The proteins of the Hepatitis C Virus: their features and interactions with intracellular protein phosphorylation
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The proteins of the Hepatitis C Virus: their features and interactions with intracellular protein phosphorylation. / Schulze zur Wiesch, J; Schmitz, H; Borowski, E; Borowski, P.
in: ARCH VIROL, Jahrgang 148, Nr. 7, 07.2003, S. 1247-67.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Review › Forschung
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TY - JOUR
T1 - The proteins of the Hepatitis C Virus: their features and interactions with intracellular protein phosphorylation
AU - Schulze zur Wiesch, J
AU - Schmitz, H
AU - Borowski, E
AU - Borowski, P
PY - 2003/7
Y1 - 2003/7
N2 - Chronic infection with Hepatitis C virus (HCV) often results in cirrhosis and enhances the probability of developing hepatocellular carcinoma (HCC). The underlying mechanisms that lead to malignant transformation of infected cells, however, remain unclear. Observations made with isolated HCV antigens and/or with HCV subgenomic replicon systems demonstrated that the products encoded in the HCV genome interfere with and disturb intracellular signal transduction, often by phosphorylation of cellular proteins. Moreover, some of the HCV-encoded proteins seem to serve as substrates for host cell protein kinases. These phosphorylations affect the biological functions of the antigens. In many cases it could be demonstrated that only short stretches of the linear sequence of the viral or cellular proteins are involved and play a crucial role for these phosphorylation events. The identification of these small polypeptide elements and the subsequent development of strategies to inhibit protein-protein interactions involving them may be the first step towards reducing the chronicity and/or of the carcinogenicity of the virus. This review summarizes current knowledge of intracellular phosphorylation processes that are affected by HCV.
AB - Chronic infection with Hepatitis C virus (HCV) often results in cirrhosis and enhances the probability of developing hepatocellular carcinoma (HCC). The underlying mechanisms that lead to malignant transformation of infected cells, however, remain unclear. Observations made with isolated HCV antigens and/or with HCV subgenomic replicon systems demonstrated that the products encoded in the HCV genome interfere with and disturb intracellular signal transduction, often by phosphorylation of cellular proteins. Moreover, some of the HCV-encoded proteins seem to serve as substrates for host cell protein kinases. These phosphorylations affect the biological functions of the antigens. In many cases it could be demonstrated that only short stretches of the linear sequence of the viral or cellular proteins are involved and play a crucial role for these phosphorylation events. The identification of these small polypeptide elements and the subsequent development of strategies to inhibit protein-protein interactions involving them may be the first step towards reducing the chronicity and/or of the carcinogenicity of the virus. This review summarizes current knowledge of intracellular phosphorylation processes that are affected by HCV.
KW - Carcinoma, Hepatocellular/virology
KW - Genome, Viral
KW - Hepacivirus/genetics
KW - Hepatitis C/complications
KW - Humans
KW - Liver Neoplasms/virology
KW - Phosphorylation
KW - Viral Proteins/genetics
U2 - 10.1007/s00705-003-0115-8
DO - 10.1007/s00705-003-0115-8
M3 - SCORING: Review article
C2 - 12827459
VL - 148
SP - 1247
EP - 1267
JO - ARCH VIROL
JF - ARCH VIROL
SN - 0304-8608
IS - 7
ER -
