Major Cause Of Posttransfusion Hepatitis Research Articles

Molecular epidemiology of SEN virus among blood donors and renal dialysis patients.

The SEN virus (SEN-V) is a single-stranded circular, non-enveloped DNA virus that has been linked to blood transfusion and is thought to be a major cause of post-transfusion hepatitis. The two SENV types, SENV-H and SENV-D, are non-A to E hepatitis viruses in those who are infected. The purpose of this study is to find out how common SENV and its variations are among renal dialysis patients and healthy blood donors. The study used a cross-sectional design, with 300 blood samples collected from KFMMC patients, 150 from healthy blood donors and 150 from renal dialysis patients, between January 2019 and January 2021. The samples were screened for the presence of SENV-D andSENV-H.using nested PCR. Molecular analysis of the SEN virus revealed that 9.3% of the samples (14 out of 150) tested positive for SEN virus infection in renal dialysis patients. The data from healthy donors revealed that 10% of the samples tested positive for the SEN virus (15 out of 150). The presence of SEN-V in healthy blood donors and renal dialysis patients demonstrates the virus's blood-borne nature and emphasizes the dangers of blood-borne transmission.

Distribution of Hepatitis C Virus Genotypes in Patients with Major β-Thalassemia in Mashhad, Northeast Iran

BACKGROUND Hepatitis C virus (HCV) is considered to be the major cause of post-transfusion hepatitis in patients with thalassemia. We aimed to determine the HCV prevalence, genotypes, and viral load among patients with major β-thalassemia in Mashhad, Iran. METHODS Medical records of all 550 patients with major β-thalassemia who referred to ThalassemiaHemophilia Center of Mashhad (Sarvar Clinic) were reviewed from October to November 2011. Plasma samples of the patients were tested for the presence of anti-HCV antibodies by enzyme linked immunosorbent assay. Real-time polymerase chain reaction (PCR) was used to determine viral genotype and HCV RNA titer. RESULTS HCV antibodies were detected in 37 individuals (6.73%) including 17 men and 20 women with mean age of 25.2 ± 8.4 years. The PCR analysis was performed for 27 patients, of whom HCV RNA was detected in 17 patients (63.0%). Viral titers were investigated in 14 subjects and a high viral load more than 600000 copies/mL was observed in 6 patients (42.9%). The most prevalent genotypes were 3a (50.0%) followed by 1a (37.5%). No significant correlation was found between genotype and age, sex, serum ferritin, liver tests, and HCV RNA titer. CONCLUSION HCV infection among patients with thalassemia is more common than general population in Mashhad, northeast Iran. The dominant HCV subtype is 3a followed by 1a. These findings could help health authorities to provide preventive measures, and practitioners to choose the right protocol of treatment for the patients.

Hepatitis C: progress and problems.

The hepatitis C virus (HCV), a single-stranded RNA virus, is the major cause of posttransfusion hepatitis. HCV isolates differ in nucleotide and amino acid sequences. Nucleotide changes are concentrated in hypervariable regions and may be related to immune selection. In most immunocompetent persons, HCV infection is diagnosed serologically, using antigens from conserved regions. Amplification of RNA may be necessary to detect infection in immunosuppressed patients. Transmission by known parenteral routes is frequent; other means of spread are less common and may represent inapparent, percutaneous dissemination. Infection can lead to classical acute hepatitis, but most infected persons have no history of acute disease. Once infected, most individuals apparently remain carriers of the virus, with varying degrees of hepatocyte damage and fibrosis ensuing. Chronic hepatitis may lead to cirrhosis and hepatocellular carcinoma. However, disease progression varies widely, from less than 2 years to cirrhosis in some patients to more than 30 years with only chronic hepatitis in others. Determinants important in deciding outcome are unknown. Alpha interferon, which results in sustained remission in selected patients, is the only available therapy. Long-term benefits from such therapy have not been demonstrated. Prevention of HCV infection by vaccination is likely to be challenging if ongoing viral mutation results in escape from neutralization and clearance.

Impact of screening blood donors for hepatitis C antibody on posttransfusion hepatitis: a prospective study with a second-generation anti-hepatitis C virus assay.

Hepatitis C is the major cause of posttransfusion hepatitis. Blood components that are positive for antibody to hepatitis C virus (anti-HCV) can transmit posttransfusion hepatitis. To investigate the effect on posttransfusion hepatitis of screening blood donors with a second-generation test for anti-HCV, 249 transfusion recipients who underwent cardiovascular surgery were prospectively followed. Six recipients who were positive for anti-HCV before transfusion and 51 subjects with incomplete follow-up were excluded from this study. Eleven (13.8%) of 80 subjects who received unscreened blood had two successive serum alanine aminotransferase levels > 90 U per L. Seven (8.8% of total) developed anti-HCV and HCV RNA and two (2.5% of total) developed IgM antibody to cytomegalovirus (IgM anti-CMV). By contrast, 3 (2.7%) of the 112 subjects who received anti-HCV-screened blood had two successive serum alanine aminotransferase levels > 90 U per L. None of these three developed anti-HCV and HCV RNA, but two (1.8% of total) showed the development of IgM anti-CMV. The study shows that screening for anti-HCV in blood donors with a second-generation test almost abrogated posttransfusion viral hepatitis C. After anti-HCV screening, other body fluid-transmitted viruses such as CMV may become important in posttransfusion hepatitis.

The histopathology of chronic hepatitis c - are there any characteristic morphologic features?

The hepatitis C virus (HCV) is the major cause of posttransfusion hepatitis, and has a high prevalence in intravenous drug users. HCV infection carries a high risk of chronicity and is associated with hepatocellular carcinoma. Archival liver biopsy material was retrieved and reviewed from patients with chronic hepatitis and HCV antibodies. The biopsy samples were formalin fixed, paraffin embedded, and stained with standard liver stains and immunoperoxidase stain for cytokeratin. 25 liver samples from 24 patients were studied. The histological features ranged from lobular inflammation only (12%), to cirrhosis (12%). The majority showed combined lobular and portal tract inflammation and could be further subcategorised by the degree of portal inflammation. Specific features observed within the lobule included lymphocytic infiltration with lobules (88%), fatty change (60%), and acidophil bodies (64%). Characteristic portal changes included lymphocyte infiltration (88%) in most cases with follicle formation, degenerate bile ducts (72%), piecemeal necrosis (84%), and portal tract granulomas (36%). Chronic HCV infection is characterised by lobular and portal tract inflammation. Fatty change, lymphoid follicles, and bile duct lesions are generally not seen in other types of viral hepatitis. The features are not only of practical diagnostic significance, but may also suggest different evolution and pathogenesis.

Prospective controlled study of post-transfusion hepatitis after cardiac surgery in a large referral hospital in India.

We studied the risk of post-transfusion hepatitis (PTH) in recipients of blood collected from voluntary donors screened for HBsAg. Two hundred and fifty patients without any previous history of liver disease or transfusion were followed up for 12 months subsequent to cardiac surgery. Thirty-five of them had closed-heart surgery without receiving transfusion and served as controls. The remaining 215 patients received single-point transfusions (mean 4 +/- 2.4 units). None of the controls and 15 (6.9%) blood recipients developed PTH. Three (20%) patients had hepatitis-B-virus-induced hepatitis while the remainder (80%) had non A, non B (NANB) hepatitis. The number of units of blood transfused and surrogate markers for development of PTH (donor alanine aminotransferase, anti-HBc and anti-HBs antibody) were not associated with the occurrence of PTH (p greater than 0.05). Nine (60%) of the 15 patients developing PTH were asymptomatic. All the patients recovered from the PTH, except one who died of fulminant hepatitis. At the end of 1 year of follow-up, none of the patients had evidence of chronic hepatitis. Only three (25%) of the patients with NANB-PTH developed anti-hepatitis C virus (HCV) antibody during the follow-up. We conclude that the incidence of PTH in India is similar to other parts of the world and NANB virus was the major cause of the PTH. The absence of chronicity and lack of seroconversion to anti-HCV antibody in the majority of the patients after 1 year of follow-up may suggest the possibility of a NANB virus other than HCV as the major cause of PTH in India.

Antibodies to hepatitis C virus in autologous blood donors.

Hepatitis C virus (HCV) is the major cause of posttransfusion hepatitis. Two anti-HCV enzyme immunoassay (EIA) kits and one recombinant immunoblot assay (RIBA) were used to test serum samples of 1476 donations from 692 autologous blood donors to assess the prevalence of anti-HCV and its relationship to transfusion history. Of all autologous blood donations, 23 (1.6%) reacted when tested with one EIA kit and 29 (2.0%) reacted when tested by the other EIA kit. Of the autologous donors, 12 (1.78%) reacted by the first EIA kit and 14 (2.02%) by the second. Discrepancies in the EIA results from different donations by the same donor were seen in seven donors. The RIBA was positive or indeterminate in 33 percent of the EIA-reactive donations and in 41 percent of EIA-reactive donors. All RIBA-positive and -indeterminate samples reacted with both EIA kits. There was no significant difference in the EIA-reactive rates of autologous and first-time homologous blood donors. Previously transfused autologous blood donors had a higher anti-HCV EIA-reactive rate than nontransfused autologous donors, but the difference was not significant. In regard to hepatitis C, the use of autologous blood for homologous transfusion appears to be as safe as the use of blood from first-time homologous donors. Universal testing of previously transfused patients for hepatitis C appears premature at this time. Discrepant anti-HCV EIA results from different donations from the same individual have implications regarding donor deferral.

Antibody to Hepatitis C Virus in Post-Transfusion Hepatitis

To evaluate the prevalence of antibodies to hepatitis C virus (anti-HCV), their relation to outcome, and the seroconversion rate in patients with post-transfusion non-A, non-B hepatitis. Retrospective analysis of prospectively collected serum specimens. A referral-based university hospital. Sixty-three consecutive patients who developed non-A, non-B post-transfusion hepatitis after open-heart surgery. All patients had follow-up with serial serum testing and clinical evaluation. The mean (+/- SD) duration of follow-up after hepatitis onset was 81 +/- 33 months (range, 13 to 132 months). Seventeen patients recovered after acute-phase illness, whereas 46 developed chronic disease which, in 30 cases, was confirmed histologically. Of 32 patients tested before transfusion, 1 (3.1%) had anti-HCV. Fifty-nine (93%) patients were anti-HCV positive during acute-phase hepatitis: Patients with "early" seroconversion (less than 15 days after hepatitis onset) did not differ from those with "late" seroconversion (greater than 60 days after onset) in epidemiologic, clinical, and biochemical features. The rate of anti-HCV positivity during acute-phase illness was not significantly different among patients who recovered (76%) compared with those who developed chronic disease (95%). At 6 to 12 months, patients whose disease resolved had lower antibody activity than those with progressive disease. Further, during long-term follow-up (1 to 9 years), 53% of patients whose disease resolved but only 6.9% of patients who had progressive disease became anti-HCV negative. Hepatitis C virus is the major cause of post-transfusion hepatitis in Italy. The time to anti-HCV seroconversion varies widely after hepatitis onset and is not significantly associated with acute-phase features or outcome of disease.

Alanine Aminotransferase and Posttransfusion Hepatitis

To the Editor.— The American Red Cross is initiating the screening of donor blood for high alanine aminotransferase (ALT) levels to reduce the incidence of posttransfusion hepatitis. Non-A, non-B hepatitis, probably caused by several viruses, is the major cause of posttransfusion hepatitis. Thirty percent of patients with posttransfusion hepatitis are symptomatic, and some develop chronic hepatic disease. Hepatitis B has been virtually eliminated as a source of posttransfusion hepatitis by testing donor blood for hepatitis B surface antigen. Aach et al1prospectively followed up 1513 transfusion recipients and found that the incidence of posttransfusion hepatitis was directly related to the ALT concentration in blood donors. The overall attack rate for non-A, non-B hepatitis was 10%, but recipients of donor units with an ALT concentration of 60 U/L or greater had a 45% attack rate. The direct relationship between transfusion hepatitis and donor ALT levels was confirmed by Alter et

A clinical approach to non-A, non-B hepatitis.

Non-A, non-B agents are currently the major cause of posttransfusion hepatitis and a major cause of chronic active hepatitis in the United States. Recent investigations suggest the clinical entity of non-A, non-B hepatitis results from infection with one of at least two distinct viruses. These viruses produce hepatitis with different incubation periods, induce different histopathologic characteristics, and have different antigenic determinants. The clinical and virologic aspects of non-A, non-B hepatitis are reviewed.