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PubMed1996

[A study on angiotensin-I converting enzyme polymorphism in CAPD patients].

To clarify the role of genes related to angiotensin-I converting enzyme (ACE), the author investigated polymorphism of the ACE gene in 60 patients undergoing chronic ambulatory peritoneal dialysis (CAPD) and 50 patients undergoing hemodialysis (HD). One hundred healthy subjects were used as controls. The polymorphism was classified into three genotypes, II, ID and DD, according to insertion (I) and deletion (D) using the polymerase chain reaction method. In dialysis patients (CAPD or HD, n = 110), 21.8% had the II genotype, 48.2% the ID genotype, and 30.0% the DD genotype. There was a significant difference in allele frequency between normal subjects (n = 100) (J = 0.63, D = 0.37) and dialysis patients (I = 0.46, D = 0.54) (chi 2 = 12.321, p < 0.001). The mean plasma ACE activity was 9.9 +/- 1.6 IU/l in CAPD patients with the II genotype, 11.6 +/- 4.7 IU/l in CAPD patients with the ID genotype, and 14.5 +/- 3.5 IU/l in CAPD patients with the DD genotype. The mean rate of decrease in residual urinary volume was 0.8 +/- 0.7% per month in CAPD patients with the II genotype 1.4 +/- 1.3% per month in CAPD patients with the ID genotype, and 2.5 +/- 2.0% per month in CAPD patients with the DD genotype. These data showed a significant decrease in urinary volume in CAPD patients with the DD genotype (p < 0.05). The mean rate of decrease in residual urinary volume was positively correlated with the plasma ACE activity (r = 0.13389, p < 0.02). In CAPD patients, the mean cardiothoracic ratio was 46.6 +/- 3.5% in cases with the II genotype, 47.6 +/- 5.5% in cases with the ID genotype, and 52.9 +/- 8.4% in cases with the DD genotype. These data indicated significant cardiac enlargement in DD genotype cases. It can be concluded that CAPD patients with the DD genotype lost their residual renal function more rapidly and had a larger heart, than patients with the other genotypes.

Adult↗

PubMed2000

Insertion/deletion polymorphism of the angiotensin I-converting enzyme gene is not associated with restenosis after coronary stent placement.

BACKGROUND: The renin-angiotensin system is thought to play a role in coronary thrombosis and restenosis. Plasma angiotensin I-converting enzyme (ACE) activity is associated with an insertion/deletion polymorphism in the gene coding for ACE. The objective of this study was to test the hypothesis that the D allele of the ACE gene is associated with a higher risk for restenosis after coronary stent placement. METHODS AND RESULTS: This prospective study included 1850 consecutive patients with coronary artery disease who underwent intracoronary stent implantation. The adverse clinical events recorded were death, myocardial infarction, and target vessel revascularization. The primary end point of the study was restenosis (>/=50% diameter stenosis at follow-up angiography performed in 84% of the patients). The secondary end point was clinical outcome 1 year after the procedure. The restenosis rate at the 6-month angiographic follow-up was 32.8% in patients with the II genotype, 34.0% for patients with the ID genotype, and 31.2% for patients with the DD genotype (P=0.62). One-year event-free survival was 77.7% in patients with genotype II, 75.2% in patients with genotype ID, and 75.5% in patients with genotype DD (P=0.54). The lack of association was also present in the subgroup of patients with a low risk for restenosis: the restenosis rate was 21.7% in II carriers, 23.4% in ID carriers, and 19.7% in DD carriers (P=0.83). CONCLUSIONS: The ACE DD genotype or D allele does not influence the 1-year clinical and angiographic outcome of patients undergoing coronary stent placement. These data suggest that routine determination of the ACE genotype may not help identify patients who are at a higher risk of thrombotic and restenotic events after coronary stent placement.

Aged↗

PubMed2005

[Angiotensin converting enzyme gene and exercise-induced silent myocardial ischemia in type 2 diabetes mellitus].

OBJECTIVE: To investigate the relationship between angiotensin converting enzyme (ACE) gene and exercise-induced silent myocardial ischemia (SI) in patients with type 2 diabetes mellitus. METHODS: One hundred and eight patients suffering from type 2 diabetes mellitus with normal rest electrocardiograph and 50 healthy individuals were selected randomly. SI was diagnosed with treadmill exercise test and ACE genotypes were detected with PCR. RESULTS: (1) The control group and type 2 diabetes mellitus group had similar distribution of ACE genotypes and alleles (P>0.05). Compared with the non-SI group, the SI group had significantly higher ACE D allele prevalence (Chi-square=4.501, P<0.05); however, the two groups had similar prevalence of ACE genotypes (P>0.05). (2) There were no significant differences in clinical characteristics and serum lipoproteins among the three ACE genotypes (II, DD,ID) of type 2 diabetes mellitus (P>0.05). (3) The prevalence of SI in DD group was found to be 68.2%, which was significantly higher than that in II genotype group (39.5%, Chi-square=4.593, P<0.05). CONCLUSION: ACE D allele increases the risk of SI in type 2 diabetes mellitus.

Adult↗

PubMed1996

Response to interferon in chronic hepatitis C due to mixed genotype infection.

We examined the response to interferon (IFN) in patients with chronic hepatitis C (CHC) due to two different genotypes of hepatitis C virus (HCV) infection. Among 64 CHC patients studied, one (2%) had HCV-RNA genotype I, 36 (56%) had genotype II, 19 (30%) had genotype III, 2 (3%) had genotype IV and 6 (9%) had both genotypes II and III. There was no significant difference in age, sex, history of blood transfusion and liver histology among patients with genotypes II, III and II + III. The HCV-RNA titre of genotype II patients was significantly higher than that of genotype III patients (P < 0.05). However, there was no significant difference in the HCV-RNA titre between genotype II + III and the other groups. The complete response rate achieved with IFN therapy was significantly higher in genotype III patients (74%) than in genotype II patients (17%; P < 0.01). Of the six patients with genotype II + III, a complete response to IFN was only achieved by two patients (33%), both of whom had a low HCV-RNA titre ( < or = 10(4.5) copies/mL) and HCV serotype 2. The remaining four patients had HCV serotype 1 and three of the patients had a high HCV-RNA titre ( > or = 10(5) copies/mL). The HCV genotype III was lost in two patients after IFN therapy. These data suggest that HCV-RNA titre and HCV serotype are important factors for predicting the efficacy of IFN therapy in patients with mixed genotype infection and show direct evidence of higher susceptibility towards CHC of patients with genotype III than genotype II.

Adolescent↗

PubMed2003

Analysis of the SAG5 locus reveals a distinct genomic organisation in virulent and avirulent strains of Toxoplasma gondii.

We have recently characterised, in the virulent strain RH of Toxoplasma gondii, three glycosylphosphatidylinositol-anchored surface antigens related to SAG1 (p30) and encoded by highly homologous, tandemly arrayed genes named SAG5A, SAG5B and SAG5C. In the present study, we compared the genomic organisation of the SAG5 locus in strains belonging to the three major genotypes of T. gondii. Southern blot analysis using a SAG5-specific probe produced two related but distinct hybridisation patterns, one exclusive of genotype I virulent strains, the other shared by avirulent strains of either genotype II or genotype III. To understand the molecular bases of this intergenotypic heterogeneity, we cloned and sequenced the SAG5 locus in the genotype II strain Me49. We found that in this isolate the SAG5B gene is missing, with SAG5A and SAG5C laying contiguously. This genomic arrangement explains the hybridisation profiles observed for all the avirulent strains examined and indicates that the presence of SAG5B is a distinctive trait of genotype I. Furthermore, we identified two novel SAG1-related genes, SAG5D and SAG5E, mapping respectively 1.8 and 4.0 kb upstream of SAG5A. SAG5D is transcribed in tachyzoites and encodes a polypeptide of 362 amino acids sharing 50% identity with SAG5A-C, whereas SAG5E is a transcribed pseudogene. We also evaluated polymorphisms at the SAG5 locus by comparing the coding regions of SAG5A-E from strains representative of the three archetypal genotypes. In agreement with the strict allelic dimorphism of T. gondii, we identified two alleles for SAG5D, whereas SAG5A, SAG5C and SAG5E were found to be three distinct nucleotide variants. The higher intergenotypic polymorphism of SAG5A, SAG5C and SAG5E suggests that these genes underwent a more rapid genetic drift than the other members of the SAG1 family. Finally, we developed a new PCR-restriction fragment length polymorphism method based on the SAG5C gene that is able to discriminate between strains of genotype I, II and III by a single endonuclease digestion.

Animals↗

PubMed1995

Relationship of genotype to level of hepatitis C viraemia determined by competitive polymerase chain reaction.

To compare the levels of hepatitis C virus (HCV) viraemia in carriers of the same genotype in various stages of chronic HCV infection, we quantified the amount of HCV RNA by competitive polymerase chain reaction and determined HCV genotype using type-specific primers. The study population included 255 patients with chronic HCV infection (asymptomatic 33, chronic hepatitis 141, liver cirrhosis 50, hepatocellular carcinoma 31). Of these 255, the prevalence of HCV RNA genotype II was 67.8%, genotype III, 17.3% and genotype IV, 14.9%; no genotype I was found. The level of HCV RNA (logarithmic transformed copy numbers per 50 microliters of serum) was significantly higher in subjects of genotype II than in those of genotypes III or IV (mean titre 5.8 +/- 1.0 vs. 5.1 +/- 1.2 and 4.8 +/- 1.1, P < 0.05, respectively). There was no significant difference in the level of HCV RNA between genotypes III and IV. Of 173 patients of genotype II, there were no significant differences between the level of HCV RNA and the stage of liver disease or in the level of HCV RNA by age. Of the 129 with genotype II with a history of blood transfusion, there was no significant difference between the level of HCV RNA of patients with and without a history of transfusion or between that of patients with a history of blood transfusion and the time elapsed since blood transfusion. The level of HCV viraemia depended on the genotype of HCV RNA and did not correlate to age or to the stage of liver disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2003

Relationship between polymorphism of the angiotensin-converting enzyme gene and the response to angiotensin-converting enzyme inhibition in hypertensive patients.

The aim of this study was to investigate the relationship between polymorphism of the anglotensin-converting enzyme (ACE) gene and the blood pressure response to ACE inhibition in a hypertensive cohort. Imidapril (5-10 mg/day) or benazepril (10-20 mg/day) was administered for 6 weeks to 517 essential hypertensives. ACE gene polymorphism was examined by the polymerase chain reaction (PCR) method and the patients were classified as having the 190-bp deletion homozygous (DD) genotype, the 490-bp insertion homozygous (II) genotype, or the 490-bp insertion, 190-bp deletion heterozygous (ID) genotype. The achieved change in systolic and diastolic blood pressure (SBP and DBP) was analyzed for association with genotypes at the ACE gene locus. The DD genotype was observed in 132 patients (25.5%), the ID genotype in 255 patients (49.3%), and the II genotype in 130 patients (25.2%). The SBP reductions in the patients with the DD genotype, II genotype, and ID genotype were -14.5 +/- 12.7 mmHg, -14.3 +/- 13.1 mmHg and -14.0 +/- 12.2 mmHg, respectively (p = 0.94). The DBP reductions in the patients with the DD genotype, II genotype, and ID genotype were -8.7 +/- 7.4 mmHg, -8.7 +/- 7.7 mmHg and -8.5 +/- 6.7 mmHg, respectively (p = 0.96). There was no significant association between the ACE gene polymorphisms and the response to ACE inhibition. These results suggest that ACE genotype does not predict the blood pressure-lowering response to antihypertensive treatment with ACE inhibition.

Aged↗

PubMed2003

Influence of the Alu-repeat I/D polymorphism in t-PA gene intron 8 on the stimulated t-PA release after venous occlusion.

Tissue type plasminogen activator (t-PA) is released from endothelium in both a constitutive and regulated fashion. In healthy subjects, an association between net t-PA release rate and a few t-PA gene polymorphisms, including the Alu-repeat I/D polymorphism in intron 8, was described. The possible influence of the Alu-repeat polymorphism on t-PA release was evaluated after a venous occlusion test (VO) in 82 patients showing an impaired fibrinolytic capacity associated with different arterial disease or with previous venous thrombosis, and in 50 healthy controls. Euglobulin lysis time, t-PA antigen (t-PA:Ag) and activity, PAI-1 antigen and activity plasma levels were assayed before and 20 minutes after VO; the Alu-repeat I/D polymorphism was determined by PCR. Defective fibrinolysis was due to reduced t-PA release in 40 patients (t-PA group) and to PAI-1 excess in 42 patients (PAI group). No differences in both genotype distribution and allele frequencies were observed between patients and controls. The t-PA:Ag increase after VO (20/0-minute levels ratio adjusted for hematocrit) was considerably higher both in controls and in PAI group patients carrying the I allele than in the DD genotype carriers (II, ID, DD: 3.77+/-0.62, 3.43+/-0.44, 2.06+/-0.32 in controls, and 3.67+/-0.23, 2.80+/-0.50, 1.62+/-0.29 in PAI group, respectively). The difference was significant between the DD and both the ID and II genotypes in controls (p<0.05), and between the DD and II genotypes in PAI-1 group (p<0.05). A slight and nonsignificant trend of association between genotype and t-PA:Ag 20/0 ratio was seen in the t-PA group patients. In conclusion, these data suggest a possible genetic modulation of t-PA-regulated secretion.

Adult↗

PubMed2000

Replication and persistence of different strains of bovine viral diarrhea virus in an in vitro embryo production system.

Recent studies have shown that exposed, in vitro-derived embryos remain contaminated with bovine viral diarrhea virus (BVDV) after washing. However, introduction of a Genotype II versus Genotype I strain of BVDV into an IVF system was reported to provide greater potential for transmission of disease. The primary objective of this study was to compare the potentials for different strains of noncytopathic BVDV to replicate in an IVF system, associate with IVF embryos and infect co-cultured cells via association with washed embryos. The secondary objective was to compare the effect of different strains of BVDV on embryonic development. Two Genotype I (SD-1 and NY-1) and 2 Genotype II (CD-87 and PA-131) strains of BVDV were evaluated. After IVM and IVF of oocytes, presumptive zygotes were washed and transferred into in vitro cultures containing uterine tubal cells (UTC) and medium that was free of BVDV-neutralizing activity. Immediately before addition of zygotes, the cultures were inoculated with 10(5) cell culture infective doses (50%, CCID50) of a strain of BVDV or maintained as a negative control. Cultures of zygotes were then incubated for 7 d. Embryonic development was observed on Days 3 and 7, and attempts were made to isolate BVDV from UTC and medium on Day 7. Also on Day 7, groups of intact, washed blastocysts were either transferred into virus-free secondary cultures containing UTC or sonicated with sonicate fluid assayed by both virus isolation and single-closed-tube reverse transcription nested polymerase chain reaction (RT-nPCR). After 3 d in secondary culture, hatched embryos were enumerated, and medium from the cultures, washed UTC and embryos were tested for BVDV by virus isolation. In addition, washed UTC and embryos were tested for BVDV using RT-nPCR. All strains of BVDV persisted and replicated in the embryo culture environment, but cleavage beyond the 4-cell stage, blastocyst development and hatching varied among cultures contaminated with different strains of virus. Further, the quantity of BVDV associated with washed embryos from both initial and secondary cultures varied among strains, but the variation was unrelated to difference in genotype (SD-1 and PA-131 greater than NY-1 and CD-87). Although all strains of BVDV replicated in UTC in the initial in vitro cultures and remained associated with washed blastocysts, susceptible UTC in the secondary in vitro cultures were seldom infected by any strain of virus.

Animals↗

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↗

PubMed1999

Angiotensin-converting-enzyme gene insertion/deletion polymorphism and response to physical training.

BACKGROUND: The function of local renin-angiotensin systems in skeletal muscle and adipose tissue remains largely unknown. A polymorphism of the human angiotensin converting enzyme (ACE) gene has been identified in which the insertion (I) rather than deletion (D) allele is associated with lower ACE activity in body tissues and increased response to some aspects of physical training. We studied the association between the ACE gene insertion or deletion polymorphism and changes in body composition related to an intensive exercise programme, to investigate the metabolic effects of local human renin-angiotensin systems. METHODS: We used three independent methods (bioimpedance, multiple skinfold-thickness assessment of whole-body composition, magnetic resonance imaging of the mid-thigh) to study changes in body composition in young male army recruits over 10 weeks of intensive physical training. FINDINGS: Participants with the II genotype had a greater anabolic response than those with one or more D alleles for fat mass (0.55 vs -0.20 kg, p=0.04 by bioimpedance) and non-fat mass (1.31 vs -0.15 kg, p=0.01 by bioimpedance). Changes in body morphology with training measured by the other methods were also dependent on genotype. INTERPRETATION: II genotype, as a marker of low ACE activity in body tissues, may conserve a positive energy balance during rigorous training, which suggests enhanced metabolic efficiency. This finding may explain some of the survival and functional benefits of therapy with ACE inhibitors.

Adipose Tissue↗

PubMed2002

[A study of insertion/delation polymorphism of the angiotensin-converting enzyme gene in pilots].

In order to understand insertion/delation (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene in pilots,and to explore the relationship between ACE gene I/D polymorphism and the performance of the pilots, the polymerase chain reaction (PCR) was used to determine the genotypes for an I/D polymorphism in intron 16 of the ACE gene in 118 pilots and 96 healthy subjects as controls. The result showed that the I/D polymorphism in intron 16 of the ACE gene was categorized into three genotypes: two deletion alleles (genotype DD), heterozygous alleles (genotype ID), and two insertion alleles (genotype II). The genotype II and I allele frequency were significantly higher in pilots (44.07% and 0.65) than that in healthy subjects (31.25% and 0.52). It is suggested that I gene of ACE may play a role in performance of the pilots.

English Abstract↗

PubMed2002

Enhanced responses of blood pressure, renal function, and aldosterone to angiotensin I in the DD genotype are blunted by low sodium intake.

Angiotensin-converting enzyme (ACE) activity is increased in the DD genotype, but the functional significance for renal function is unknown. Blunted responses of BP and proteinuria to ACE inhibition among DD renal patients during periods of high sodium intake were reported. It was therefore hypothesized that sodium status affects the phenotype in the ACE I/D polymorphism. The effects of angiotensin I (AngI) and AngII among 27 healthy subjects, with both low (50 mmol sodium/d) and liberal (200 mmol sodium/d) sodium intakes, were studied. Baseline mean arterial pressure (MAP) values, renal hemodynamic parameters, and renin-angiotensin system parameters were similar for all genotypes with either sodium intake level. With liberal sodium intake, the increases in MAP, renal vascular resistance, and aldosterone levels during AngI infusion (8 ng/kg per min) were significantly higher for the DD genotype, compared with the ID and II genotypes (all parameters presented as percent changes +/- 95% confidence intervals), with mean MAP increases of 22 +/- 2% (DD genotype), 13 +/- 5% (ID genotype), and 12 +/- 6% (II genotype) (P < 0.05), mean increases in renal vascular resistance of 100.1 +/- 19.7% (DD genotype), 73.0 +/- 16.3% (ID genotype), and 63.2 +/- 16.9% (II genotype) (P < 0.05), and increases in aldosterone levels of 650 +/- 189% (DD genotype), 343 +/- 71% (ID genotype), and 254 +/- 99% (II genotype) (P < 0.05). Also, the decrease in GFR was more pronounced for the DD genotype, with mean decreases of 17.9 +/- 4.7% (DD genotype), 8.8 +/- 3.4% (ID genotype), and 6.4 +/- 5.9% (II genotype) (P < 0.05). The effective renal plasma flow, plasma AngII concentration, and plasma renin activity values were similar for the genotypes. In contrast, with low sodium intake, the responses to AngI were similar for all genotypes. The responses to AngII were also similar for all genotypes, with either sodium intake level. In conclusion, the responses of MAP, renal hemodynamic parameters, and aldosterone concentrations to AngI are enhanced for the DD genotype with liberal but not low sodium intake. These results support the presence of gene-environment interactions between ACE genotypes and dietary sodium intake.

Adult↗

PubMed1996

Genotypes of sarco(endo)plasmic reticulum Ca(2+)-dependent ATPase II gene in substrains of spontaneously hypertensive rats.

OBJECTIVE: To search for a genetic marker of the sarco(endo)plasmic reticulum Ca(2+)-dependent ATPase (SERCA) II gene in spontaneously hypertensive rats (SHRs) and to investigate differences in blood pressure and intracellular Ca2+ among some substrains of SHRs and Wistar-Kyoto (WKY) rats related to their SERCA II genotypes. DESIGN AND METHODS: The coding region of the SERCA II gene was sequenced in SHRs. Blood pressure and intracellular Ca2+ concentration ([Ca2+]i) in platelets were measured in substrains of SHRs and WKY rats with different SERCA II genotypes. RESULTS: A point mutation that provided restriction fragment length polymorphisms (RFLPs) by HindIII or Saul was found in the SERCA II gene. The polymerase chain reaction (PCR) products were digested by HindIII in SHR substrains and WKY-Kyoto rats, whereas they were digested by Saul in normotensive strains and SHR-Toho. Among SHR-Kyoto, SHR-Toho, WKY-Kyoto and WKY-Charles River, the substrains with the HindIII-digested SERCA II genotype showed slightly but significantly higher systolic blood pressure and augmented agonist-stimulated [Ca2+]i than those with the Saul-digested genotype. CONCLUSIONS: RFLPs were found in the SERCA II gene. In the substrain analysis of SHRs and WKY rats, higher blood pressure and increased [Ca2+]i were associated with the SERCA II genotype digested by HindIII. The SERCA II gene locus has the potential to contribute to the development of hypertension and abnormal intracellular Ca2+ metabolism in SHRs. These RFLPs in the SERCA II gene should be a useful genetic marker.

Animals↗

PubMed2001

Prevalence of hepatitis C genotypes in Indian patients and their clinical significance.

AIM: To study the significance of hepatitis C genotypes in relation to severity of liver disease, progression of liver disease and response to treatment. METHODS: Sixty one consecutive patients with hepatitis C infection were evaluated with detailed history, clinical examination, biochemical, imaging and virological profile, liver histology whenever feasible. Hepatitis C infection was confirmed with AntiHCV third generation ELISA assay. HCVRNA by PCR and HCV genotyping by direct sequencing. RESULTS: Demographic profile of patients was as M:F 36:25, mean age 46.3 +/- 13.6 years (range 10 to 70 years). Clinical presentations of these patients were as cirrhosis 23, cirrhosis with HCC 3, chronic hepatitis 22, acute hepatitis 4, asymptomatic with normal enzymes nine. Distribution of genotypes was as follows; 13/61 (21%) genotype I, 15/61 (25%) genotypes II and 33/61 (54%) genotype III. Cirrhosis was significantly common in genotype I (77%) when compared to genotype II and III (33%); p < 0.001. Mean time of presenting as cirrhosis was much faster in genotype I (8.7 +/- 6.7 years) as compared to other genotypes (type II 12.8 +/- 4.2 years and genotype III 15.8 +/- 6.9 years). Genotype distribution in CRF and renal transplant patient was genotype I 8/23 (35%), genotype II 5/23 (22%) and genotype III 10/23 (43%). Fourteen patients were treated with interferon and ribavarine combination for one year. Sustained response seen in 8/14 (57%). All these patients had genotype non 1. All the four patients with Genotype I were non-responders. CONCLUSION: Hepatitis C genotype III is common in India, Genotype I runs a more severe course, faster progression and non responders to interferon as compared with genotype II and III.

Adolescent↗

PubMed2006

[Hepatitis E virus of different genotypes contains multiple-type antigenic epitopes].

Monoclonal antibodies (McAbs) were prepared against a recombinant protein p166Us derived from US-1 strain of hepatitis E virus (HEV). The immune reactivity of the McAbs to seven p166s derived from different genotypes and subtypes of HEV, which included p166Bur (genotype I a), p166Pak (genotype I b), p166Mor (genotype I c), p166Mex (genotype II), p166Us (genotype III), p166Nz (swine HEV, genotype III) and p166Chn (genotype IV), was tested by an indirect enzyme-linked immunosorbent assay (ELISA) and a Western blotting assay. The immunological relationship between the McAbs and native HEV particles or anti-HEV positive serum samples was analyzed by an antigen-competitive or antibody-competitive ELISA. Totally, six McAb-producible hybridoma cell lines, designated by the name of 4D3, 2E3, 11E11, 12H5, 3A3 and 1F1 respectively, were cloned and obtained in this study. The McAb of 4D3 could react to all of the seven p166 recombinant proteins. This kind of reaction could be inhibited by each of 4 genotypes of native HEV particles or anti-HEV positive serum samples. The McAbs produced by 2E3, 11E11 and 12H5 reacted to p166Us, p166Nz and p166Chn, but did not react to p166Bur, p166Pak, p166Mor and p166Mex. The reaction of McAb of 2E3, as an example of the McAbs of 2E3, 11E11 and 12H5, could be only inhibited by genotype III and IV HEV or anti-HEV positive serum. The McAb of 3A3 could bind to p166Us as well as p166Nz. The McAb produced by 1F1 was reactive to the p166Us only. However, neither of I , II , IV genotype HEV particles or antisera could inhibit both of their reactions to p166Us. The data as mentioned above suggested that there are multiple-type antigenic epitopes such as genotype I, II, III and IV common, III and IV common, and III specific epitopes within HEV ORF2 encoded p166 proteins of different genotypes and subtypes of HEV. Moreover, the antigenic epitopes on recombinant protein p166s and these on native HEV particles possess identical immunological characteristics.

Animals↗

PubMed2000

Effect of Ava II and NcoI polymorphisms at the low density lipoprotein receptor gene on plasma lipid levels in a group of Thai subjects.

The contribution of common genetic variations at the LDL receptor gene in determining interindividual differences in plasma lipid levels in the general population has been observed in several studies. In this study, we employed the PCR-RFLP method to investigate such an effect of the common Ava II (exon 13) and Nco I (exon 18) polymorphisms at the low density lipoprotein (LDL) receptor gene locus in 54 normolipidemic Thai subjects. The mean LDL-C level was slightly higher in the Ava II (+/+) genotype than the other Ava II genotypes. This difference was significant at the 5 per cent level although there were only three homozygotes with Ava II (+/+) genotype. The average effect of Ava II (+) allele was to increase LDL-C level by 6.75 mg/dl. A gene-dosage effect was not observed for this polymorphism. In addition, the subjects with Ava II (+/+) genotype also tended to have high serum total cholesterol and triglyceride and low HDL-C levels. Nco I polymorphism revealed no statistically significant effect on lipid levels in these subjects. However, the subjects with (+) allele tended to have high levels of LDL-C, serum total cholesterol and triglyceride.

Alleles↗

PubMed1996

Relationship between the angiotensin converting enzyme gene polymorphism and the effects of enalapril on left ventricular hypertrophy and impaired diastolic filling in essential hypertension: M-mode and pulsed Doppler echocardiographic studies.

OBJECTIVE: To investigate the relationship between the angiotensin converting enzyme (ACE) gene polymorphism and the effects of the ACE inhibitor enalapril on left ventricular hypertrophy and impaired diastolic filling. DESIGN AND METHODS: Enalapril (5-10 mg/day) was administered for 12 months to 60 previously untreated patients with essential hypertension. M-mode and pulsed Doppler echocardiography were performed before and after treatment, and changes in various parameters after treatment with enalapril were examined. ACE gene polymorphism was examined by the polymerase chain reaction method and the patients were classified as having the 190 bp deletion homozygous (DD) genotype, the 490 bp insertion homozygous (II) genotype or the 490 bp insertion 190 bp deletion heterozygous (ID) genotype. RESULTS: The DD genotype was observed in 10 patients (17%), the ID genotype in 24 patients (40%) and the II genotype in 26 patients (43%). Plasma ACE activity before treatment with enalapril was significantly higher in seven patients with DD genotype than it was in 18 patients with ID genotype and in 14 patients with II genotype. In all of the 60 patients, the left ventricular mass index, the peak atrial systolic velocity:early diastolic velocity ratio and the deceleration time from the peak of the early diastolic wave to the baseline in transmitral flow velocity were decreased significantly after treatment with enalapril. The changes in left ventricular mass index and atrial systolic velocity:early diastolic velocity ratio after enalapril administration were significantly greater in the DD genotype group than they were in the other two genotype groups. CONCLUSION: Enalapril-induced regression of left ventricular hypertrophy and improvement in left ventricular impaired diastolic filling were significantly greater in the DD genotype group than they were in the ID and II genotype groups, suggesting that the circulating and tissue renin-angiotensin systems, particularly the former system, are most active in hypertensive patients with the DD genotype.

Adult↗