scholarly journals Marrow transplantation from hepatitis C virus seropositive donors: transmission rate and clinical course

Blood ◽  
1994 ◽  
Vol 84 (9) ◽  
pp. 3229-3235 ◽  
Author(s):  
MC Shuhart ◽  
D Myerson ◽  
BH Childs ◽  
JD Fingeroth ◽  
JJ Perry ◽  
...  

Abstract Bone marrow transplant recipients are at risk for acquiring hepatitis C infection from the donated marrow. Twelve patients who were hepatitis C virus (HCV) RNA-negative pretransplant received marrow from anti-HCV seropositive donors. HCV RNA was present in the sera of seven of these donors. After transplant, serial serum specimens were obtained from all marrow recipients for determination of HCV RNA and aminotransferase levels. All seven recipients of marrow from HCV RNA-positive donors were HCV RNA-positive after marrow infusion; none cleared virus from the serum. All five recipients of marrow from anti-HCV seropositive, HCV RNA-negative donors remained free of HCV RNA in serum up to day 100. Abnormal serum aminotransferases were common in both HCV RNA- negative and HCV RNA-positive marrow recipients. One HCV-infected recipient developed marked elevation in aminotransferases after immunosuppressive drugs were stopped. We conclude that the presence of HCV RNA in the serum of marrow donors is an accurate predictor of HCV infection in marrow recipients. The acute infection was subclinical in all patients. The long-term risk of chronic hepatitis C virus infection in these patients remains to be determined.

Blood ◽  
1994 ◽  
Vol 84 (9) ◽  
pp. 3229-3235 ◽  
Author(s):  
MC Shuhart ◽  
D Myerson ◽  
BH Childs ◽  
JD Fingeroth ◽  
JJ Perry ◽  
...  

Bone marrow transplant recipients are at risk for acquiring hepatitis C infection from the donated marrow. Twelve patients who were hepatitis C virus (HCV) RNA-negative pretransplant received marrow from anti-HCV seropositive donors. HCV RNA was present in the sera of seven of these donors. After transplant, serial serum specimens were obtained from all marrow recipients for determination of HCV RNA and aminotransferase levels. All seven recipients of marrow from HCV RNA-positive donors were HCV RNA-positive after marrow infusion; none cleared virus from the serum. All five recipients of marrow from anti-HCV seropositive, HCV RNA-negative donors remained free of HCV RNA in serum up to day 100. Abnormal serum aminotransferases were common in both HCV RNA- negative and HCV RNA-positive marrow recipients. One HCV-infected recipient developed marked elevation in aminotransferases after immunosuppressive drugs were stopped. We conclude that the presence of HCV RNA in the serum of marrow donors is an accurate predictor of HCV infection in marrow recipients. The acute infection was subclinical in all patients. The long-term risk of chronic hepatitis C virus infection in these patients remains to be determined.


PEDIATRICS ◽  
1994 ◽  
Vol 94 (6) ◽  
pp. 919-922
Author(s):  
Suguru Matsuoka ◽  
Katsuyoshi Tatara ◽  
Yasunobu Hayabuchi ◽  
Yoshiyuki Taguchi ◽  
Kazuhiro Mori ◽  
...  

Objective. We studied the time course of hepatic dysfunction, seropositivity to hepatitis C virus (HCV) antibodies, viremia, and histologic evidence of hepatic injury to evaluate the course of HCV infection in children infected by blood transfusion. Patients and methods. Twenty-nine patients (ages 4 to 18 years) who underwent open-heart surgeries for congenital heart disease were grouped into three categories based on alterations in serum alanine aminotransferase (ALT) levels: Group A, acute infection; Group B, subacute infection; and Group C, chronic infection. Results. In Group C, all 13 patients had detectable HCV RNA in serum. In contrast, all patients in Group A had no detectable HCV RNA. In Group B, one of nine patients had detectable HCV RNA and two of four patients examined had persistent chronic hepatitis by histologic criteria. Antibodies directed against C100-3 antigen or core-antigen were more useful than second-generation HCV antibody assays in determining the relationship between viremia and immunologic response. Infection with HCV genotype II and the presence of higher HCV RNA copy numbers were associated with histologic evidence of hepatic damage. Conclusion. An abnormal ALT value is frequently associated with viremia, and biochemically resolved acute infection reflects clearance of HCV. However, a normal ALT does not always reflect an absence of hepatocyte damage and HCV replication in patients with subacute disease. The measures outlined in this study are useful indicators of disease activity during the chronic phase of post-transfusion HCV infection.


2004 ◽  
Vol 85 (9) ◽  
pp. 2515-2523 ◽  
Author(s):  
Séverine Deforges ◽  
Alexey Evlashev ◽  
Magali Perret ◽  
Mireille Sodoyer ◽  
Stéphane Pouzol ◽  
...  

Previous work on hepatitis C virus (HCV) led to the discovery of a new form of virus particle associating virus and lipoprotein elements. These hybrid particles (LVP for lipo-viro-particles) are enriched in triglycerides and contain at least apolipoprotein B (apoB), HCV RNA and core protein. These findings suggest that LVP synthesis could occur in liver and intestine, the two main organs specialized in the production of apoB-containing lipoprotein. To identify the site of LVP production, the genetic diversity and phylogenetic relationship of HCV quasispecies from purified LVP, whole serum and liver biopsies from chronically infected patients were studied. HCV quasispecies from LVP and liver differed significantly, suggesting that LVP were not predominantly synthesized in the liver but might also originate in the intestine. The authors therefore searched for the presence of HCV in the small intestine. Paraffin-embedded intestinal biopsies from 10 chronically HCV-infected patients and from 12 HCV RNA-negative controls (10 anti-HCV antibody-negative and two anti-HCV antibody-positive patients) were tested for HCV protein expression. HCV NS3 and NS5A proteins were stained in small intestine epithelial cells in four of the 10 chronically infected patients, and not in controls. Cells expressing HCV proteins were apoB-producing enterocytes but not mucus-secreting cells. These data indicate that the small intestine can be infected by HCV, and identify this organ as a potential reservoir and replication site. This further emphasizes the interaction between lipoprotein metabolism and HCV, and offers new insights into hepatitis C infection and pathophysiology.


2021 ◽  
Vol 14 (10) ◽  
Author(s):  
Servet Oztürk ◽  
Canan Ağalar

Background: Anti-hepatitis C virus (anti-HCV) is the only screening test being used in the diagnosis of hepatitis C. In this study, we examined anti-HCV positivity rates in our hospital. Objectives: The aim of administering the anti-HCV test was to distinguish patients with hepatitis C infection from false positivity in patients with reactive results. Methods: The anti-HCV tests were performed at Fatih Sultan Mehmet Training and Research Hospital in Istanbul, Turkey, between January 1, 2015 and December 31, 2019. The patients were evaluated retrospectively in terms of age, gender, anti-HCV titer, the clinic for which the examination was requested, the reason for the examination, and the history of hepatitis C. Results: In this study, 511 patients who had two negative polymerase chain reaction (PCR) results were evaluated as false positive cases and enrolled. The cut-off value was found to be 7.5 IU/ml, with the highest sensitivity of 94.4% and specificity of 94.5% (area under the curve [AUC]: 0.982). The lowest anti-HCV titer (5.2) was from patients without acute hepatitis, who were HCV-RNA positive and diagnosed with chronic hepatitis C. Conclusions: It may be more appropriate to report anti-HCV cut-off value of 0 - 5 as negative, 5 - 7.5 as borderline, and > 7.5 as positive. Working with a more acceptable cut-off level with a greater number of tests can help identify patients with asymptomatic HCV infection. Also, it can possibly reduce the cost due to a decrease in the number of PCR tests administered.


2000 ◽  
Vol 14 (7) ◽  
pp. 593-598 ◽  
Author(s):  
N Yamaguchi ◽  
K Tokushige ◽  
K Yamauchi ◽  
N Hayashi

The humoral immune response to acute infection by hepatitis C virus (HCV) is not yet perfectly clear in terms of immunoglobulin (Ig) response, diversity of HCV antigen, and the relation with hepatitis severity and antibody response.  Serum IgM and IgG anti-HCV levels in patients with HCV and either acute hepatitis (AH) or fulminant hepatitis (FH) were investigated; the diversity of HCV antigen was investigated by RIBA test III.  Of 22 AH patients, 12 (54.5%) were positive for IgM anti-HCV, mainly reacting to HCV core protein. The mean interval until the appearance of IgM anti-HCV after onset was 24.1±26.2 days. IgG anti-HCV mainly reacted to both core and NS-3 antigen, appearing 42.6±42.1 days after onset.  From a serial study of 15 AH patients, it was considered that in seven AH patients (46.7%), the IgM response would precede the IgG response. In another two AH patients, IgM anti-HCV was not detected during the acute disease phase. Of 48 chronic hepatitis patients with HCV-RNA, 40 patients were positive for IgM anti-HCV.  Therefore, IgM anti-HCV was useful for diagnosis in some of the AH patients, but it was difficult to use for distinguishing between acute and chronic infection. All four FH patients with HCV-RNA were positive for both IgM and IgG antibody to HCV at onset. Their antibody titres were higher than those of AH patients. These results suggested that, as in FH due to HBV, FH due to HCV could induce strong and rapid humoral immunity.  


2000 ◽  
Vol 38 (2) ◽  
pp. 575-577 ◽  
Author(s):  
Chloe L. Thio ◽  
Karen R. Nolt ◽  
Jacquie Astemborski ◽  
David Vlahov ◽  
Kenrad E. Nelson ◽  
...  

Immunosuppression from human immunodeficiency virus (HIV) may impair antibody formation, and false-negative hepatitis C virus antibody (anti-HCV) tests have been reported in individuals coinfected with HIV and HCV. It is unknown if the frequency of false-negative tests is sufficiently high to change screening recommendations in this setting. Thus, the prevalence of false-negative results for anti-HCV by third-generation tests was determined with samples from HIV-infected individuals. Sera from 559 HIV-infected and 944 HIV-negative prospectively followed injection drug users were tested for anti-HCV by a third-generation enzyme immunoassay and for HCV RNA by using a branched DNA assay and the HCV COBAS AMPLICOR system. Of 559 HIV-infected participants, 547 (97.8%) were anti-HCV positive. One of the remaining 12 anti-HCV-negative participants was HCV RNA positive, and she later developed detectable anti-HCV. Of the 944 HIV-negative participants, 825 (87.4%) were anti-HCV positive. One of the remaining 119 anti-HCV-negative participants was HCV RNA positive, and she also developed detectable anti-HCV at a later visit. These data indicate that HIV infection does not alter the approach to hepatitis C virus screening, which should be performed with third-generation assays for anti-HCV unless acute infection is suspected.


Blood ◽  
1997 ◽  
Vol 90 (3) ◽  
pp. 1309-1314 ◽  
Author(s):  
Giuseppe Rossi ◽  
Alessandra Tucci ◽  
Elisabetta Cariani ◽  
Antonella Ravaggi ◽  
Angelo Rossini ◽  
...  

The influence of immunodeficiency on the course of hepatitis C virus (HCV) infection is still debated, although a worsening effect has been suggested. We compared the characteristics of hepatitis C in two groups of hematologic patients with different levels of immunocompetence who acquired the same virus strain after treatment with contaminated intravenous immunoglobulins (IVIG). Indications for IVIG therapy were idiopathic thrombocytopenic purpura (ITP) in six patients and hypogammaglobulinemia in 7 patients with various hematologic disorders, who were defined immunodeficient (ID). Infection rate was 100%. Five ID patients never developed HCV antibodies despite serum HCV-RNA positivity. The same HCV genotype was shown in 10 patients tested. Moreover, E1-E2 gene partial nucleotide sequencing, performed in four patients, showed identical or closely related amino acid sequences, thus strongly supporting the hypothesis of a common source of infection. Clinical acute infection did not differ significantly between the two groups, but subsequent liver failure developed in five of the seven ID patients and in none of the ITP patients (P = .04). Liver biopsy, performed in three cases, documented HCV as the only cause of liver damage. Six ID patients died, with liver disease being the primary cause of death in four cases and a contributory cause in two cases. Their median survival after IVIG was 12 months, significantly worse than that of ITP patients (P = .0028). We conclude that immunodeficiency markedly worsens the course of IVIG-acquired HCV infection in hematologic patients.


Blood ◽  
1997 ◽  
Vol 90 (3) ◽  
pp. 1309-1314 ◽  
Author(s):  
Giuseppe Rossi ◽  
Alessandra Tucci ◽  
Elisabetta Cariani ◽  
Antonella Ravaggi ◽  
Angelo Rossini ◽  
...  

Abstract The influence of immunodeficiency on the course of hepatitis C virus (HCV) infection is still debated, although a worsening effect has been suggested. We compared the characteristics of hepatitis C in two groups of hematologic patients with different levels of immunocompetence who acquired the same virus strain after treatment with contaminated intravenous immunoglobulins (IVIG). Indications for IVIG therapy were idiopathic thrombocytopenic purpura (ITP) in six patients and hypogammaglobulinemia in 7 patients with various hematologic disorders, who were defined immunodeficient (ID). Infection rate was 100%. Five ID patients never developed HCV antibodies despite serum HCV-RNA positivity. The same HCV genotype was shown in 10 patients tested. Moreover, E1-E2 gene partial nucleotide sequencing, performed in four patients, showed identical or closely related amino acid sequences, thus strongly supporting the hypothesis of a common source of infection. Clinical acute infection did not differ significantly between the two groups, but subsequent liver failure developed in five of the seven ID patients and in none of the ITP patients (P = .04). Liver biopsy, performed in three cases, documented HCV as the only cause of liver damage. Six ID patients died, with liver disease being the primary cause of death in four cases and a contributory cause in two cases. Their median survival after IVIG was 12 months, significantly worse than that of ITP patients (P = .0028). We conclude that immunodeficiency markedly worsens the course of IVIG-acquired HCV infection in hematologic patients.


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