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Journal of Virology, June 2009, p. 5806-5814, Vol. 83, No. 11
0022-538X/09/$08.00+0     doi:10.1128/JVI.00033-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

The Marmoset Model of GB Virus B Infections: Adaptation to Host Phenotypic Variation{triangledown}

Trudie Weatherford,1,3 Deborah Chavez,1 Kathleen M. Brasky,2 and Robert E. Lanford1,2,3*

Department of Virology and Immunology,1 Southwest National Primate Research Center, Southwest Foundation for Biomedical Research, 7620 NW Loop 410, San Antonio, Texas 78227,2 Department of Microbiology and Immunology, University of Texas Health Science Center, 7703 Floyd Curl Dr., San Antonio, Texas 782293

Received 7 January 2009/ Accepted 6 March 2009

Worldwide, approximately 170 million people are chronically infected with hepatitis C virus (HCV), and chronic infection frequently progresses to serious liver disease, including cirrhosis and hepatocellular carcinoma. GB virus B (GBV-B), the virus phylogenetically most closely related to HCV, causes hepatitis in tamarins. We have demonstrated the suitability of the tamarin as a host for GBV-B and as a surrogate nonhuman primate model for HCV infection, and we have initiated studies of GBV-B infection in a closely related species, the common marmoset (Callithrix jacchus). Here, we demonstrate that marmosets exhibit two phenotypes upon infection with GBV-B: the susceptible phenotype and the partially resistant phenotype. In addition, we identify changes that may correlate with adaptation of the virus to the partially resistant host. GBV-B was serially passaged five times through 14 marmosets as one lineage and two times through 6 marmosets as a second lineage. Virus adapted to the marmosets and eventually exhibited robust infections in two separate lineages, lineages 1 and 2. A third lineage was initiated with a molecular clone, and again, susceptible and partially resistant phenotypes were observed. Three isolates were fully sequenced (from lineage 1), and 21 nucleotide changes were observed, with six amino acid changes. We speculate that the marmoset partially resistant phenotype may be due to a polymorphism in the marmoset population that affects critical virus-host interactions and that wild-type GBV-B is capable of rapidly adapting to this altered host.

* Corresponding author. Mailing address: Department of Virology and Immunology, Southwest Foundation for Biomedical Research, 7620 NW Loop 410, San Antonio, TX 78227. Phone: (210) 258-9445. Fax: (210) 670-3329. E-mail: rlanford{at}icarus.sfbr.org

{triangledown} Published ahead of print on 11 March 2009.

Journal of Virology, June 2009, p. 5806-5814, Vol. 83, No. 11
0022-538X/09/$08.00+0     doi:10.1128/JVI.00033-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Weatherford, T., Chavez, D., Brasky, K. M., Lemon, S. M., Martin, A., Lanford, R. E. (2009). Lack of Adaptation of Chimeric GB Virus B/Hepatitis C Virus in the Marmoset Model: Possible Effects of Bottleneck. J. Virol. 83: 8062-8075 [Abstract] [Full Text]  


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