Infections and the Liver

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Infections and the Liver. / Eksteen, Johannes.

In: Digestive Diseases, Vol. 29, No. 2, 01.01.2011, p. 184-190.

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Eksteen, Johannes. / Infections and the Liver. In: Digestive Diseases. 2011 ; Vol. 29, No. 2. pp. 184-190.

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@article{e66ba1e42bde4c56ad54252f2d079190,
title = "Infections and the Liver",
abstract = "Background: Hepatitis B (HBV) and hepatitis C virus (HCV) have infected nearly half a billion individuals worldwide and are major indications for liver transplantation. Key requirements to successful outcomes with modern antiviral drugs are favourable host factors. Results: Single nucleotide polymorphisms near the IL28B gene location which encode for interferon (IFN)-lambda 3 have a large effect in determining the likelihood of patients obtaining a cure from pegylated IFN-alpha and ribavirin combination therapy or spontaneous clearance of the HCV. 80% of patients who carry two copies of this advantageous variant cleared the virus during IFN therapy and remained virus-free with a sustained viral response. This mutation is more common in Caucasian and Asian populations, whereas it is only found in the 40-50% of sub-Saharan Africans who are known to be more resistant to combination therapy. Similarly, host factors control tolerance to chronic HBV infection and can fluctuate over time with increased risk of progression to cirrhosis and particularly liver cancer. Loss of viral tolerance with reactivation and hepatitis is increasingly seen with the widespread use of biological treatments for diseases such as inflammatory bowel disease or rheumatoid arthritis. Natural disasters and conflicts in some parts of the world have also seen an increase in cases of hepatitis A and E virus infection and highlighted the global public health burden from viral-induced hepatitis. Conclusions: Increased appreciation of the interaction between host factors and the viral life cycles is likely to significantly alter the way we target these infections in the future. Copyright (C) 2011 S. Karger AG, Basel",
keywords = "Hepatitis B infection, Cirrhosis, Hepatitis C infection, IL28B gene",
author = "Johannes Eksteen",
year = "2011",
month = jan,
day = "1",
doi = "10.1159/000323884",
language = "English",
volume = "29",
pages = "184--190",
journal = "Digestive Diseases",
issn = "0257-2753",
publisher = "Karger",
number = "2",

}

RIS

TY - JOUR

T1 - Infections and the Liver

AU - Eksteen, Johannes

PY - 2011/1/1

Y1 - 2011/1/1

N2 - Background: Hepatitis B (HBV) and hepatitis C virus (HCV) have infected nearly half a billion individuals worldwide and are major indications for liver transplantation. Key requirements to successful outcomes with modern antiviral drugs are favourable host factors. Results: Single nucleotide polymorphisms near the IL28B gene location which encode for interferon (IFN)-lambda 3 have a large effect in determining the likelihood of patients obtaining a cure from pegylated IFN-alpha and ribavirin combination therapy or spontaneous clearance of the HCV. 80% of patients who carry two copies of this advantageous variant cleared the virus during IFN therapy and remained virus-free with a sustained viral response. This mutation is more common in Caucasian and Asian populations, whereas it is only found in the 40-50% of sub-Saharan Africans who are known to be more resistant to combination therapy. Similarly, host factors control tolerance to chronic HBV infection and can fluctuate over time with increased risk of progression to cirrhosis and particularly liver cancer. Loss of viral tolerance with reactivation and hepatitis is increasingly seen with the widespread use of biological treatments for diseases such as inflammatory bowel disease or rheumatoid arthritis. Natural disasters and conflicts in some parts of the world have also seen an increase in cases of hepatitis A and E virus infection and highlighted the global public health burden from viral-induced hepatitis. Conclusions: Increased appreciation of the interaction between host factors and the viral life cycles is likely to significantly alter the way we target these infections in the future. Copyright (C) 2011 S. Karger AG, Basel

AB - Background: Hepatitis B (HBV) and hepatitis C virus (HCV) have infected nearly half a billion individuals worldwide and are major indications for liver transplantation. Key requirements to successful outcomes with modern antiviral drugs are favourable host factors. Results: Single nucleotide polymorphisms near the IL28B gene location which encode for interferon (IFN)-lambda 3 have a large effect in determining the likelihood of patients obtaining a cure from pegylated IFN-alpha and ribavirin combination therapy or spontaneous clearance of the HCV. 80% of patients who carry two copies of this advantageous variant cleared the virus during IFN therapy and remained virus-free with a sustained viral response. This mutation is more common in Caucasian and Asian populations, whereas it is only found in the 40-50% of sub-Saharan Africans who are known to be more resistant to combination therapy. Similarly, host factors control tolerance to chronic HBV infection and can fluctuate over time with increased risk of progression to cirrhosis and particularly liver cancer. Loss of viral tolerance with reactivation and hepatitis is increasingly seen with the widespread use of biological treatments for diseases such as inflammatory bowel disease or rheumatoid arthritis. Natural disasters and conflicts in some parts of the world have also seen an increase in cases of hepatitis A and E virus infection and highlighted the global public health burden from viral-induced hepatitis. Conclusions: Increased appreciation of the interaction between host factors and the viral life cycles is likely to significantly alter the way we target these infections in the future. Copyright (C) 2011 S. Karger AG, Basel

KW - Hepatitis B infection

KW - Cirrhosis

KW - Hepatitis C infection

KW - IL28B gene

U2 - 10.1159/000323884

DO - 10.1159/000323884

M3 - Article

C2 - 21734383

VL - 29

SP - 184

EP - 190

JO - Digestive Diseases

JF - Digestive Diseases

SN - 0257-2753

IS - 2

ER -