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Science 14 April 2000:
Vol. 288. no. 5464, pp. 339 - 344
DOI: 10.1126/science.288.5464.339
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Reports

The Outcome of Acute Hepatitis C Predicted by the Evolution of the Viral Quasispecies

Patrizia Farci, 12* Atsushi Shimoda, 3 Alessandra Coiana, 1 Giacomo Diaz, 4 Giovanna Peddis, 1 Jacqueline C. Melpolder, 5 Antonello Strazzera, 1 David Y. Chien, 6 Santiago J. Munoz, 7 Angelo Balestrieri, 1 Robert H. Purcell, 2 Harvey J. Alter 5

The mechanisms by which hepatitis C virus (HCV) induces chronic infection in the vast majority of infected individuals are unknown. Sequences within the HCV E1 and E2 envelope genes were analyzed during the acute phase of hepatitis C in 12 patients with different clinical outcomes. Acute resolving hepatitis was associated with relative evolutionary stasis of the heterogeneous viral population (quasispecies), whereas progressing hepatitis correlated with genetic evolution of HCV. Consistent with the hypothesis of selective pressure by the host immune system, the sequence changes occurred almost exclusively within the hypervariable region 1 of the E2 gene and were temporally correlated with antibody seroconversion. These data indicate that the evolutionary dynamics of the HCV quasispecies during the acute phase of hepatitis C predict whether the infection will resolve or become chronic.

1 Department of Medical Sciences, University of Cagliari, Via San Giorgio 12, 09124 Cagliari, Italy.
2 Hepatitis Viruses Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health (NIH), Bethesda, MD 20892, USA.
3 Department of Internal Medicine, Kanazawa University, Kanazawa 920-8641, Japan.
4 Department of Cytomorphology, University of Cagliari, 09124 Cagliari, Italy.
5 Department of Transfusion Medicine, Warren G. Magnuson Clinical Center, NIH, Bethesda, MD 20892, USA.
6 Chiron Corporation, Emeryville, CA 94507, USA.
7 Albert Einstein Medical Center, Philadelphia, PA 19141, USA.
*   To whom correspondence should be addressed. E-mail: farcip{at}pacs.unica.it

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Mapping B-Cell Epitopes of Hepatitis C Virus E2 Glycoprotein Using Human Monoclonal Antibodies from Phage Display Libraries.
F. Bugli, N. Mancini, C.-Y. Kang, C. Di Campli, A. Grieco, A. Manzin, A. Gabrielli, A. Gasbarrini, G. Fadda, P. E. Varaldo, et al. (2001)
J. Virol. 75, 9986-9990
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Hepatitis C virus replication is directly inhibited by IFN-alpha in a full-length binary expression system.
R. T. Chung, W. He, A. Saquib, A. M. Contreras, R. J. Xavier, A. Chawla, T. C. Wang, and E. V. Schmidt (2001)
PNAS
   Abstract »    Full Text »    PDF »
Hepatitis C Virus Infection.
G. M. Lauer and B. D. Walker (2001)
N. Engl. J. Med. 345, 41-52
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Sustained Dysfunction of Antiviral CD8+ T Lymphocytes after Infection with Hepatitis C Virus.
N. H. Gruener, F. Lechner, M.-C. Jung, H. Diepolder, T. Gerlach, G. Lauer, B. Walker, J. Sullivan, R. Phillips, G. R. Pape, et al. (2001)
J. Virol. 75, 5550-5558
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Molecular intermediates of fitness gain of an RNA virus: characterization of a mutant spectrum by biological and molecular cloning.
A. Arias, E. Lázaro, C. Escarmís, and E. Domingo (2001)
J. Gen. Virol. 82, 1049-1060
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Characterization of Hepatitis C Virus Core-Specific Immune Responses Primed in Rhesus Macaques by a Nonclassical ISCOM Vaccine.
N. K. Polakos, D. Drane, J. Cox, P. Ng, M. J. Selby, D. Chien, D. T. O'Hagan, M. Houghton,