Hepatitis C virus infection of cholangiocarcinoma cell lines

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Hepatitis C virus infection of cholangiocarcinoma cell lines. / Fletcher, N. F.; Humphreys, E. A.; Jennings, E.; Osburn, W.; Lissauer, Samantha; Wilson, G. K.; Van Ijzendoorn, S. C.; Baumert, T. F.; Balfe, P.; Afford, S.; Mckeating, J.

In: Journal of General Virology, Vol. 96, No. 6, 06.2015, p. 1380-1388.

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@article{d71dad53143940d0800e9c349e38db94,
title = "Hepatitis C virus infection of cholangiocarcinoma cell lines",
abstract = "Hepatitis C virus (HCV) infects the liver and hepatocytes are the major cell type supporting viral replication. Hepatocytes and cholangiocytes derive from a common hepatic progenitor cell that proliferates during inflammatory conditions, raising the possibility that cholangiocytes may support HCV replication and contribute to the hepatic reservoir. We screened cholangiocytes along with a panel of cholangiocarcinoma-derived cell lines for their ability to support HCV entry and replication. While primary cholangiocytes were refractory to infection and lacked expression of several entry factors, two cholangiocarcinoma lines, CC-LP-1 and Sk-ChA-1, supported efficient HCV entry; furthermore, Sk-ChA-1 cells supported full virus replication. In vivo cholangiocarcinomas expressed all of the essential HCV entry factors; however, cholangiocytes adjacent to the tumor and in normal tissue showed a similar pattern of receptor expression to ex vivo isolated cholangiocytes, lacking SR-BI expression, explaining their inability to support infection. This study provides the first report that HCV can infect cholangiocarcinoma cells and suggests that these heterogeneous tumors may provide a reservoir for HCV replication in vivo.",
author = "Fletcher, {N. F.} and Humphreys, {E. A.} and E. Jennings and W. Osburn and Samantha Lissauer and Wilson, {G. K.} and {Van Ijzendoorn}, {S. C.} and Baumert, {T. F.} and P. Balfe and S. Afford and J. Mckeating",
year = "2015",
month = jun
doi = "10.1099/vir.0.000090",
language = "English",
volume = "96",
pages = "1380--1388",
journal = "Journal of General Virology",
issn = "0022-1317",
publisher = "Microbiology Society",
number = "6",

}

RIS

TY - JOUR

T1 - Hepatitis C virus infection of cholangiocarcinoma cell lines

AU - Fletcher, N. F.

AU - Humphreys, E. A.

AU - Jennings, E.

AU - Osburn, W.

AU - Lissauer, Samantha

AU - Wilson, G. K.

AU - Van Ijzendoorn, S. C.

AU - Baumert, T. F.

AU - Balfe, P.

AU - Afford, S.

AU - Mckeating, J.

PY - 2015/6

Y1 - 2015/6

N2 - Hepatitis C virus (HCV) infects the liver and hepatocytes are the major cell type supporting viral replication. Hepatocytes and cholangiocytes derive from a common hepatic progenitor cell that proliferates during inflammatory conditions, raising the possibility that cholangiocytes may support HCV replication and contribute to the hepatic reservoir. We screened cholangiocytes along with a panel of cholangiocarcinoma-derived cell lines for their ability to support HCV entry and replication. While primary cholangiocytes were refractory to infection and lacked expression of several entry factors, two cholangiocarcinoma lines, CC-LP-1 and Sk-ChA-1, supported efficient HCV entry; furthermore, Sk-ChA-1 cells supported full virus replication. In vivo cholangiocarcinomas expressed all of the essential HCV entry factors; however, cholangiocytes adjacent to the tumor and in normal tissue showed a similar pattern of receptor expression to ex vivo isolated cholangiocytes, lacking SR-BI expression, explaining their inability to support infection. This study provides the first report that HCV can infect cholangiocarcinoma cells and suggests that these heterogeneous tumors may provide a reservoir for HCV replication in vivo.

AB - Hepatitis C virus (HCV) infects the liver and hepatocytes are the major cell type supporting viral replication. Hepatocytes and cholangiocytes derive from a common hepatic progenitor cell that proliferates during inflammatory conditions, raising the possibility that cholangiocytes may support HCV replication and contribute to the hepatic reservoir. We screened cholangiocytes along with a panel of cholangiocarcinoma-derived cell lines for their ability to support HCV entry and replication. While primary cholangiocytes were refractory to infection and lacked expression of several entry factors, two cholangiocarcinoma lines, CC-LP-1 and Sk-ChA-1, supported efficient HCV entry; furthermore, Sk-ChA-1 cells supported full virus replication. In vivo cholangiocarcinomas expressed all of the essential HCV entry factors; however, cholangiocytes adjacent to the tumor and in normal tissue showed a similar pattern of receptor expression to ex vivo isolated cholangiocytes, lacking SR-BI expression, explaining their inability to support infection. This study provides the first report that HCV can infect cholangiocarcinoma cells and suggests that these heterogeneous tumors may provide a reservoir for HCV replication in vivo.

U2 - 10.1099/vir.0.000090

DO - 10.1099/vir.0.000090

M3 - Article

C2 - 25701818

VL - 96

SP - 1380

EP - 1388

JO - Journal of General Virology

JF - Journal of General Virology

SN - 0022-1317

IS - 6

ER -