Infect Dis ; 18(1): 334, 2018 07 17.
Artigo em Inglês | MEDLINE | ID: mdl-30016934

RESUMO

BACKGROUND: Human anelloviruses (TTV, TTMDV and TTMV) are at high prevalence all across the globe, having also a controversial disease-inducing potential. This study aimed to estimate the prevalence of anelloviral DNA in the Romanian human population and to investigate the association of infections with common pathologies in Romanian population. METHODS: After informed consent, blood samples were collected from 2000 subjects represented by: clinically healthy individuals (n = 701) and a group of patients with pathologies linked to low grade inflammation or alteration of carbohydrate metabolism (n = 1299). All samples were analysed for the presence of TTV, TTMDV and TTMV DNA by hemi-nested PCR. RESULTS: The prevalence of TTV, TTMDV and TTMV in the studied population was 68.2, 54.4%, respectively 40.1%, lower than the recent reports from other geographic regions. The three viral species were significantly more frequent in the group of patients compared to the healthy subjects and were associated with type 2 diabetes mellitus. The presence of anelloviral DNA was also associated with medical procedures (e.g. haemodialysis/transfusions, surgical procedures) and previous hepatitis A virus infection. Lifestyle choices related to alcohol consumption, smoking, physical activity and living environment were not associated with differences in distribution of the three viruses. CONCLUSION: Further evidence is needed to establish a correlation between infection with human anelloviruses and a pathology or group of pathologies.


Assuntos
Infecções por Vírus de DNA/diagnóstico , Adulto , Anelloviridae/genética , Anelloviridae/isolamento & purificação , Estudos de Casos e Controles , Infecções por Vírus de DNA/complicações , Infecções por Vírus de DNA/epidemiologia , DNA Viral/sangue , Diabetes Mellitus Tipo 2/complicações , Feminino , Hepatite A/patologia , Humanos , Estilo de Vida , Masculino , Pessoa de Meia-Idade , Prevalência , Romênia/epidemiologia
6.
J Virol ; 92(9)2018 05 01.
Artigo em Inglês | MEDLINE | ID: mdl-29437974

RESUMO

The hepatitis A virus (HAV) cellular receptor 1 (HAVCR1), classified as CD365, was initially discovered as an HAV cellular receptor using an expression cloning strategy. Due to the lack of HAV receptor-negative replication-competent cells, it was not possible to fully prove that HAVCR1 was a functional HAV receptor. However, biochemistry, classical virology, and epidemiology studies further supported the functional role of HAVCR1 as an HAV receptor. Here, we show that an anti-HAVCR1 monoclonal antibody that protected African green monkey kidney (AGMK) cells against HAV infection only partially protected monkey Vero E6 cells and human hepatoma Huh7 cells, indicating that these two cell lines express alternative yet unidentified HAV receptors. Therefore, we focused our work on AGMK cells to further characterize the function of HAVCR1 as an HAV receptor. Advances in clustered regularly interspaced short palindromic repeat/Cas9 technology allowed us to knock out the monkey ortholog of HAVCR1 in AGMK cells. The resulting AGMK HAVCR1 knockout (KO) cells lost susceptibility to HAV infection, including HAV-free viral particles (vpHAV) and exosomes purified from HAV-infected cells (exo-HAV). Transfection of HAVCR1 cDNA into AGMK HAVCR1 KO cells restored susceptibility to vpHAV and exo-HAV infection. Furthermore, transfection of the mouse ortholog of HAVCR1, mHavcr1, also restored the susceptibility of AGMK HAVCR1 KO cells to HAV infection. Taken together, our data clearly show that HAVCR1 and mHavcr1 are functional HAV receptors that mediate HAV infection. This work paves the way for the identification of alternative HAV receptors to gain a complete understanding of their interplay with HAVCR1 in the cell entry and pathogenic processes of HAV.IMPORTANCE HAVCR1, an HAV receptor, is expressed in different cell types, including regulatory immune cells and antigen-presenting cells. How HAV evades the immune response during a long incubation period of up to 4 weeks and the mechanism by which the subsequent necroinflammatory process clears the infection remain a puzzle that most likely involves the HAV-HAVCR1 interaction. Based on negative data, a recent paper from the S. M. Lemon and W. Maury laboratories (A. Das, A. Hirai-Yuki, O. Gonzalez-Lopez, B. Rhein, S. Moller-Tank, R. Brouillette, L. Hensley, I. Misumi, W. Lovell, J. M. Cullen, J. K. Whitmire, W. Maury, and S. M. Lemon, mBio 8:e00969-17, 2017, https://doi.org/10.1128/mBio.00969-17) suggested that HAVCR1 is not a functional HAV receptor, nor it is it required for HAV infection. However, our data, based on regain of the HAV receptor function in HAVCR1 knockout cells transfected with HAVCR1 cDNA, disagree with their findings. Our positive data show conclusively that HAVCR1 is indeed a functional HAV receptor and lays the ground for the identification of alternative HAV receptors and how they interact with HAVCR1 in cell entry and the pathogenesis of HAV.


Assuntos
Anticorpos Monoclonais/imunologia , Receptor Celular 1 do Vírus da Hepatite A/imunologia , Receptor Celular 1 do Vírus da Hepatite A/metabolismo , Vírus da Hepatite A/metabolismo , Animais , Sistemas CRISPR-Cas/genética , Linhagem Celular Tumoral , Edição de Genes/métodos , Técnicas de Inativação de Genes , Hepatite A/patologia , Receptor Celular 1 do Vírus da Hepatite A/genética , Humanos , Camundongos , Células Vero
7.
Arch Virol ; 163(5): 1187-1193, 2018 May.
Artigo em Inglês | MEDLINE | ID: mdl-29387970

RESUMO

To establish an animal model for the newly identified Marmota Himalayana hepatovirus, MHHAV, so as to develop a better understanding of the infection of hepatitis A viruses. Five experimental woodchucks (Marmota monax) were inoculated intravenously with the purified MHHAV from wild woodchuck feces. One animal injected with PBS was defined as a control. Feces and blood were routinely collected. After the animals were subjected to necropsy, different tissues were collected. The presence of viral RNA and negative sense viral RNA was analyzed in all the samples and histopathological and in situ hybridization analysis was performed for the tissues. MHHAV infection caused fever but no severe symptoms or death. Virus was shed in feces beginning at 2 dpi, and MHHAV RNA persisted in feces for ~2 months, with a biphasic increase, and in blood for ~30 days. Viral RNA was detected in all the tissues, with high levels in the liver and spleen. Negative-strand viral RNA was detected only in the liver. Furthermore, the animals showed histological signs of hepatitis at 45 dpi. MHHAV can infect M. monax and is associated with hepatic disease. Therefore, this animal can be used as a model of HAV pathogenesis and to evaluate antiviral and anticancer therapeutics.


Assuntos
Modelos Animais de Doenças , Vírus da Hepatite A/patogenicidade , Hepatite A , Hepatite Viral Animal , Marmota , Animais , Fezes/virologia , Hepatite A/patologia , Hepatite A/fisiopatologia , Hepatite A/virologia , Vírus da Hepatite A/genética , Vírus da Hepatite A/isolamento & purificação , Vírus da Hepatite A/fisiologia , Hepatite Viral Animal/patologia , Hepatite Viral Animal/fisiopatologia , Hepatite Viral Animal/virologia , Fígado/patologia , Fígado/virologia , RNA Viral/isolamento & purificação , Baço/patologia , Baço/virologia
8.
Artigo em Inglês | MEDLINE | ID: mdl-29440324

RESUMO

Hepatitis A virus (HAV) is transmitted by the fecal-oral route and is a major cause of acute viral hepatitis. The clinical manifestations of HAV infection range from asymptomatic infection to acute liver failure (ALF), but do not include progression to chronic hepatitis. Risk factors for severe acute hepatitis A are older age (>40 years) and preexisting liver disease. Some patients may show atypical clinical features such as relapsing hepatitis, prolonged cholestasis, or extrahepatic manifestations. Almost all hepatitis A patients spontaneously recover with supportive care. However, in the case of ALF (<1%), intensive care and urgent decision on liver transplantation are required. Liver injury during hepatitis A is not directly caused by HAV but is known to be caused by immune-mediated mechanisms. In this review, the natural history and clinical manifestations of hepatitis A are described. In addition, mechanisms of immunopathogenesis in hepatitis A are discussed.


Assuntos
Hepatite A/patologia , Falência Hepática Aguda/diagnóstico , Transplante de Fígado , Fígado/fisiopatologia , Doença Aguda , Progressão da Doença , Hepatite A/complicações , Vacinas contra Hepatite A/uso terapêutico , Vírus da Hepatite A/imunologia , Humanos , Falência Hepática Aguda/virologia , Fatores de Risco
9.
Viral Immunol ; 31(3): 223-232, 2018 04.
Artigo em Inglês | MEDLINE | ID: mdl-29099687

RESUMO

Bilirubin (BR), a metabolite with increased concentrations in plasma during viral hepatitis, has been recognized as a potential immune-modulator. We recently reported that conjugated BR (CB) augments regulatory T cell (Treg) suppressor activity during acute hepatitis A virus (HAV) infection. However, the mechanisms related to the effects of CB on Treg function in the course of hepatotropic viral diseases have not been elucidated. T cell immunoglobulin domain and mucin domain 3 (TIM-3), via its interactions with galectin-9 (GAL-9), is a receptor associated with enhanced Treg function. Thus, TIM-3 expression may be related to the crosstalk between CB and Tregs during HAV infection. Herein, in vitro treatment with high concentrations of CB upregulated TIM-3 expression on Tregs from healthy donors. CB treatment in vitro did not induce de novo Treg generation, and in vitro stimulation with TGF-ß, which shows increased secretion during HAV infection, resulted in a trend toward increased TIM-3 expression on Tregs and CD4+ T lymphocytes (TLs) from healthy donors. Interestingly, an upregulation of TIM-3 expression on CD4+CD25+ T cells and an increase in the proportion of CD4+ TLs expressing GAL-9 were found in HAV-infected patients with abnormal CB values relative to healthy controls. In addition, a statistically significantly reduction in IL-17F production was observed after treatment of CD4+ TLs from healthy donors with high doses of CB in vitro. In summary, our results suggest that CB might regulate Treg activity via a TIM-3-mediated mechanism, ultimately leading to an anti-inflammatory hepatoprotective effect.


Assuntos
Bilirrubina/metabolismo , Receptor Celular 2 do Vírus da Hepatite A/biossíntese , Hepatite A/patologia , Fatores Imunológicos/metabolismo , Linfócitos T Reguladores/efeitos dos fármacos , Regulação para Cima , Adolescente , Antígenos CD4/análise , Criança , Pré-Escolar , Feminino , Humanos , Lactente , Interleucina-17/análise , Subunidade alfa de Receptor de Interleucina-2/análise , Masculino , Linfócitos T Reguladores/química
10.
Pancreatology ; 17(2): 166-175, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28236520

RESUMO

BACKGROUND: Acute pancreatitis (AP) in patients with fulminant viral hepatitis is well recognized and its mortality depends on the severity of hepatitis rather than pancreatitis. Acute pancreatitis associated with non-fulminant acute hepatitis A (AHA) has been rarely described, and is considered to have a benign course with good response to conservative management. OBJECTIVE: To perform a systematic review of the frequency and prognosis of AP associated with fulminant or non-fulminant AHA. RATIONALE: An increasing number of reports describe AP associated with AHA. Some life-threatening complications related to AP may occur, and death has been reported. In addition, it is possible that early diagnosis of these cases may help in reducing the morbidity and mortality. DATA SOURCES: Ovid Medline In-Process & Other Non-Indexed Citations, Ovid MEDLINE, Ovid EMBASE, Ovid Cochrane Central Register of Controlled Trials, Ovid Cochrane Database of Systematic Reviews, Scopus, Google Scholar, and reference lists of relevant articles. STUDY SELECTION: All available studies discussing AP associated with fulminant or non-fulminant AHA. DATA EXTRACTION AND ASSESSMENT: Two blinded independent observers extracted and assessed the frequency of AP associated with AHA based on large studies including all cases of AHA observed during a prolonged period of time, diagnosis of AHA based on anti-HAV IgM, diagnosis of fulminant hepatitis (FH) based on the American Association for the study of Liver Diseases (AASLD) position paper, diagnosis of AP based on the American College of Gastroenterology (ACG) guidelines, diagnosis of AP associated with AHA based on Makharia's association, and diagnosis of AP severity based on the Revision of the Atlanta Classification (RAC). We have developed a tool for risk of bias assessment of case reports and case-series and applied it to the included studies. RESULTS: The frequency of reported AP associated with AHA is 0-0.1%. Thirty-eight publications with a total of 54 patients meeting the inclusion criteria have been published. Twenty-two studies had a low risk for bias, 10 had moderate risk and 6 had high risk. Patients originated from all continents but most of them were from Asia. The median age at diagnosis was 16 years (range: 2-81) with a male to female ratio of 2. The median interval between the onset of jaundice and onset of AP pain was 4 days (range: 0-30). AP was severe in 9% of patients. The median hospital stay for AP was 8 days (range: 3-35). Most cases occur in patients without FH (94%). Mortality was reported in 2 patients (3.7%). CONCLUSION: Acute pancreatitis associated with AHA is rare with an estimated frequency of 0-0.1%. Fifty-four documented cases, mostly in Asian patients, have been reported. The median age of patients is 16 years with a M/F ratio of 2. Acute pancreatitis occurs less than one week after the onset of jaundice and mostly in patients without FH. Acute pancreatitis in this setting is severe in 9% of patients with a mortality rate similar to all other causes of AP.


Assuntos
Hepatite A/complicações , Hepatite A/patologia , Pancreatite/etiologia , Humanos , Pancreatite/patologia
11.
Clin J Gastroenterol ; 10(1): 52-56, 2017 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-27848147

RESUMO

We describe a case of acute liver failure (ALF) without hepatic encephalopathy with marked elevation of aminotransferase due to hepatitis A, according to the revised Japanese criteria of ALF. This liver biopsy of the patient showed compatible to acute viral hepatitis and she immediately recovered without intensive care. She had no comorbid disorders. Of interest, phylogenetic tree analysis using almost complete genomes of hepatitis A virus (HAV) demonstrated that the HAV isolate from her belonged to the HAV subgenotype IA strain and was similar to the HAJFF-Kan12 strain (99% nucleotide identity) or FH1 strain (98% nucleotide identity), which is associated with severe or fulminant hepatitis A. Careful interpretation of the association between HAV genome variations and severity of hepatitis A is needed and the mechanism of the severe hepatitis should be explored.


Assuntos
Aspartato Aminotransferases/sangue , Vírus da Hepatite A Humana/genética , Hepatite A/virologia , Falência Hepática Aguda/virologia , Adulto , Biomarcadores/sangue , Biópsia , Ensaios Enzimáticos Clínicos , Feminino , Hepatite A/diagnóstico por imagem , Hepatite A/enzimologia , Hepatite A/patologia , Vírus da Hepatite A Humana/classificação , Vírus da Hepatite A Humana/isolamento & purificação , Humanos , Fígado/patologia , Falência Hepática Aguda/diagnóstico por imagem , Falência Hepática Aguda/enzimologia , Falência Hepática Aguda/patologia , Filogenia , Tomografia Computadorizada por Raios X
12.
Science ; 353(6307): 1541-1545, 2016 09 30.
Artigo em Inglês | MEDLINE | ID: mdl-27633528

RESUMO

Hepatotropic viruses are important causes of human disease, but the intrahepatic immune response to hepatitis viruses is poorly understood because of a lack of tractable small- animal models. We describe a murine model of hepatitis A virus (HAV) infection that recapitulates critical features of type A hepatitis in humans. We demonstrate that the capacity of HAV to evade MAVS-mediated type I interferon responses defines its host species range. HAV-induced liver injury was associated with interferon-independent intrinsic hepatocellular apoptosis and hepatic inflammation that unexpectedly resulted from MAVS and IRF3/7 signaling. This murine model thus reveals a previously undefined link between innate immune responses to virus infection and acute liver injury, providing a new paradigm for viral pathogenesis in the liver.


Assuntos
Proteínas Adaptadoras de Transdução de Sinal/imunologia , Modelos Animais de Doenças , Vírus da Hepatite A/imunologia , Hepatite A/imunologia , Interações Hospedeiro-Patógeno/imunologia , Fígado/imunologia , Camundongos , Proteínas Adaptadoras de Transdução de Sinal/genética , Animais , Apoptose , Hepatite A/patologia , Hepatite A/virologia , Hepatócitos/imunologia , Hepatócitos/patologia , Hepatócitos/virologia , Humanos , Fator Regulador 3 de Interferon/genética , Fator Regulador 3 de Interferon/imunologia , Fator Regulador 7 de Interferon/genética , Fator Regulador 7 de Interferon/imunologia , Interferon Tipo I/imunologia , Fígado/patologia , Fígado/virologia , Camundongos Knockout , Receptor de Interferon alfa e beta/genética , Receptor de Interferon alfa e beta/imunologia , Receptores de Interferon/genética , Receptores de Interferon/imunologia , Transdução de Sinais/imunologia , Especificidade da Espécie
13.
Pathologe ; 37(3): 269-74, 2016 May.
Artigo em Alemão | MEDLINE | ID: mdl-26919849

RESUMO

Q fever is a worldwide distributed zoonotic disease with a mostly benign course, which regularly reoccurs in Germany. This report is about a patient with sporadic serologically proven Q fever, which also showed typical histopathological findings with nonspecific granulomatous hepatitis, usually seen in acute disease. The bone marrow biopsy revealed so-called doughnut granulomas, which are not pathognomonic but a typical finding in Q fever. This case report impressively underlines that the histomorphological findings can make a decisive contribution to the clarification by extended differential diagnostics, even though it plays a subordinate role in the routine diagnostics of disseminated Q fever.


Assuntos
Doença Granulomatosa Crônica/diagnóstico , Doença Granulomatosa Crônica/patologia , Hepatite A/diagnóstico , Hepatite A/patologia , Febre Q/diagnóstico , Febre Q/patologia , Doenças Raras , Adulto , Antibacterianos/uso terapêutico , Valva Aórtica/patologia , Biópsia por Agulha , Medula Óssea/patologia , Diagnóstico Diferencial , Quimioterapia Combinada , Endocardite Bacteriana/diagnóstico , Endocardite Bacteriana/tratamento farmacológico , Endocardite Bacteriana/patologia , Doença Granulomatosa Crônica/tratamento farmacológico , Hepatite A/tratamento farmacológico , Humanos , Fígado/patologia , Masculino , Febre Q/tratamento farmacológico , Recidiva
14.
Indian Pediatr ; 53(1): 67-9, 2016 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-26840680

RESUMO

BACKGROUND: Auxiliary partial orthotopic liver transplantation is a technique where part of diseased native liver is removed and replaced with healthy donor liver so that, the left behind native liver could later regenerate. CASE CHARACTERISTICS: 2 year 6 month old girl with acute liver failure due to Hepatitis A. She underwent a successful auxiliary partial orthotopic liver transplantation. OUTCOME: Successful native liver regeneration and immunosuppression withdrawal after two and half years of surgery. MESSAGE: In selective cases of acute liver failure, auxiliary partial orthotopic liver transplantation could provide a chance for native liver regeneration and immunosuppression-free life.


Assuntos
Hepatite A , Cirrose Hepática , Falência Hepática Aguda , Transplante de Fígado , Pré-Escolar , Feminino , Hepatite A/complicações , Hepatite A/patologia , Humanos , Fígado/patologia , Cirrose Hepática/etiologia , Cirrose Hepática/patologia , Cirrose Hepática/cirurgia , Falência Hepática Aguda/etiologia , Falência Hepática Aguda/patologia , Falência Hepática Aguda/cirurgia
15.
Clin. transl. oncol. (Print) ; 18(2): 220-227, feb. 2016. tab, graf, ilus
Artigo em Inglês | IBECS | ID: ibc-148228

RESUMO

Objective. To examine the expression of cortactin in epithelial ovarian cancer, and discuss the relationship between the expression of cortactin and the clinical pathology characteristics in epithelial ovarian cancer, as well as clinical significance. Methods. The expression of cortactin was detected using real-time fluorescence quantitative PCR and immunohistochemical SP method in epithelial ovarian cancer. Results. (1) The relative content of cortactin mRNA in epithelial ovarian cancer tissue was higher than that in benign control tissue, and expression was related to histological classification and FIGO stage. (2) Cortactin protein was localized in the cytoplasm and membrane of tumor cells. The positive rate of cortactin was 73.3 % in epithelial ovarian cancer, and the rate of cortactin expression was related to histological classification. (3) The average survival period of epithelial ovarian cancer patients with positive expression of cortactin was 19.5 ± 1.2 months (95 % CI 14.6–21.4 months), compared with 34.5 ± 4.3 months in the negative expression group (95 % CI 22.1–25.9 months). Univariate survival analysis showed that: negative expression of cortactin had a significant survival advantage (χ 2 = 5.739, P = 0.017). A cox regression model for multivariate analysis revealed that cortactin was an independent prognostic factor for epithelial ovarian cancer (P = 0.001; RR = 6.452, 95 % CI 2.289–7.112). Conclusions. Negative expression of cortactin was an independent prognostic factor and had a survival advantage. This suggested that cells with poor differentiation showed increasing motility. Cortactin is closely related to poor prognosis (AU)


No disponible


Assuntos
Humanos , Masculino , Feminino , Cortactina/administração & dosagem , Cortactina/metabolismo , Neoplasias Ovarianas/diagnóstico , Neoplasias Ovarianas/mortalidade , Linfonodos/anormalidades , Linfonodos/metabolismo , Ascite/metabolismo , Hepatite A/patologia , Neoplasias Pancreáticas/patologia , Cortactina , Cortactina/farmacologia , Neoplasias Ovarianas/complicações , Neoplasias Ovarianas/metabolismo , Linfonodos/fisiologia , Ascite/complicações , Hepatite A/complicações , Intervalo Livre de Doença , Neoplasias Pancreáticas/complicações
16.
J Korean Med Sci ; 31(1): 67-72, 2016 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-26770040

RESUMO

The hepatitis A virus (HAV) has been the leading cause of viral hepatitis in Korea since the 2000s. We aimed to describe the current status and regional differences in hepatitis A incidence. We studied the total number of hepatitis A cases reported to the Korea Centers for Disease Control and Prevention through the National Infectious Diseases Surveillance System between 2011 and 2013. Additionally, National Health Insurance Review and Assessment Service data and national population data from Statistics Korea were used. In total, 7,585 hepatitis A cases were reported; 5,521 (10.9 cases per 100,000 populations), 1,197 (2.3 cases per 100,000 populations), and 867 (1.7 cases per 100,000 populations) in 2011, 2012, and 2013, respectively. Fifty-eight patients were infected outside of the country and 7,527 patients represented autochthonous HAV infection cases. Autochthonous HAV infection occurred more frequently among men than women (4,619 cases, 6.1 cases per 100,000 population vs. 2,908 cases, 3.9 cases per 100,000 population). The incidence rate was higher in the 20-29 yr-old group (2,309 cases, 11.6 cases per 100,000 populations) and 30-39 yr-old group (3,306 cases, 13.6 cases per 100,000 populations). The majority of cases were reported from March to June (53.6%, 4,038/7,527). Geographic analyses revealed a consistently high relative risk (RR) of HAV infection in mid-western regions (2011, RR, 1.25, P=0.019; 2012, RR, 2.53, P<0.001; 2013, RR, 1.86, P<0.001). In summary, we report that hepatitis A incidence has been decreasing gradually from 2011 to 2013 and that some regions show the highest prevalence rates of HAV infection in Korea.


Assuntos
Hepatite A/epidemiologia , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Criança , Bases de Dados Factuais , Feminino , Hepatite A/patologia , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , República da Coreia/epidemiologia , Risco , Estações do Ano , Fatores Sexuais , Adulto Jovem
19.
J Infect Dev Ctries ; 8(3): 326-30, 2014 Mar 13.
Artigo em Inglês | MEDLINE | ID: mdl-24619264

RESUMO

INTRODUCTION: Hepatitis A is the most common form of acute viral hepatitis worldwide, especially in children. The clinical severity of the hepatitis A virus (HAV) infection varies from an asymptomatic infection to a fulminant disease. In this study, we aimed to evaluate characteristics of pediatric patients diagnosed with HAV infection. METHODOLOGY: Patients younger than 18 years of age admitted between January 1, 2006 and January 1, 2011 to our hospital, an important reference center located in the middle part of Turkey, diagnosed as having hepatitis A were evaluated. RESULTS: Of 427 patients, 49.4% were female and 50.6% were male. Hospitalization rate of the patients was 28.3%. The reason for hospitalization was vomitting in 58.7% of the patients and abdominal pain in 28%. The mean time of hospitalization was 5.2 ± 4.5 (1-40) days. There was no significant difference in hospitalization time by age. Vomiting and abdominal pain were significantly more common, and PT and aPTT levels were significantly elevated in patients with elevated AST and ALT levels over 1000 IU/L (p < 0.001). PT elevation was present in 15.2% of the patients, aPTT elevation in 11.9%, leukopenia in 16.6%, and thrombocytopenia in 2.6%. In terms of atypical course, four patients (0.9%) had cholestatic hepatitis, one had recurrent hepatitis, and one had fulminant hepatitis, yet no mortality was observed. CONCLUSIONS: Atypical courses of hepatitis A were more scarce in pediatric patients, but careful follow-up of patients with AST and ALT levels > 1000 IU/L is necessary.


Assuntos
Vírus da Hepatite A/isolamento & purificação , Hepatite A/patologia , Adolescente , Análise Química do Sangue , Criança , Pré-Escolar , Feminino , Hepatite A/diagnóstico , Hepatite A/virologia , Humanos , Lactente , Masculino , Estudos Retrospectivos , Turquia
20.
J Med Virol ; 86(2): 202-8, 2014 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-24243548

RESUMO

Clinical infection by hepatitis A virus (HAV) is generally self-limited but in some cases can progress to liver failure. Here, an HAV outbreak investigation among children with acute liver failure in a highly endemic country is presented. In addition, a sensitive method for HAV whole genome amplification and sequencing suitable for analysis of clinical samples is described. In this setting, two fatal cases attributed to acute liver failure and two asymptomatic cases living in the same household were identified. In a second household, one HAV case was observed with jaundice which resolved spontaneously. Partial molecular characterization showed that both households were infected by HAV subtype IA; however, the infecting strains in the two households were different. The HAV outbreak strains recovered from all cases grouped together within cluster IA1, which contains closely related HAV strains from the United States commonly associated with international travelers. Full-genome HAV sequences obtained from the household with the acute liver failure cases were related (genetic distances ranging from 0.01% to 0.04%), indicating a common-source infection. Interestingly, the strain recovered from the asymptomatic household contact was nearly identical to the strain causing acute liver failure. The whole genome sequence from the case in the second household was distinctly different from the strains associated with acute liver failure. Thus, infection with almost identical HAV strains resulted in drastically different clinical outcomes.


Assuntos
Surtos de Doenças , Genoma Viral , Vírus da Hepatite A/genética , Hepatite A/complicações , Hepatite A/epidemiologia , Falência Hepática Aguda/epidemiologia , Adolescente , Criança , Análise por Conglomerados , Feminino , Hepatite A/patologia , Hepatite A/virologia , Vírus da Hepatite A/isolamento & purificação , Humanos , Falência Hepática Aguda/patologia , Falência Hepática Aguda/virologia , Masculino , Dados de Sequência Molecular , Filogenia , RNA Viral/genética , Análise de Sequência de DNA , Estados Unidos
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