Volume 66, Issue 4 pp. 468-471
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Lack of susceptibility of Chacma baboons (Papio ursinus orientalis) to hepatitis C virus infection

N.P. Sithebe

N.P. Sithebe

MRC, CANSA, University Molecular Hepatology Research Unit, Department of Medicine, University of the Witwatersrand, Johannesburg, South Africa

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M.C. Kew

Corresponding Author

M.C. Kew

MRC, CANSA, University Molecular Hepatology Research Unit, Department of Medicine, University of the Witwatersrand, Johannesburg, South Africa

Department of Medicine, Medical School, 7 York Road, Parktown 2193, Johannesburg, South Africa.===Search for more papers by this author
M.J. Mphahlele

M.J. Mphahlele

Department of Virology, Medical University of Southern Pretoria, Pretoria, South Africa

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A.C. Paterson

A.C. Paterson

Department of Anatomical Pathology, South African Institute for Medical Research and University of the Witwatersrand, Johannesburg, South Africa

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G. Lecatsas

G. Lecatsas

Department of Virology, Medical University of Southern Pretoria, Pretoria, South Africa

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A. Kramvis

A. Kramvis

MRC, CANSA, University Molecular Hepatology Research Unit, Department of Medicine, University of the Witwatersrand, Johannesburg, South Africa

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W. de Klerk

W. de Klerk

Laboratory Animal Centre, Medical University of Southern Africa, Pretoria, South Africa

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First published: 05 February 2002
Citations: 11

Abstract

The main reason to ascertain whether baboons are susceptible to infection with hepatitis C virus (HCV) is the need to replace chimpanzees, which are endangered, as an animal model for undertaking research into the biology and host–virus interactions of HCV, and for developing a vaccine against this virus. A second reason is that baboons are a possible source of xenografts for human liver transplantation. We inoculated serum containing HCV into four Chacma baboons and monitored them for 52 weeks for evidence of infection. Serum was tested for antibody to HCV, HCV RNA, and aminotransferase concentrations at 2-week intervals for 26 weeks and thereafter at 4-week intervals. Liver tissue was examined at 28 and 52 weeks for histopathological changes and viral RNA, and at 52 weeks for viral particles using electron microscopy. Reverse transcription-polymerase chain reaction assay was used to detect HCV RNA, and the results were confirmed by Southern hybridization. Serum aminotransferase concentrations remained within the normal range and liver histology was normal during the follow-up period. Passive transmission of anti-HCV to the baboons was observed during the first 4 weeks. HCV RNA was not detectable in any serum or liver sample and electron microscopy failed to reveal viral particles in liver tissue. In conclusion, we did not find Chacma baboons to be susceptible to infection with HCV, although we cannot deny that in an immunosuppressed liver transplant recipient, infection of a baboon xenograft might occur. Another animal model for HCV infection must be sought. J. Med. Virol. 66:468–471, 2002. © 2002 Wiley-Liss, Inc.

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