Negative strand of hepatitis C virus RNA in the liver of patients with chronic hepatitis C after interferon treatment

Tomimatsu, Masahiko; Endou, Hitoshi; Takahashi, H.; Iga, Daijiro; Kato, Yoshikazu; Tamai, Norio; Nakajima, Hiroyuki; Okano, Akira; Mori, Haruki; Higuchi, Hisashi

doi:10.1111/j.1440-1746.1997.tb00525.x

Cited by 11 publications

(7 citation statements)

References 21 publications

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“…The other sample was frozen immediately and then stored at À808C until PCR testing. Positive and negative HCV RNA strands in the liver were amplified independently by specific RT-seminested PCR as described elsewhere [Tomimatsu et al, 1997]. Briefly, after denaturation of the RNA extracted from the liver, synthesis of the positive and negative HCV cDNA strands was done with an antisense primer YCA (5 0 ACTCGCAAGCACCC-TATCAG3 0 ) or a sense primer YCS13 (5 0 GAGGAAC-TACTGTCTTCACG3 0 ) derived from the 5 0 -noncoding region, respectively.…”

Section: Laboratory Testsmentioning

confidence: 99%

Histological improvement of chronic liver disease after spontaneous serum hepatitis C virus clearance

Sugiyasu

Yuki

Nagaoka³

et al. 2002

Journal of Medical Virology

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The long-term histological and virological outcomes of spontaneous circulating hepatitis C virus (HCV) clearance were studied in chronic liver disease. Between 1979 and 1984, three patients underwent laparoscopy for chronic non-A, non-B liver disease, and two were found to have cirrhosis and one with chronic active hepatitis. After HCV assays became available in 1990, they were positive persistently for HCV antibody without serum HCV RNA. Reductions of antibody levels to HCV core and/or nonstructural proteins were observed, and liver biopsies were undertaken between 1995 and 2000. Liver biopsies at 11-19 years after laparoscopy disclosed marked alleviation of liver inflammation and fibrosis in each case although a low grade of inflammation remained. The two patients with cirrhosis no longer showed histological features of cirrhosis, and the poor liver function in one patient had been ameliorated. Liver specimens from two patients were subjected to polymerase chain reaction to detect positive and negative HCV RNA strands and hepatitis B virus DNA. Only the positive HCV RNA strand was detected for one patient who had previously cirrhosis. Liver specimens were examined from another six nonviremic HCV-seropositive individuals without chronic liver disease. Five patients displayed low-grade liver inflammation without evident fibrosis, but none had any viral genome in the liver. These findings suggest that spontaneous circulating HCV clearance in chronic liver disease confers favorable liver histological outcome, although occult HCV infection persists. J. Med. Virol. 69:41-49, 2003.

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Section: Laboratory Testsmentioning

confidence: 99%

Histological improvement of chronic liver disease after spontaneous serum hepatitis C virus clearance

Sugiyasu

Yuki

Nagaoka³

et al. 2002

Journal of Medical Virology

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“…None of their 69 aviremic individuals with hepatitis C infection had a detectable PBMC-associated HCV-RNA. The HCV-RNA detection rates in liver biopsy specimens varied widely among studies ranging from 0% to 83% [ 20 – 23 ]. Haydon et al other studies detected HCV-RNA in liver biopsy tissues in 10 of 12 individuals (83%) using RT-PCR [ 20 ].…”

Section: Introductionmentioning

confidence: 99%

A New Twist to a Chronic HCV Infection: Occult Hepatitis C

Attar

Thiel²

2015

Gastroenterology Research and Practice

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Background. The prevalence of occult hepatitis C infection (OCI) in the population of HCV-RNA negative but anti-HCV positive individuals is presently unknown. OCI may be responsible for clinically overt recurrent disease following an apparent sustained viral response (SVR) weeks to years later. Purpose. To review the available current literature regarding OCI, prevalence, pathogenic mechanisms, clinical characteristics, and future directions. Data Sources. Searching MEDLINE, article references, and national and international meeting abstracts for the diagnosis of OCI (1990–2014). Data Synthesis. The long-term followup of individuals with an OCI suggests that the infection can be transient with the loss of detectable HCV-RNA in PPBMCs after 12–18 months or alternatively exist intermittently and potentially long term. The ultimate outcome of HCV infection is decided by interplay between host immune responses, antiviral therapies, and the various well-identified viral evasion mechanisms as well as the presence of HCV infection within extrahepatic tissues. Conclusion. The currently widely held assumption of a HCV-cure in individuals having had “SVR” after 8–12 weeks of a course of DAA therapy as recently defined may not be entirely valid. Careful longitudinal followup utilizing highly sensitive assays and unique approaches to viral isolation are needed.

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“…13 Others have shown an association of HCV-replicative status with outcomes after interferon alfa therapy. 14,15 The association of pre-or posttransplantation HCV replication and long-term outcome following liver transplantation remains unclear. Because there is an initial decrease in serum HCV viral load within the first 2 days after transplantation, followed by a marked elevation over pretransplantation quantities, a rapid turnover of virions over the first posttransplantation days has been proposed.…”

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confidence: 99%

Hepatitis C-induced hepatic allograft injury is associated with a pretransplantation elevated viral replication rate

et al. 2000

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Hepatitis C virus (HCV) allograft infection after liverEnd-stage liver disease associated with hepatitis C virus (HCV) infection is the leading indication for liver transplantation. 1 Although the recurrence of posttransplantation viremia is nearly universal, 2-4 the rate and extent of HCV-induced allograft injury is variable. 5 At present, mechanisms of injury and reliable predictors of aggressive allograft injury induced by HCV remain elusive.HCV is a positive-sense, single-strand RNA virus that presumably requires a negative-strand RNA-replicative intermediate. Previous nontransplantation studies have demonstrated intra-and extrahepatic replication determined by the presence of negative-strand HCV RNA. 6-12 Evaluation of HCVreplicative intermediates has suggested that persistent infection may be partly the result of intrahepatic viral replication. 13 Others have shown an association of HCV-replicative status with outcomes after interferon alfa therapy. 14,15 The association of pre-or posttransplantation HCV replication and long-term outcome following liver transplantation remains unclear. Because there is an initial decrease in serum HCV viral load within the first 2 days after transplantation, followed by a marked elevation over pretransplantation quantities, a rapid turnover of virions over the first posttransplantation days has been proposed. 16 However, although intrahepatic HCV replication is noted to occur as early as 7 days after liver transplantation, viral replication in the early posttransplantation period is not associated with the development of recurrent hepatitis. 17 Others have demonstrated a correlation between the extent of allograft fibrosis with the rate of posttransplantation HCV replication at the time of biopsy. 18 The association of viral replication with increased propensity for allograft infection has been firmly established for hepatitis B virus. [19][20][21][22] Whether pretransplantation HCV viral replication rate predicts progression of liver disease remains to be determined. Although recognizing HCV and hepatitis B virus are clearly different, previous experience with hepatitis B lead to the hypothesis that pretransplantation, and possibly posttransplantation, HCV intrahepatic replication status would be associated with outcome. The purpose of the present study was to prospectively evaluate the differences in pre-and posttransplantation intrahepatic HCV replication in a cohort of HCV liver-transplant recipients undergoing protocol biopsies. PATIENTS AND METHODSPatients and Clinical Monitoring. The University of Virginia Human Investigation Committee approved this study. Informed consent in writing was obtained from patients as approved by our hospital practices committee in conformation with the ethical guidelines of the 1975 Declaration of Helsinki. Twenty-four liver transplantations in 23 consecutive patients with end-stage liver disease caused by Abbreviations: HCV, hepatitis C virus; RT-PCR, reverse-transcriptase polymerase chain reaction; Eq, equivalent(s).

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Negative strand of hepatitis C virus RNA in the liver of patients with chronic hepatitis C after interferon treatment

Cited by 11 publications

References 21 publications

Histological improvement of chronic liver disease after spontaneous serum hepatitis C virus clearance

Histological improvement of chronic liver disease after spontaneous serum hepatitis C virus clearance

A New Twist to a Chronic HCV Infection: Occult Hepatitis C

Hepatitis C-induced hepatic allograft injury is associated with a pretransplantation elevated viral replication rate

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