TT virus: a mother-to-child transmitted rather than bloodborne virus.
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Amniotic Fluid↗
Biomedical subjects
Y Katano
Publications and source records attributed to Y Katano.
Methods and conclusions in the clinical study of TT virus.
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DNA Virus Infections↗
Why is the interferon sensitivity-determining region (ISDR) system useful in Japan?
BACKGROUND/AIMS: The amino acid sequence of NS5A2209-2248, named the "interferon sensitivity-determining region" (ISDR), has been reported to correlate with responsiveness of interferon (IFN) therapy to patients with the hepatitis C virus (HCV) genotype-1b, by several Japanese authors. However, European authors have failed to find this phenomenon, suggesting a difference in HCV-1b isolates between Japan and Europe. METHODS: We compared the HCV-1b nucleotide sequences of our Japanese patients and those of other countries quoted from GenBank, using the envelope 1 sequence. RESULTS: A phylogenetic tree analysis revealed two characteristic groups from a geographical viewpoint: one group (NJ group) consists of almost entirely non-Japanese isolates, and the other (J group) of almost entirely Japanese isolates. The isolates other than the NJ and J groups are characterized by their specific nucleotide residue, constructing an individual group (W group). Japanese HCV-1b isolates consist of the J group and W group (approximately 40% and 60%, respectively). Comparative study between the two groups in Japanese patients treated with IFN revealed a strong correlation between ISDR type and IFN responsiveness only in the J group, but not in the W group. CONCLUSIONS: These observations convinced us that the existence of the Japan-specific J group is one reason why the ISDR system is useful only in Japan.
Base Sequence↗
Infection with TT virus, a novel transfusion-transmissible DNA virus, in haemophiliacs and in blood products.
We evaluated the characteristics and rate of infection with TT virus (TTV), a novel DNA virus, in Japanese haemophiliacs. TTV DNA was measured in 60 haemophiliacs by semi-nested polymerase chain reaction. Co-infection with hepatitis C virus (HCV), hepatitis G virus (HGV) and human immunodeficiency virus (HIV) was also evaluated. In addition, the rate of detection of TTV DNA in blood products was evaluated. TTV DNA was detected in 35/60 haemophiliacs (58.3%). There were no differences in the backgrounds or characteristics between haemophiliacs with and without TTV infection, except for higher levels of IgG and IgM in patients with TTV infection. In patients infected with TTV of types other than type 1, which are rarely detected in Japan, the rate of co-infection with HCV of imported types was high; TTV of types other than type 1 in Japanese haemophiliacs were probably transmitted by imported blood products. TTV DNA was detected in over half of the blood products tested, but TTV DNA concentrations in these products were lower than in the serum of haemophiliacs.
Adolescent↗
Reactive lymphoid hyperplasia of liver coexisting with chronic thyroiditis: radiographical characteristics of the disorder.
BACKGROUND: Reactive lymphoid hyperplasia of the liver is an extremely rare entity, with six cases reported so far. METHODS: We encountered a 47-year-old Japanese female with reactive lymphoid hyperplasia of the liver, which coexisted with chronic thyroiditis. The lesion was discovered incidentally as a hypo-echoic mass with a hyper-echoic rim at a routine ultrasonography examination. It increased from 12 to 17 mm diameter in 6 months. Radiological studies, such as contrast-enhanced computerized tomography (CT) and angiography demonstrated a hypervascular lesion. RESULTS: It was consequently diagnosed as a neoplasm with malignant potentiality and she underwent partial hepatectomy. The lesion was composed of small mature lymphocytes which formed prominent lymphoid follicles with germinal centres, scattered plasma cells and stromal fibrosis. Immunohistochemical study revealed polyclonal origins of the involved lymphocytes. DNA analysis for the immunoglobulin heavy gene and the T cell receptor beta gene using Southern blot hybridization showed no monoclonality. The following features have characterized the images in past cases, as well as ours: hypo-echoic mass, occasionally with a rim, in ultrasonography and hypervascularity, shown by angiography and enhanced CT.
Angiography↗
Conformational epitopes detected by cross-reactive antibodies to envelope 2 glycoprotein of the hepatitis C virus.
The prevalence of anti-E2 antibody in persons chronically infected with hepatitis C virus (HCV) is high irrespective of viral genotype, and this cross-reactive antibody is thought to react with a conformational epitope. To investigate the characteristics of this anti-E2 antibody, the immunoreactivity of sera from HCV-1b-infected patients was measured against various modified forms of E2 glycoprotein derived from HCV-H (genotype 1a) by an immunofluorescence technique. Twelve of 18 patients were positive for anti-E2 antibody, and 10 of the 12 required a minimal amino acid (aa) region including aa 406-644 for strong reactivity, suggesting that the major E2 antibody has a conformational epitope in this region. Subsequent analysis using mutant E2 glycoproteins designed to lose N-glycosylation potential at varying sites revealed seven important N-glycosylation sites in this region. Four of these (aa 423, 430, 448, and 576) are indispensable for an antibody response.
Amino Acid Sequence↗
Fatal liver failure in haemophiliacs with HIV-induced immunodeficiency: observation of six patients.
We observed six cases of haemophiliacs with HIV-induced immunodeficiency who died from fatal liver failure despite the absence of evident cirrhosis. They all had the infection with hepatitis viruses (two patients with hepatitis B and D viruses and four patients with hepatitis C virus) and their CD4 counts were severely decreased. They were much younger than cirrhotic haemophiliacs without HIV. Their serum levels of hyaluronic acid and type IV collagen were lower than those in haemophiliacs with cirrhosis, and were normal. No patients had experienced symptoms or concomitant diseases characteristic of cirrhosis, such as ascites, jaundice, oesophageal/gastric varices or hepatocellular carcinoma, except for one case who had a history of mild ascites. The characteristics of this liver failure were different from liver failure resulting from cirrhosis caused by chronic hepatitis, which suggests liver failure that is specific to patients with immunodeficiency. This kind of liver failure can be a factor threatening survival in patients with HIV infection and with hepatitis virus co-infection in an immunodeficient state.
Acquired Immunodeficiency Syndrome↗
Inhibition of the expression of the gene for the angiotensin AT1 receptor by angiotensin II in the rat adrenal gland.
The expression of angiotensin AT1A and AT1B receptor mRNA after continuous angiotensin II administration was investigated in the rat adrenal gland. Angiotensin AT1 receptor mRNA detected by Northern blot analysis decreased to 52.7+/-16.1% of control after the administration of angiotensin II (20 microg/h) for 24 h, and to 70.8+/-8.0% after 1 week. A low dose of angiotensin II (0.2 microg/h) also decreased angiotensin AT1 receptor mRNA to 73.0+/-5.5% after 1 week. Competitive reverse transcription and polymerase chain reaction (RT-PCR) experiments revealed that both angiotensin AT1A and AT1B receptor mRNAs decreased after administration of angiotensin II (20 or 0.2 microg/h) for 1 week. Analysis of the angiotensin AT1A promoter by using luciferase-reporter system showed that angiotensin II (up to 1 microM) did not have any effects on the promoter activity (106+/-5.7% after 0.1 microM angiotensin II stimulation) in Y1 cells and cultured vascular smooth muscle cells, although phorbol myristate acetate (PMA) decreased the promoter activity by about 40% compared with control. These results suggest that angiotensin AT1 receptor gene expression in the rat adrenal gland is inhibited by angiotensin II and it may not be due to suppression of promoter activity. Other mechanisms such as destabilization of angiotensin AT1 receptor mRNA or angiotensin II-induced increased blood pressure may be involved in the inhibition.
Adrenal Glands↗
Assessment and treatment of liver disease in Japanese haemophilia patients.
We studied the prevalence of the hepatitis C virus (HCV), human immunodeficiency virus (HIV) and GB virus C or hepatitis G virus (GBV-C/HGV), and characteristics of infections in Japanese haemophilia patients. Haemophilia patients were highly infected with HCV (88.2%) because of frequent use of unheated blood concentrates. Analysis for HCV genotypes revealed characteristics of HCV infection in haemophilia patients. Japanese haemophilia patients were highly infected with rare genotypes in Japan: genotype 1a (26.5%), genotype 3 (14.5%) and genotype 4 (2.4%). HIV infection was observed in 32.3% of haemophilia patients. HCV quasispecies (clones) and direct sequencing were investigated in patients with a single HCV genotype in the hypervariable region 1 of HCV, which resulted in a high degree of diversity. This indicates that even a single genotype of HCV might have multiple origins. GBV-C/HGV infection was noted in 20.9% of Japanese haemophilia patients. Over 40 haemophilia patients with chronic hepatitis C have been treated with interferon alpha for 6 months at total doses of 480-720 million units. About 38% showed clearance of HCV RNA from serum. Six patients with HIV infection were included in the study and they did not show eradication of HCV from the serum. This might derive from that they had high serum HCV RNA titers and genotype 1a or 1b. Histologic assessment was performed in 36 haemophilia patients with HCV. No case showed a histologically normal liver. Hepatic fibrosis in the biopsy specimens was classified into five stages of fibrosis and compared with serum hepatic fibrosis markers. Serum hyaluronic acid mostly correlated with hepatic fibrosis (r = 0.78, P < 0.0001) followed by type IV collagen (r = 0.38, P < 0.05). This suggests that estimation of serum fibrosis markers might be substituted for liver biopsy in haemophilia patients.
HIV Infections↗
Prophylactic endoscopic ligation of high-risk oesophageal varices in a cirrhotic patient with severe haemophilia A.
One of the main complications in cirrhosis is haemorrhage from oesophageal varices. It is serious and often fatal, especially in cirrhotic patients with haemophilia. We describe the use of endoscopic variceal ligation (EVL) for prophylaxis of oesophageal variceal bleeding in a high-risk patient, a 40-year-old Japanese man, with severe haemophilia A and liver cirrhosis caused by hepatitis C virus. He had large, coil-shaped varices with a red colour sign, predicting the likelihood of haemorrhage. Administration of omeprazole and factor VIII concentrate achieved rapid healing of the post-EVL ulcers and prevented bleeding from them. Four EVL sessions eradicated oesophageal varices completely, and he has had no recurrence of varices for 2 years, indicating that the procedure was of considerable benefit.
Adult↗
Serum hyaluronan as a marker of liver fibrosis in hemophiliacs with hepatitis C virus-associated chronic liver disease.
We measured serum type III procollagen peptide, type IV collagen (IV-C), and hyaluronan (HA) in 36 hemophiliacs with hepatitis C virus (HCV)-related chronic liver disease. We also measured these markers in 19 interferon (IFN)-treated patients before and after a 6-month course of IFN-alpha. The serum concentrations of IV-C and HA were correlated with the stage of fibrosis (IV-C r = 0.38; HA r = 0.78). These markers fell only in complete responders showing sustained clearance of serum HCV RNA by IFN. These results suggest that, in hemophiliacs with chronic liver disease, serum HA measurement might be an alternative to liver biopsy and reflect the response to IFN.
Adolescent↗
Serum levels of soluble intercellular adhesion molecule-1 and soluble vascular cell adhesion molecule-1 in asymptomatic carriers of hepatitis C virus.
High levels of serum-soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) have been noted in patients with chronic hepatitis C. This study aimed to measure serum levels of sICAM-1 and sVCAM-1 in asymptomatic hepatitis C virus carriers and clarify the clinical significance of measuring soluble forms. Serum levels of sICAM-1 were significantly higher than in healthy controls but serum sVCAM-1 levels did not differ statistically from those in healthy controls. Liver biopsy obtained from 12 asymptomatic hepatitis C virus carriers showed evidence of hepatitis. Estimating sICAM-1 and sVCAM-1 in asymptomatic carriers may be helpful, especially in cases in which liver biopsy is not possible.
Adult↗
Quasispecies nature of hepatitis C virus (HCV) in patients with chronic hepatitis C with mixed HCV subtypes.
The quasispecies nature of hepatitis C virus (HCV) in patients with mixed HCV subtype infection was compared with that in patients with single HCV subtype infection. The number of HCV quasispecies was compared between 35 patients with mixed HCV subtype infection and 83 patients with single subtype infection. Subtype was determined by primers deduced from the core region and by line probe assay respectively. The number of quasispecies was evaluated by polymerase chain reaction amplification of hypervariable region 1 and by fluorescence single-strand conformation polymorphism analysis. There was no difference in clinical background between patients with mixed subtype infection and patients with single subtype infection. The number of quasispecies in patients with multiple subtype HCV infection was larger than in patients with single subtype HCV infection. The immunologic environments which allow the coexistence of more HCV quasispecies in patients with multiple HCV subtype infection differs from that in patients with single HCV subtype infection.
Adult↗
Naive and memory T cell infiltrates in chronic hepatitis C: phenotypic changes with interferon treatment.
The phenotypes of infiltrating lymphocytes in liver with chronic hepatitis C, including changes associated with interferon (IFN) treatment, were characterized. Specimens obtained from 22 patients treated with IFN were examined using avidin-biotin-peroxidase immunohistochemistry. In areas of lobular and periportal inflammation, most lymphocytes were CD8+ T cells of the CD45RO+ (memory) subset. The centres of lymphoid follicles were occupied by CD20+ B cells and a few CD4+ T cells which were CD45RA+ (naive subset). Follicular centres were surrounded mainly with CD4+ T cells. CD8+ T cells, mostly CD45RO+, were scattered through the mantle zones of follicles and extended around them. No significant changes in CD45RA+ lobular infiltrates accompanied IFN treatment. On the other hand, the number of CD45RO+ lobular infiltrates decreased after IFN treatment in complete responders (P < 0.01). Moreover, there were significant correlations between CD45RO+ cell counts and serum alanine aminotransferase concentrations, CD45RO+ cell counts and the liver histologic grade and CD45RO+ cell counts and CD8+ cell counts. These results suggest that CD8+ memory T cells participate in hepatocyte injury in chronic hepatitis C, and that a decrease of CD8+ memory T cells correlates with the decreased liver inflammation with IFN treatment.
Adult↗
Serum levels of tissue inhibitor of metalloproteinases-2 and of precursor form of matrix metalloproteinase-2 in patients with liver disease.
Serum levels of tissue inhibitor of metalloproteinases-2 (TIMP2) and of precursor form of matrix metalloproteinase-2 (proMMP2) were determined in patients with chronic hepatitis and hepatocellular carcinoma by a one-step sandwich enzyme immunoassay. Serum levels of TIMP2 and proMMP2 were significantly higher in patients with chronic liver disease, than in normal controls. Serum levels of TIMP2 showed a weak negative correlation with the serum albumin level and prothrombin time (PT). Serum levels of proMMP2 in patients with chronic hepatitis were strongly correlated with those of type IV collagen and were negatively correlated with PT and serum albumin levels. Serum proMMP2 levels were also significantly correlated with histological stages. These data indicate that serum levels of proMMP2 might be useful in the follow-up of patients with chronic hepatitis.
Adult↗
Serum hyaluronic acid reflects the effect of interferon treatment on hepatic fibrosis in patients with chronic hepatitis C.
Changes in serum hyaluronic acid (HA) in 35 patients treated with interferon (IFN) were studied and the histological change in fibrosis was analysed. Serum HA levels and hepatitis C virus (HCV) RNA were followed from the start of therapy to 12 months after completion of treatment. Histological changes in pre- and post-treatment liver biopsies were assessed using a modified Knodell's scoring system. The serum levels of HA (r = 0.79; P < 0.0001) correlated with the degree of fibrosis more closely than with that of amino terminal peptides of type III procollagen (PIIIP; r = 0.45; P < 0.05) or type IV collagen (IV-C; r = 0.42; P < 0.05). Only complete responders (CR) had a significant decrease in serum levels of HA and IV-C (P < 0.05), in parallel with histological improvement (P < 0.01). Neither partial responders (PR) nor non-responders (NR) had significant changes in histological scores and in serum levels of fibrotic markers. Significant differences were observed between CR and NR, both in HA levels (P < 0.01) and PIIIP levels (P < 0.05) 12 months after the cessation of treatment. These results suggest that serum HA is an indicator of the extent of fibrosis in chronic hepatitis C. Serial determinations of serum HA levels may be of use for monitoring the histological response of hepatic fibrosis to IFN treatment in chronic hepatitis C.
Adult↗
Idiopathic adulthood ductopenia.
In 1981, a 26 year old man occasionally demonstrated elevated serum transaminase concentrations. He had no history of medication, or a personal or family history of jaundice, except for prolonged physiological jaundice as a neonate. Serum hepatitis B surface antigen, hepatitis C virus antibody and anti-mitochondrial antibody were absent. A wedge biopsy specimen revealed ductular proliferation, mild inflammation of the portal area and disappearance of bile ducts from 80% of the portal tracts. Serial sections demonstrated a vanishing bile duct. Endoscopic retrograde choledochopancreatography, portography and arteriography demonstrated no abnormalities. In 1994, the patient died of hepatic failure following a 12 year observation period. He was subsequently diagnosed with idiopathic adulthood ductopenia on the basis of the criteria proposed by Ludwig.
Adult↗
Evidence of redox-linked signaling for producing a giant signal complex.
Previously we showed that a thiol-reactive heavy metal, HgCl2, crosslinked multiple cell surface receptors through a ligand-independent pathway, which produced massive aggregates of phosphotyrosine (PTYR)-containing proteins beneath plasma membrane [Nakashima et al. (1994): J Immunol 152: 1064-1071]. In this study we characterized these unique aggregates at the molecular level. The lysates in Brij 96 of thymocytes treated with HgCl2 were separated into the supernatant and pellet fractions by simple centrifugation. Selected PTYR-containing proteins and p56lck appeared in the pellet fraction as quickly as 5 s after exposure to HgCl2, and were further increased in amount by 5 min. Although the mechanism of triggering these events was redox-linked, the majority of proteins in the Brij 96-insoluble aggregates were dissociated in SDS-PAGE under nonreducing condition. This suggested that PTYR-containing proteins and p56lck themselves do not form dimer or polymer directly by thiol-mediated bond. The pellet fraction was further found to include some other signal delivery elements, such as GTPase activating protein, phosphatidylinositol 3 kinase, and mitogen-activated protein kinase. Finally, all of these signal elements and selected PTYR-containing proteins were collected in the same fraction by the sucrose density gradient centrifugation. These results suggest a unique redox-linked pathway of formation of a giant signal complex.
Animals↗