Infection with chronic hepatitis C virus and liver transplantation: A role for interferon therapy before transplantation

Thomas, Ryan M.; Brems, John J.; Guzman-Hartman, Grace; Yong, Sherri; Cavaliere, Patricia; Thiel, David H. Van

doi:10.1053/jlts.2003.50166

Cited by 134 publications

(94 citation statements)

References 21 publications

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“…Predictors of viral clearance include non-genotype 1 and an early virological response [22][23][24][25] . The absence of a ≥ 2 log10 reduction in HCV RNA between baseline and wk 4 has a strong negative predictive value [22][23][24]26,27] . This absence of an early virological response can be used as a guide to stopping treatment [26] .…”

Section: Predictors Of Antiviral Therapy Response and Tolerancementioning

confidence: 99%

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Strategies to reduce hepatitis C virus recurrence after liver transplantation

Ciria

Pleguezuelo²,

Khorsandi³

et al. 2013

WJH

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Hepatitis C virus (HCV) is a major health problem that leads to chronic hepatitis, cirrhosis and hepatocellular carcinoma, being the most frequent indication for liver transplantation in several countries. Unfortunately, HCV re-infects the liver graft almost invariably following reperfusion, with an accelerated history of recurrence, leading to 10%-30% of patients progressing to cirrhosis within 5 years of transplantation. In this sense, some groups have even advocated for not retransplanting this patients, as lower patient and graft outcomes have been reported. However, the management of HCV recurrence is being optimized and several strategies to reduce post-transplant recurrence could improve outcomes, decrease the rate of re-transplantation and optimize the use of available grafts. Three moments may be the focus of potential actions in order to decrease the impact of viral recurrence: the pretransplant moment, the transplant environment and the post-transplant management. In the pre-transplant setting, it is not well established if reducing the pre transplant viral load affects the risk for HCV progression after transplant. Obviously, antiviral treatment can render the patient HCV RNA negative post transplant but the long-term benefit has not yet been fully established to justify the cost and clinical risk. In the transplant moment, factors as donor age, cold ischemia time, graft steatosis and ischemia/reperfusion injury may lead to a higher and more aggressive viral recurrence. After the transplant, discussion about immunosuppression and the moment to start the treatment (prophylactic, pre-emptive or once-confirmed) together with new antiviral drugs are of interest. This review aims to help clinicians have a global overview of posttransplant HCV recurrence and strategies to reduce its impact on our patients.

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Section: Predictors Of Antiviral Therapy Response and Tolerancementioning

confidence: 99%

“…Many of the reported studies were designed to focus on the safety and tolerability of AVT, rather than HCV recurrence patterns and clinical course post LTx [22][23][24][26][27][28][29][30][31] . A number of different antiviral regimens and treatment periods have been studied.…”

Section: Evidence Regarding Pre-transplant Antiviral Therapymentioning

confidence: 99%

Strategies to reduce hepatitis C virus recurrence after liver transplantation

Ciria

Pleguezuelo²,

Khorsandi³

et al. 2013

WJH

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“…Finally, insulin resistance secondary to HCV infection may further impair response to combination therapy [31] . Several repor ts on antiviral therapy in HCVinfected cirrhotic patients who sustained one or more episodes of liver decompensation are available in the literature [32][33][34][35][36] (Table 1): The results indicate that these patients might tolerate current antiviral regimens. However, unstandardized dosages of antiviral drugs that have been administered for a variable and different treatment length may have underestimated and differentiated outcomes and virologic response rates in previous reports.…”

Section: Hcv Cirrhosis In Decompensated Phasementioning

confidence: 99%

Antiviral therapy in hepatitis C virus cirrhotic patients in compensated and decompensated condition

Iacobellis

Ippolito

Andriulli

2008

WJG

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The main goals of treating cirrhotic patients with antiviral therapy are to attain sustained viral clearance (SVR), halt disease progression, and prevent reinfection of the liver graft. However, while the medical need is great, the use of interferon and ribavirin might expose these patients to severe treated-related side effects as a large proportion of them have pre-existing hematological cytopenias. We have reviewed potential benefits and risks associated with antiviral drugs in patients with liver cirrhosis, due to hepatitis C virus (HCV) infection. In cases presenting with bridging fibrosis or cirrhosis, current regimens of antiviral therapy have attained a 44%-48% rate of SVR. In cirrhotic patients with portal hypertension, the SVR rate was 22% overall, 12.5% in patients with genotype 1, and 66.7% in those with genotypes 2 and 3 following therapy with low doses of either Peg-IFN alpha2b and of ribavirin. In patients with decompensated cirrhosis, full dosages of Peg-IFN alpha-2b and of ribavirin produced a SVR rate of 35% overall, 16% in patients with genotype 1 and 4, and 59% in those with genotype 2 and 3. Use of hematological cytokines will either ensure full course of treatment to be accomplished with and prevent development of treatment-associated side effects. Major benefits after HCV eradication were partial recovery of liver metabolic activity, prevention of hepatitis C recurrence after transplantation, and removal of some patients from the waiting list for liver transplant. Several observations highlighted that therapy is inadvisable for individuals with poor hepatic reserve (Child-PughTurcotte score ≥ 10). Although SVR rates are low in decompensated cirrhotics due to hepatitis C, these patients have the most to gain as successful antiviral therapy is potentially lifesaving.

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“…The propensity of HCV to infect the immune system is consistent with a significantly greater prevalence of lymphoproliferative disorders, such as non-Hodgkin's lymphoma and mixed cryoglobulinemia, and perhaps mucosa-associated lymphoid tissue lymphoma, in patients infected with HCV (4,10,13,40,42). It also is possible that HCV residing in immune cells, like other persistent viral infections (5,14,26,29), is an important contributor to longterm virus persistence and that the infected immune cells are reservoirs from which infection can spread, for example, in patients grafted with new livers due to HCV-related end-stage disease or in recipients of seemingly HCV-negative donor organs (24,25,39).…”

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confidence: 99%

Hepatitis C Virus Infection of Human T Lymphocytes Is Mediated by CD5

Sarhan

Pham

Chen

et al. 2012

J Virol

109

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Hepatitis C virus (HCV) is one of the main causes of chronic liver disease. Although infection of hepatocytes is mainly responsible for manifestations of hepatitis C, the virus also invades the immune system by a yet-to-be-identified mechanism. Using human T cell lines and primary T lymphocytes as targets and patient-derived HCV as inocula, we aimed to identify how HCV gains entry into these cells. HCV replication was determined by detection of the HCV RNA replicative (negative) strand and viral proteins, while specific antibodies, knocking down gene expression and making otherwise-resistant cells prone to HCV, were employed to identify a receptor molecule determining T lymphocyte permissiveness to HCV infection. The results revealed that T cell susceptibility to HCV requires CD5, a lymphocyte-specific glycoprotein belonging to the scavenger receptor cysteine-rich family. Blocking of T cell CD5 with antibody or silencing with specific short hairpin RNA (shRNA) decreased cell susceptibility to HCV, while increasing CD5 expression by mitogen stimulation had the opposite effect. Moreover, transfection of naturally CD5-deficient HEK-293 fibroblasts with CD5 facilitated infection of these otherwise HCV-resistant cells. In contrast to T cells, hepatocytes do not express CD5. The data revealed that CD5 is a molecule important for HCV entry into human T lymphocytes. This finding provides direct insight into the mechanism of HCV lymphotropism and defines a target for potential interventions against HCV propagating in this extrahepatic compartment.

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Infection with chronic hepatitis C virus and liver transplantation: A role for interferon therapy before transplantation

Cited by 134 publications

References 21 publications

Strategies to reduce hepatitis C virus recurrence after liver transplantation

Strategies to reduce hepatitis C virus recurrence after liver transplantation

Antiviral therapy in hepatitis C virus cirrhotic patients in compensated and decompensated condition

Hepatitis C Virus Infection of Human T Lymphocytes Is Mediated by CD5

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