Hepatitis C Superinfection in Hepatitis C Virus (Hcv)-Infected Patients Transplanted With an HCV-Infected Kidney

Widell, Anders; Månsson, Siv; Persson, Nils H.; Thysell, Hans; Hermodsson, Svante; Blohmé, I

doi:10.1097/00007890-199510150-00004

Cited by 110 publications

(50 citation statements)

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“…The persistence of such mixed infection has been reported previously, though most longitudinal studies have found that only one strain persists, with exclusion of the other (7,21,48). Another recent study examining IDUs with HCV superinfection also found no evidence for recombination (1).…”

Section: Discussionmentioning

confidence: 57%

Progression of Fibrosis during Chronic Hepatitis C Is Associated with Rapid Virus Evolution

Wang

Netski²,

Astemborski

et al. 2007

J Virol

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Hepatic fibrosis is the primary mediator of disease due to chronic infection with hepatitis C virus (HCV).HCV exists as a quasispecies in each infected individual, and longitudinal viral sequence changes may reveal viral dynamics and the selection pressures applied by the host immune system. Thus, we hypothesized that patterns of sequence change might reveal the immunopathogenesis of fibrosis progression. We tested this hypothesis by studying individuals enrolled in a prospective study of chronic HCV-related hepatic fibrosis with little or no fibrosis at first biopsy (stage 0 or 1) and a second planned liver biopsy sample obtained 4 years later. Serum was obtained from five individuals with fast progression (FP; defined as a >2-stage change between visits) and 10 carefully matched individuals with slow progression (SP; defined as a <2-stage change between visits). We sequenced multiple cloned hemigenomic cDNAs from each person spanning six genes (core through NS3). Phylogenetic analysis revealed temporal shifts in phylogenetic clustering over time, suggesting frequent quasispecies replacement rather than simple diversification. In addition, mixed infections were detected in three subjects, with coexistence in two subjects (one FP, one SP) of subtypes 1a and 1b throughout the 4-year biopsy interval. Subjects with FP had a higher rate of evolution than subjects with SP, with a preponderance of synonymous changes, suggesting purifying selection, except in hypervariable region 1, where positive selection pressure is frequently detected. Thus, in a small but carefully matched cohort we found evidence for rapid neutral evolution of HCV in persons with rapid progression of hepatic fibrosis, suggesting higher turnover of infected cells.

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Section: Discussionmentioning

confidence: 57%

Progression of Fibrosis during Chronic Hepatitis C Is Associated with Rapid Virus Evolution

Wang

Netski²,

Astemborski

et al. 2007

J Virol

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“…The full range of clinical manifestations of posttransplantation HCV and posttransplantation diabetes, other than their apparent adverse association with survival, could not be determined. Previous studies have shown that whether the donor or recipient HCV viral strain predominates after transplantation is unpredictable (34). Because of the lower prevalence but higher virulence of HCV in the United States compared with other countries (35), results of the present analysis may not be applicable outside the United States.…”

Section: Discussionmentioning

confidence: 86%

Impact of Diabetes and Hepatitis after Kidney Transplantation on Patients Who Are Affected by Hepatitis C Virus

Abbott

Lentine

Bucci

et al. 2004

Journal of the American Society of Nephrology

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Abstract. Complications associated with use of donor hepatitis C-positive kidneys (DHCVϩ) have been attributed primarily to posttransplantation liver disease (as a result of hepatitis C disease). The role of posttransplantation diabetes has not been explored in this setting. With the use of the United States Renal Data System database, 28,942 Medicare KT recipients were studied from January 1, 1996, through July 31, 2000. Cox proportional hazards regression models were used to calculate adjusted hazard ratios (AHR) for the association of sero-pairs for HCV (Dϩ/RϪ, Dϩ/Rϩ, DϪ/Rϩ and DϪ/RϪ) with Medicare claims for de novo posttransplantation HCV and posttransplantation diabetes. The peak risk for posttransplantation HCV was in the first 6 mo after transplantation. The incidence of posttransplantation HCV after transplantation was 9.1% in Dϩ/RϪ, 6.3% in Dϩ/Rϩ, 2.4% in DϪ/Rϩ, and 0.2% in DϪ/RϪ. The incidence of posttransplantation diabetes after transplantation also peaked early and was 43.8% in Dϩ/RϪ, 46.6% in Dϩ/Rϩ, 32.3% in DϪ/Rϩ, and 25.4% in DϪ/RϪ. Associations for both complications were significant in adjusted analysis (Cox regression). Both posttransplantation HCV (AHR, 3.36; 95% confidence interval, 2.44 to 4.61) and posttransplantation diabetes (AHR, 1.81; 95% confidence interval, 1.54 to 2.11) were independently associated with an increased risk of death, but posttransplantation diabetes accounted for more years of life lost, particularly among recipients of DHCVϩ kidneys. Posttransplantation diabetes may contribute substantially to the increased risk of death associated with use of DHCVϩ kidneys and accounts for more years of life lost than posttransplantation HCV. Because HCV infection acquired after transplantation is so difficult to treat, methods that have been shown to reduce viral transmission warrant renewed attention.

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“…Morales et al 42 found that, after 25 months of follow-up, transplanting kidney from HCV-positive donors into HCV-RNA-positive recipients resulted in no difference in clinical outcome compared with HCV-positive recipients who had received kidneys from HCV-negative donors. A major concern is superinfection by HCV, as reported by Widell et al 43 with biochemical worsening (persistent elevation in ALT activity) 14 to 24 months after RT in previously infected patients. A recent series from the United States 44 has shown that the use of renal allografts from HCV-positive donors for HCV-positive recipients did not affect short-term graft or patient survival; in addition, the waiting times for these patients were lowered.…”

Section: Kidney Donor With Hcv-positive Serologymentioning

confidence: 95%

“…43 Sustained biochemical and virologic response rates were 0% to 67% and 15.8% to 64%, respectively (Table 3). In a large, controlled trial, Huraib et al 45 showed a significant decrease in the histologic activity index (HAI) after IFN therapy, 4.27 Ϯ 1.19 to 1.64 Ϯ 0.67 (P ϭ .004); a significant difference between the HAI scores at the end of the study periods between IFN and placebo groups occurred, 1.64 Ϯ 0.67 versus 5.5 Ϯ 1.35 (P Ͻ .0007).…”

Section: Therapy Of Hepatitis C In Esrd: Current Statusmentioning

confidence: 98%

Hepatitis C infection and the patient with end-stage renal disease

2002

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Hepatitis C virus (HCV) remains common in patients with end-stage renal disease (ESRD)and is an important cause of liver disease in this population. Acquisition of HCV infection continues to occur in dialysis patients because of nosocomial spread. The natural history of HCV in dialysis patients remains controversial because the course of HCV typically extends over decades, whereas dialysis patients have higher morbidity and mortality rates than those of the general population limiting long-term follow-up. However, recent reports suggest that HCV infection affects the survival of chronic dialysis patients as well as renal transplant ( L iver disease is a significant cause of morbidity and mortality in patients with end-stage renal disease (ESRD) treated by dialysis or transplantation. 1 Viral hepatitis was suspected to be prevalent in patients with ESRD maintained on chronic hemodialysis (HD) nearly 3 decades ago. Development of diagnostic testing for hepatitis B virus (HBV) confirmed a high incidence and prevalence of HBV infection both in patients and staff in HD units. A number of measures mandated by the Centers for Disease Control, including isolation of hepatitis B surface antigen-positive patients, dedicated dialysis machines, and regular surveillance for HBV infection, dramatically reduced the spread of HBV in this setting by the late 1970s. However, many cases of liver disease in ESRD were unexplained and were ascribed to non-A, non-B hepatitis. Once the hepatitis C virus (HCV) was cloned, 2 it rapidly became evident that HCV was frequent in patients with ESRD on HD and that HCV transmission was occurring within HD units in the absence of the usual parenteral risk factors (i.e., blood transfusion or illicit drug use) ( Table 1). A number of other important facets of HCV infection in ESRD patients have been recognized, including false-negative serologic tests and an absence of biochemical dysfunction despite viremia. However, despite this, progressive liver disease can occur and is a particular concern in the patient who is a renal transplantation (RT) recipient. Epidemiology and Diagnosis of HCV Infection in ESRDWith first-and second-generation serologic testing for HCV available, a number of investigators 3 reported a high prevalence of anti-HCV seropositivity in patients with ESRD on chronic dialysis, most of whom were also viremic by polymerase chain reaction (PCR). A high rate of false-negative serologic testing was also noted. Bukh et al. 4 reported that 2.6% of dialysis patients seronegative by second-generation enzyme-linked immunosorbent assay (ELISA) were viremic by PCR. However, the more recent

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Hepatitis C Superinfection in Hepatitis C Virus (Hcv)-Infected Patients Transplanted With an HCV-Infected Kidney

Cited by 110 publications

References 0 publications

Progression of Fibrosis during Chronic Hepatitis C Is Associated with Rapid Virus Evolution

Progression of Fibrosis during Chronic Hepatitis C Is Associated with Rapid Virus Evolution

Impact of Diabetes and Hepatitis after Kidney Transplantation on Patients Who Are Affected by Hepatitis C Virus

Hepatitis C infection and the patient with end-stage renal disease

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