Hepatitis C virus viral kinetics during α-2a or α-2b pegylated interferon plus ribavirin therapy in liver transplant recipients with different immunosuppression regimes

Berenguer, Marina; Ortíz-Cantó, Cecilia; Abellán, Juan J.; Aguilera, Victoria; Rubín, Ángel; Prieto, M.; López‐Labrador, F. Xavier

doi:10.1016/j.jcv.2011.12.005

Cited by 7 publications

(6 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…2c). In apparent agreement, whereas it is well-known that chronic HCV patients who respond to IFN-a therapy often experience a rapid and sharp reduction of viral load within the first few days upon treatment [26,27], we observed that three of four chronic HEV patients had only minor fluctuation of viral load within first 2 weeks of pegylated IFN-a treatment, although all the patients eventually cleared the virus (Fig. 2d).…”

Section: Hev Compared To Hcv Is Less Sensitive To Ifn-a Treatmentsupporting

confidence: 87%

Disparity of basal and therapeutically activated interferon signalling in constraining hepatitis E virus infection

Zhou

Wang

et al. 2015

Journal of Viral Hepatitis

View full text Add to dashboard Cite

Hepatitis E virus (HEV) represents one of the foremost causes of acute hepatitis globally. Although there is no proven medication for hepatitis E, pegylated interferon-α (IFN-α) has been used as off-label drug for treating HEV. However, the efficacy and molecular mechanisms of how IFN signalling interacts with HEV remain undefined. As IFN-α has been approved for treating chronic hepatitis C (HCV) for decades and the role of interferon signalling has been well studied in HCV infection, this study aimed to comprehensively investigate virus-host interactions in HEV infection with focusing on the IFN signalling, in comparison with HCV infection. A comprehensive screen of human cytokines and chemokines revealed that IFN-α was the sole humoral factor inhibiting HEV replication. IFN-α treatment exerted a rapid and potent antiviral activity against HCV, whereas it had moderate and delayed anti-HEV effects in vitro and in patients. Surprisingly, blocking the basal IFN pathway by inhibiting JAK1 to phosphorylate STAT1 has resulted in drastic facilitation of HEV, but not HCV infection. Gene silencing of the key components of JAK-STAT cascade of the IFN signalling, including JAK1, STAT1 and interferon regulatory factor 9 (IRF9), stimulated HEV infection. In conclusion, compared to HCV, HEV is less sensitive to IFN treatment. In contrast, the basal IFN cascade could effectively restrict HEV infection. This bears significant implications in management of HEV patients and future therapeutic development.

show abstract

Section: Hev Compared To Hcv Is Less Sensitive To Ifn-a Treatmentsupporting

confidence: 87%

Disparity of basal and therapeutically activated interferon signalling in constraining hepatitis E virus infection

Zhou

Wang

et al. 2015

Journal of Viral Hepatitis

View full text Add to dashboard Cite

show abstract

“…7, 8 Combination therapy with PEG‐IFN and ribavirin remains the recommended regimen after LT because SVR rates are higher than those with interferon (IFN)‐based dual therapy or PEG‐IFN alone. Unfortunately, studies of post‐LT treatment have generally led to disappointing SVR rates because of the high proportions of patients with genotype 1 and previous nonresponse, the poor tolerability of PEG‐IFN and ribavirin, and concomitant immunosuppression, which affects viral kinetics and renders the interpretation of traditional stopping rules complex 9. When more than 40 treatment trials of PEG‐IFN or IFN with ribavirin were pooled, the composite SVRs were 27% and 24%, respectively 10.…”

Section: Antiviral Therapy For the Treatment Of Significant Recurrentmentioning

confidence: 99%

Hepatitis C virus: Management of recurrent disease

Verna

2013

Clinical Liver Disease

View full text Add to dashboard Cite

“…Non-1 genotype [26, 27, 199, 202, 213, 218, 220, 234, 235], absence of prior antiviral therapy [194], early virologic response (evaluated after 3 months) [27, 28, 202, 205, 207–210, 214, 215, 217–221, 223, 235], rapid virologic response (evaluated after 1 month) [206, 208, 220], adherence to therapy [27, 202, 207, 211, 213, 216–218], low baseline viral load [27, 208, 211–213, 216, 221, 222], low pretreatment fibrosis stage [26, 28, 204], younger donor age [26, 28, 221, 234], polymorphisms close to the IL-28B gene [66–69], and cyclosporine-based immunosuppression [26, 234, 236] are associated with an improved SVR. Most studies demonstrated improved biochemical and histologic findings, even in virologic nonresponders [222, 237], but whether antiviral therapy slows disease progression in nonresponders has not yet been demonstrated.…”

Section: Antiviral Treatmentmentioning

confidence: 99%

Liver Transplantation and Hepatitis C

Akamatsu

Sugawara

2012

International Journal of Hepatology

View full text Add to dashboard Cite

Hepatitis-C-virus- (HCV-) related end-stage cirrhosis is the primary indication for liver transplantation in many countries. Unfortunately, however, HCV is not eliminated by transplantation and graft reinfection is universal, resulting in fibrosis, cirrhosis, and finally graft decompensation. The use of poor quality organs, particularly from older donors, has a highly negative impact on the severity of recurrence and patient/graft survival. Although immunosuppressive regimens have a considerable impact on the outcome, the optimal regimen after liver transplantation for HCV-infected patients remains unclear. Disease progression monitoring with protocol biopsy and new noninvasive methods is essential for predicting patient/graft outcome and starting antiviral treatment with the appropriate timing. Antiviral treatment with pegylated interferon and ribavirin is currently considered the most promising regimen with a sustained viral response rate of around 30% to 35%, although the survival benefit of this regimen remains to be investigated. Living-donor liver transplantation is now widely accepted as an established treatment for HCV cirrhosis and the results are equivalent to those of deceased donor liver transplantation.

show abstract

Hepatitis C virus viral kinetics during α-2a or α-2b pegylated interferon plus ribavirin therapy in liver transplant recipients with different immunosuppression regimes

Cited by 7 publications

References 55 publications

Disparity of basal and therapeutically activated interferon signalling in constraining hepatitis E virus infection

Disparity of basal and therapeutically activated interferon signalling in constraining hepatitis E virus infection

Hepatitis C virus: Management of recurrent disease

Liver Transplantation and Hepatitis C

Contact Info

Product

Resources

About