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J Virol, March 1998, p. 1725-1730, Vol. 72, No. 3
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Immunity in Chimpanzees Chronically Infected with Hepatitis C Virus: Role of Minor Quasispecies in Reinfection

Colby A. Wyatt, Linda Andrus, Betsy Brotman, Fannie Huang, Dong-Hun Lee, and Alfred M. Prince*

Laboratories of Virology and Parasitology and of Microchemistry, The Lindsley F. Kimball Research Institute of the New York Blood Center, New York, New York 10021

Received 30 January 1997/Accepted 18 November 1997

We have previously reported that chimpanzees chronically infected with hepatitis C virus (HCV) could be reinfected, even with the original infecting strain. In this study we tested the hypothesis that this might reflect the presence of minor quasispecies to which there was little or no immunity. To evaluate this hypothesis, we sequenced multiple clones taken at intervals after primary infection and rechallenge from four chronically infected chimpanzees. The inoculum used in these studies (HCV-H, genotype 1a) revealed 17 separate variants among 46 clones sequenced. Following challenge, each of the four challenged animals showed marked alterations of their quasispecies distribution. The new variants, which appeared 1 to 6 weeks after challenge, were either identical to or closely resembled variants present in the challenge inoculum. These results, paralleled by an increase in viremia in some of the challenged animals, suggest that quasispecies in the challenge inoculum were responsible for signs of reinfection and that there was little immunity. However, the newly emerged quasispecies completely took over infection in only one animal. In the remaining three chimpanzees the prechallenge quasispecies were able to persist. The natural evolution of infection within chimpanzees resulted in variants able to compete with the inoculum variants. Whether through reexposure or the natural progression of infection, newly emerged quasispecies are likely to play a role in the pathogenesis of chronic HCV infection.

* Corresponding author. Mailing address: The New York Blood Center, 310 E. 67th St., New York, NY 10021. Phone: (212) 570-3279. Fax: (212) 570-3180. E-mail: aprince{at}NYBC.org.




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Copyright © 1998 by the American Society for Microbiology. All rights reserved.