Biomedical subjects

M Mayumi

Publications and source records attributed to M Mayumi.

At least 127 records · Page 7Linked to original sources

PubMed1995

Hepatitis B virus strains with mutations in the core promoter in patients with fulminant hepatitis.

OBJECTIVE: Fulminant hepatitis B can be induced by hepatitis B virus (HBV) strains with mutations in the precore region that cannot encode hepatitis B e antigen (HBeAg). Such mutations are rarely seen in HBV DNA clones from patients with fulminant hepatitis B in the United States and France. Thus, the other mutations in HBV strains causing fulminant hepatitis B need to be identified. DESIGN: Retrospective clinical, serologic, and molecular biological studies of patients with fulminant hepatitis B. SETTING: University and city hospitals in Japan. PATIENTS: 43 patients with fulminant hepatitis B. MEASUREMENTS: The precore region coding for a part of the HBeAg precursor and the core promoter regulating the transcription of precore messenger RNA were sequenced in HBV DNA clones. RESULTS: A point mutation from G to A at nucleotide 1896 in the precore region was detected in 519 (98%) of 529 HBV DNA clones from 38 patients. Two point mutations in the core promoter, from A to T at nucleotide 1762 and from G to A at nucleotide 1764, were detected in all 130 clones from the remaining 5 patients, who did not have mutations in the precore region, and in 20 (63%) of 32 clones from a patient with chronic hepatitis B who had transmitted HBV to 1 of these other 5 patients. Mutations in the core promoter were also detected in clones from 26 (68%) of the 38 patients with the precore mutation at nucleotide 1896. Neither HBeAg nor antibody to HBeAg was detected in 37 (90%) of the 41 patients tested. CONCLUSIONS: In Japan, fulminant hepatitis B is closely associated with HBV strains that do not produce HBeAg because of mutations in the precore region, which affect translation of HBeAg, or because of mutations in the core promoter, which affect transcription of the HBeAg coding region.

Acute Disease↗

PubMed1995

Cis-acting DNA elements of mouse granulocyte-macrophage colony-stimulating factor gene responsive to Fc epsilon receptor cross-linking stimulation in the mouse mast cell line MC/9.

Mouse mast cells produce many kinds of cytokines in response to cross-linking of high affinity Fc epsilon receptor (Fc epsilon RI). Among these cytokines, granulocyte-macrophage CSF (GM-CSF) gene induction in mouse mast cells has been reported to be regulated at both the transcriptional level and the post-transcriptional level. We analyzed the mechanism of the transcriptional regulation of GM-CSF gene induction through Fc epsilon RI cross-linking stimulation in the mouse mast cell line MC/9. In MC/9, the GM-CSF gene was activated transcriptionally by Fc epsilon RI cross-linking stimulation. The 5' deletion analysis of GM-CSF gene promoter indicated that the 5' boundary of the responsive promoter region lay between positions -113 and -95. When the deletion was extended to positions -72 or -60, the stimulatory effect was significantly diminished. We then examined 3' deletion of pmGMCAT -113 from position -60. This analysis indicated that the 3' boundary lay between positions -84 and -72. No subfragments of the region spanning positions -113 to -72 could cover the full induction level. A site-directed mutagenesis experiment revealed that the sequence spanning positions -108 to -72 was needed for full activation. These data indicate that GM-CSF gene in mast cells is activated mainly through the sequence spanning positions -108 to -72.

Animals↗

PubMed1995

Serum levels of interleukin 4 and soluble CD23 in children with allergic disorders.

UNLABELLED: In order to clarify the clinical significance of serum interleukin 4 (IL-4) levels, we measured serum IL-4 concentrations in allergic and non-allergic children using a highly sensitive sandwich ELISA. The limit of detection of the assay was 0.15 pg/ml in serum samples. Serum IL-4 was detected in 96.3% (53/55) of non-allergic controls, in 92.9% (183/197) of allergic children, in 70% (7/10) of cord blood samples and in 86.7% (26/30) of neonates. The IL-4 levels in sera from non-allergic controls were relatively constant during the ages examined and all samples were under 1.5 pg/ml. In allergic children, the serum levels of IL-4 were significantly elevated, particularly at age 13-24 months. The serum levels of IL-4 did not differ in children with different clinical manifestations of allergy, such as bronchial asthma, and atopic dermatitis. The serum level of soluble CD23 (sCD23) showed an age-dependent change in allergic and non-allergic children and was significantly higher in allergic than in non-allergic infants aged 7 to 12 months, but not in other age groups. There was no significant correlation among serum levels of IL-4, sCD23 and IgE. CONCLUSION: It is suggested that the measurement of serum IL-4 and sCD23 is helpful in the examination of allergic patients in infancy and early childhood, but neither the serum level of IL-4 nor sCD23 directly reflects in vivo IgE production.

Asthma↗

PubMed1995

Physical interaction with monocytes rescues human mature CD4+ T-cell lines from anti-CD3-induced apoptosis.

Crosslinking of the TcR-CD3 complex with immobilized anti-CD3 antibodies without sufficient co-stimulation induced cell death in human mature CD4+ T-cell lines. In these T cells, DNA fragmentation and morphological characteristics of apoptosis were seen. The anti-CD3-induced apoptosis was inhibited by co-culture with monocytes. The rescue signal provided by monocytes does not need to be present simultaneously with signals mediated by anti-CD3. When T cells were precultured with monocytes for 24 h before anti-CD3 stimulation and then the monocytes were removed from the culture, anti-CD3-induced T-cell apoptosis was also inhibited. To determine whether the monocyte-derived rescue signals were transduced by soluble factors or by direct cell-to-cell interaction with monocytes, we precultured T cells with monocytes separated by a micropore membrane which prevented T cell-monocyte physical interaction but not the diffusion of secreted molecules. In this system, rescue signals could not reach the T cells. To further assess the importance of physical interaction, we precultured T cells with fixed monocytes. T cells could not be rescued from apoptosis under these experimental conditions, either. The results considered collectively suggest that sufficient physical interaction with viable monocytes is important for the rescue of anti-CD3-induced apoptosis of CD4+ T cells.

Antibodies, Monoclonal↗

PubMed1995

Cold activation of complement as a marker of hepatitis C viremia in sera from blood donors.

Sera from 49,088 blood donors were tested for markers of hepatitis C virus (HCV) infection and decreased hemolytic activity after they had been stored at 4 degrees C for 24 h, a phenomenon known as the cold activation of complement. Antibody to HCV (anti-HCV) was detected in 315 (0.64%) units, of which 181 (57%) were positive for HCV RNA. The cold activation of complement was detected in 170 (0.35%) units, and HCV RNA was detected in 140 (82%) of them. Thus, the cold activation of complement was observed in 140 (77%) of 181 blood units with HCV RNA. The close association of HCV viremia with the cold activation of complement would be useful as a surrogate test in preventing post-transfusion HCV infection in developing areas where anti-HCV assays are not easily performed.

Biomarkers↗

PubMed1995

Classifying hepatitis C virus genotypes.

Hepatitis C virus (HCV) is the major aetiological agent for blood-borne non-A, non-B hepatitis worldwide. Since its discovery in 1989, at least 28 HCV genotypes have been reported, which differ by > 20% in the nucleotide sequence of the entire genome (approximately 9500 nucleotides) or the sequence of the E1 gene (576 nucleotides). Different HCV genotypes have distinct geographical distributions, and may be associated with variations in viral replication and disease-inducing activity, as well as poor response to interferons in patients with chronic hepatitis C.

Genetic Techniques↗

PubMed1995

Role of LFA-1/ICAM-1-dependent cell adhesion in CD40-mediated inhibition of anti-IgM antibody-induced B-cell death.

Cross-linking of surface IgM by anti-IgM antibody caused activation-induced cell death of a surface IgM+, IgD+ human B lymphoma cell line, B104. The dying B104 cells did not show the morphology of apoptosis but did show that of necrosis. However, anti-IgM antibody caused apoptosis of another surface IgM+, IgD+ human B lymphoma cell line, DND-39. The influx of extracellular Ca2+ was necessary for the cell deaths of B104 and DND-39 caused by anti-IgM antibody. Their cell deaths were inhibited by cyclosporine. The anti-IgM antibody-induced cell death of DND-39, but not that of B104, was prevented by costimulation with anti-CD40 antibody. In human peripheral blood B-cells, anti-IgM antibody inhibited cell cycle transition induced by Staphylococcus aureus Cowan I at the G2/M interphase without inhibition of DNA synthesis. In this system, too, anti-CD40 antibody canceled the inhibitory signal transduced through surface IgM and increased the number of M phase cells. Blocking antibodies against the leukocyte function-associated antigen-I/intercellular adhesion molecule-1 system decreased the rescue effect of anti-CD40 antibody in both DND-39 cells and peripheral B-cells, which shows that leukocyte function-associated antigen-1/intercellular adhesion molecule-1-dependent cell adhesion plays an important role in the CD40-mediated inhibition of surface IgM-mediated negative signals.

Animals↗

PubMed1995

A common-source outbreak of fulminant hepatitis B in hemodialysis patients induced by precore mutant.

From September 9 to October 3, 1994, five patients on maintenance hemodialysis in a dialysis unit in Tokyo contracted hepatitis B virus (HBV) infection successively, and four of them died of fulminant hepatitis. The unit treated 181 patients three times a week on eight shifts, and all five afflicted patients were on the same shift along with 27 other patients. HBV DNA clones from the hepatitis patients had a point mutation converting codon 28 in the precore region to a stop codon, which aborts the synthesis and secretion of hepatitis B e antigen, and showed a sequence similarity of > 99.5% within 645 base pairs covering the X gene and precore region. There were two HBV carriers with antibody to hepatitis B e antigen who were receiving hemodialysis on the same shift. HBV DNA clones from one of them had the stop codon 28 in the precore region, and a sequence similarity of > 99.7% to those from the five patients. Based on these results, it was deduced that the fulminant HBV strain was transmitted from the carrier to five patients, and resulted in the death of four. The outbreak indicates that immunocompromised hosts like hemodialysis patients can develop fulminant hepatitis B if and when they are infected with extremely virulent HBV strains.

Acute Disease↗

PubMed1995

Hepatitis C virus variants from Thailand classifiable into five novel genotypes in the sixth (6b), seventh (7c, 7d) and ninth (9b, 9c) major genetic groups.

Nine (10%) out of 90 hepatitis C virus (HCV) isolates from hepatitis patients and commercial blood donors in Thailand were not classifiable into any of genotypes I/1a, II/1b, III/2a, IV/2b, V/3a or VI/3b by RT-PCR with type-specific primers deduced from the HCV core gene. These isolates were sequenced over a 1.6 kb stretch of the 5'-terminal sequence and 1.1 kb of the 3'-terminal sequence covering 30% of the entire genome. Based on two-by-two comparison and phylogenetic analyses of the nine Thailand isolates among themselves and with known full or partial sequences of previously reported HCV isolates, the Thailand isolates were classified into five genotypes not reported previously, viz. 6b, 7c, 7d, 9b and 9c. Along with HCV isolates reported already, they make at least nine major genetic groups of HCV which further break down into at least 28 genotypes with sequence similarity in the E1 gene (576 bp) of < or = 80%. As many more HCV isolates of distinct genotypes are expected to be found throughout the world, it will become increasingly difficult to classify them by comparison of any partial sequences of the genome. Complete sequence data will be required for the full characterization and classification of HCV genotypes.

Amino Acid Sequence↗

PubMed1995

Selective induction of interleukin-4- and interferon-y-producing T cells from cord blood naive T cells. Effects of costimulatory signaling through CD28.

We investigated the effect of costimulation through CD28 and CD11a on the differentiation of human naive CD4+ T cells with restricted cytokine production profiles. Interleukin (IL)-4 and interferon-gamma (IFN-gamma) were measured by ELISA and IL-2 was detected by a bioassay. Naive CD4+ T cells proliferated and produced IL-2 upon cross-linking of CD3, and costimulation through CD28 enhanced IL-2 production. After repeated stimulation, CD4+ T cells which were stimulated in the absence of costimulation through CD28 lost their ability to secrete IL-2 and started secreting IL-4 and IFN-gamma. Instead in the presence of costimulation through CD28, they secreted IL-2, IL-4 and IFN-gamma. Blocking of endogenous IL-4 activity with anti-IL-4 Ab suppressed the IL-4 secretion and proliferation of T cells.

CD28 Antigens↗

PubMed1995

IgM-mediated B cell apoptosis.

Cross-linking of surface immunoglobulin M (sIgM) on normal mature B cells induces different signaling consequences, including DNA synthesis (positive signaling) and cell cycle arrest and/or death by apoptosis (negative signaling). Presumably, the difference depends on the intensity of sIgM cross-linking: relatively weak cross-linking induces DNA synthesis, moderate cross-linking induces DNA synthesis with cell cycle arrest at the G2/M interphase, and intense cross-linking induces apoptosis. In vivo experiments with transgenic mice have shown that relatively weak cross-linking of sIgM by soluble antigens induces anergy in autoreactive B cells, whereas intense sIgM cross-linking by membrane-bound forms of antigens induces deletion of them. However, it is still unknown whether the different intensities of sIgM cross-linking generate qualitatively different signals responsible for DNA synthesis or cell death or whether they generate qualitatively the same but quantitatively different signals, and the quantitative difference is responsible for the induction of positive or negative signaling. The sIgM-mediated negative signaling presumably plays an important role in the induction and maintenance of B cell tolerance, and sIgD and sIgG also possess the machinery necessary for negative signaling. Negative signaling through sIgM is dependent on tyrosine kinase(s) and Ca2+ influx and is sensitive to cyclosporin A in certain types of B cells but not in all B cells. It has been suggested that there are different intracellular signaling pathways that transduce negative signaling via sIgM, and that activation-induced B cell death by sIgM cross-linking does not necessarily show DNA fragmentation and the morphology of apoptosis. On the other hand, sIgM-mediated B cell death may be inhibited in the presence of appropriate co-stimulators such as IL-4, alpha-, and beta-interferons and CD40-mediated signaling. The CD40-mediated signaling effectively inhibits sIgM-mediated B cell apoptosis in many but not all experimental systems. Although homotypic cell adhesion through the LFA-1/ICAM-1 dependent pathway was shown to be involved in certain types of CD40-mediated inhibition of sIgM-mediated negative signaling, it is still not known how the cytokines and CD40-mediated signaling inhibit sIgM-mediated B cell death. The molecular mechanisms responsible for sIgM-mediated negative signaling and for the inhibitory signaling against sIgM-mediated negative signaling need further elucidation.

Animals↗

PubMed1994

Hepatitis C virus variants from Vietnam are classifiable into the seventh, eighth, and ninth major genetic groups.

Thirty-four (41%) of 83 hepatitis C virus (HCV) isolates from commercial blood donors in Vietnam were not classifiable into genotype I/1a, II/1b, III/2a, IV/2b, or V/3a; for 15 of them, the sequence was determined for 1.6 kb in the 5'-terminal region and 1.1 kb in the 3'-terminal region. Comparison of the 15 Vietnamese isolates among themselves and with reported full or partial HCV genomic sequences indicated that they were classifiable into four major groups (groups 6-9) divided into six genotypes (6a, 7a, 7b, 8a, 8b, and 9a). Vietnamese HCV isolates of genotypes 7a, 7b, 8a, 8b, and 9a were significantly different from those classified into groups 4, 5, and 6 based on divergence within partial sequences; those of genotype 6a were homologous to a Hong Kong isolate (HK2) of genotype 6a. Phylogenetic trees based on the envelope 1 (E1) gene (576 bp) of 55 isolates and a part of the nonstructural 5 (NS5) region (1093 bp) of 43 isolates revealed at least nine major groups, three of which (groups 7, 8, and 9) were identified only in Vietnamese blood donors. With a prospect that many more HCV isolates with significant sequence divergence will be reported from all over the world, the domain of the HCV genome to be compared and criteria for grouping/typing and genotyping/subtyping will have to be determined, so that they may be correlated with virological, epidemiological, and clinical characteristics.

Base Sequence↗

PubMed1994

Involvement of LFA-1/intracellular adhesion molecule-1-dependent cell adhesion in CD40-mediated inhibition of human B lymphoma cell death induced by surface IgM crosslinking.

B cells have been shown to receive negative signals for their growth through crosslinking of surface IgM (sIgM), and it has been demonstrated that anti-IgM Abs induce B cell death. Proliferation of B cells in response to Ag stimulation in vivo may thus require additional signals that inhibit the sIgM-transduced negative signals. Signaling through CD40 has been proposed as a candidate for such costimulatory signals. To investigate the role of CD40-transduced signals in sIgM-mediated B cell death, we used a human B cell line (DND-39) that expresses sIgM, sIgD, and CD40. Crosslinking of sIgM, but not sIgD, by Abs induced DND-39 cell death. The dying cells showed the morphology of apoptosis and DNA fragmentation. Anti-CD40 Abs induced homotypic adhesion of DND-39 cells and rescued them from anti-IgM Ab-induced cell death. Anti-CD40 Abs inhibited anti-IgM Ab-induced cell death when added within 3 h after stimulation with anti-IgM Ab. Treatment with Abs against CD11a, CD18, or CD54 inhibited not only the homotypic adhesion but also the inhibition of anti-IgM Ab-induced apoptosis by anti-CD40 Ab. CD11a antisense decreased the surface CD11a expression, the anti-CD40 Ab-induced homotypic adhesion, and the inhibitory effect of anti-CD40 Ab on anti-IgM Ab-induced apoptosis. The data show that LFA-1/ICAM-1-dependent cell adhesion induced by signaling through CD40 plays an important role in the inhibition of anti-IgM Ab-induced apoptosis of DND-39 cells.

Antigens, CD↗

PubMed1994

Hepatitis C virus infection in spouses of patients with type C chronic liver disease.

OBJECTIVE: Survey for markers of hepatitis C virus (HCV) infection in spouses of patients with HCV-related chronic liver disease. DESIGN: Cross-sectional clinical, serologic, and molecular biological study of spouses of patients with HCV viremia and chronic liver disease. SETTING: University and city hospitals. PARTICIPANTS: Spouses (52 men and 102 women; mean age, 56 +/- 11 years) of 154 patients with HCV viremia (102 men and 52 women; mean age, 58 +/- 10 years), of whom 66 had chronic hepatitis, 49 had liver cirrhosis, and 39 had primary hepatocellular carcinoma. METHODS: Tests for HCV-associated antibodies were done using a second-generation enzyme immunoassay and immunoassays with synthetic oligopeptides deduced from the HCV core gene. Hepatitis C virus RNA was detected by polymerase chain reaction with primers deduced from the 5'-noncoding region and HCV genotypes by reaction with type-specific primers deduced from the HCV core gene. RESULTS: Hepatitis C virus-associated antibodies were detected in 42 (27%) spouses, of whom 25 were also positive for HCV RNA. Of 112 (73%) spouses without detectable antibodies, 2 had chronic liver disease. The development of markers of HCV infection in spouses increased with the duration of marriage, ranging from 1 to 60 years (30 +/- 11 years). CONCLUSIONS: Spouses of patients with HCV viremia and chronic liver disease have an increased risk for acquiring HCV, which is proportional to the duration of marriage. They should be followed routinely for markers of HCV infection and liver disease.

Aged↗

PubMed1994

Involvement of CD11b/CD18 in enhanced neutrophil adhesion by Fc gamma receptor stimulation.

Neutrophils showed a rapid and transient adhesion to immunoglobulin G (IgG)-coated plates compared with their adhesion to bovine serum albumin (BSA)-coated plates: the adhesion reached a peak after 15 min of incubation and then gradually returned to almost the basal state in 60 min. The addition of monomeric IgG or anti-Fc gamma RII monoclonal antibody (mAb) (IV.3) suppressed the increase in adhesion, whereas anti-Fc gamma RIII mAb (3G8) was hardly effective, indicating that the interaction of Fc gamma R, especially Fc gamma RII, with coated IgG is involved in the process. Adhesion was also blocked by cytochalasin B, suggesting that functional actin filament structures are crucial. Protein kinase inhibitors, erbstatin and genistein, inhibited the adhesion in a dose-dependent manner. The adhesion was inhibited by anti-CD11b (M1/70) and anti-CD18 (MHM23, TS1/18) mAbs. Moreover, neutrophils from a patient with complete leukocyte adhesion deficiency syndrome did not show increased adhesion to IgG-coated plates. The adhesion of neutrophils to fibrinogen- and BSA-coated plates was also increased when Fc gamma R was stimulated in the fluid phase with soluble aggregated IgG, which was also inhibited by anti-CD11b mAb. Stimulation of neutrophil Fc gamma R with soluble aggregated IgG enhanced the expression of CD11b in concert with the enhanced adhesion. These data collectively suggest that stimulation via Fc gamma R evokes a tyrosine kinase-dependent and actin filament-dependent intracellular signal that enhances the specific and nonspecific adhesive activity of neutrophils, presumably through the activation of CD11b/CD18.

Adult↗

PubMed1994

Genotypes and titers of hepatitis C virus for predicting response to interferon in patients with chronic hepatitis C.

Interferon induces remission in about 50% of patients with chronic hepatitis C, but it is difficult to predict which patients will respond. Host and viral factors were evaluated for correlation with response to interferon in patients with chronic hepatitis C. Recombinant interferon alpha-2b with a total dose of 480-560 million units was given to 136 patients, of whom 74 (54%) responded. Genotypes of hepatitis C virus (HCV) in sera, I, II, III, IV, and V, were determined by polymerase chain reaction (PCR) with type-specific primers. In 72 patients, pretreatment levels of HCV RNA were titrated by PCR in serial tenfold dilutions of RNA extracted from serum. Response to interferon occurred in 34 (40%) of 85 patients infected with HCV of genotype II, less frequently than in 22 (85%) of 26 with genotype III (P < 0.001) or in 7 (70%) of 10 with genotype IV. Of 51 patients with genotype II HCV, 6 of 8 (75%) with HCV RNA titers < 10(6) responded, more frequently than 4 of 43 (9%) with titers > or = 10(6) (P < 0.001). Responders were younger than non-responders (45.7 +/- 11.7 vs. 50.3 +/- 9.6 yr) and had received transfusions less frequently (26/74 or 35% vs. 37/62 or 60%, P < 0.01). Response to interferon correlated inversely with the severity of liver histopathology. These results indicate that response to interferon is influenced by HCV genotypes and pretreatment levels of HCV RNA in serum.

Adult↗

PubMed1994

Hepatitis B virus subtypes and hepatitis C virus genotypes in patients with chronic liver disease or on maintenance hemodialysis in Indonesia.

Hepatitis B surface antigen (HBsAg) and hepatitis C virus (HCV) RNA were surveyed in patients in Yogyakarta, Indonesia, and their subtypes and genotypes were determined by serological methods and polymerase chain reaction with type-specific primers, respectively. Of 149 patients with chronic liver disease including 24 with chronic hepatitis, 86 with liver cirrhosis, and 39 with primary hepatocellular carcinoma, HBsAg was detected in 40 (27%) and HCV RNA in 48 (32%); one patient was positive both for HBsAg and HCV RNA. Thus, the cause of chronic liver disease was not identified in 62 (42%) patients. Of 58 patients on maintenance hemodialysis, four (7%) were positive for HBsAg and 44 (76%) for HCV RNA. Subtype adw was found in 34 (74%) of 46 HBsAg samples and adr in five (11%); compound subtypes, such as adyw and adyr were detected in the remaining seven (15%). Among HCV RNA samples from 48 patients with chronic liver disease, 23 (48%) were of genotype II, 17 (35%) of genotype III and one (2%) of genotype V, in a distribution strikingly different from that of 44 samples from patients on maintenance hemodialysis, 39 (89%) of which were of genotype I and only one (2%) of genotype II. Genotypes were not classifiable in seven (15%) patients with liver disease and four (9%) patients on hemodialysis despite high HCV RNA titers in them all. These results indicate that different HCV genotypes prevail in patients with distinct diseases, as well as unclassifiable HCV genotypes in Indonesia.

Adult↗

PubMed1994

Hepatitis C virus infection in patients with chronic liver disease or chronic renal failure and blood donors in Thailand.

Hepatitis C virus (HCV) RNA and genotypes, as well as markers of hepatitis B virus infection, were surveyed in 171 patients with chronic liver disease, 276 patients with chronic renal failure, and 961 blood donors in Thailand. HCV RNA was detected in 30 (23%) of 128 patients with non-alcoholic chronic liver disease and hepatitis B surface antigen (HBsAg) in 60 (47%), and both HCV RNA and HBsAg in 3; the cause of liver disease was not established in 41 (32%) patients. HCV RNA was detected in 44 (20%) of 221 patients on maintenance hemodialysis or with kidney transplantation, but in none of 55 patients on peritoneal dialysis. Antibodies to synthetic HCV core peptides were detected in 39 (4.1%) of sera from 961 blood donors, and HCV RNA was detected in 8 (0.8%). Of the 90 HCV RNA samples from patients and donors, genotype V prevailed (46%) followed by II (22%), I (14%), III (3%), and VI (2%); genotypes were not classifiable into any of I-VI in the remaining 10%. There were six sera which contained HCV RNA, but were without antibody to HCV detectable by the second-generation enzyme immunoassay. HCV RNA titers were high in four patients with kidney transplantation, but low in one patient with chronic liver disease and one patient on maintenance hemodialysis. HCV RNA at high titer (> or = 10(4)/ml) was not classifiable in one patient. These results indicate HCV of novel genotypes in Thailand, seronegative HCV infection in patients with kidney transplantation, and a low risk of HCV infection in patients treated by peritoneal dialysis.

Adult↗