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Journal of Virology, March 2000, p. 2541-2549, Vol. 74, No. 6
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Evolutionary Rate and Genetic Drift of Hepatitis C Virus Are Not Correlated with the Host Immune Response: Studies of Infected Donor-Recipient Clusters

Jean-Pierre Allain,1,* Yan Dong,1,2 Anne-Mieke Vandamme,3 Vincent Moulton,4 and Marco Salemi3

Division of Transfusion Medicine, Department of Haematology,1 and National Blood Service,2 East Anglia Blood Centre, Cambridge, United Kingdom; Riga Institute for Medical Research, KU, Leuven, Belgium3; and FMI, Physics and Mathematics Department, Mid Sweden University, Sundsvall, Sweden4

Received 2 September 1999/Accepted 13 December 1999

Six donor-recipient clusters of hepatitis C virus (HCV)-infected individuals were studied. For five clusters the period of infection of the donor could be estimated, and for all six clusters the time of infection of the recipients from the donor via blood transfusion was also precisely known. Detailed phylogenetic analyses were carried out to investigate the genomic evolution of the viral quasispecies within infected individuals in each cluster. The molecular clock analysis showed that HCV quasispecies within a patient are evolving at the same rate and that donors that have been infected for longer time tend to have a lower evolutionary rate. Phylogenetic analysis based on the split decomposition method revealed different evolutionary patterns in different donor-recipient clusters. Reactivity of antibody against the first hypervariable region (HVR1) of HCV in donor and recipient sera was evaluated and correlated to the calculated evolutionary rate. Results indicate that anti-HVR1 reactivity was related more to the overall level of humoral immune response of the host than to the HVR1 sequence itself, suggesting that the particular sequence of the HVR1 peptides is not the determinant of reactivity. Moreover, no correlation was found between the evolutionary rate or the heterogeneity of the viral quasispecies in the patients and the strength of the immune response to HVR1 epitopes. Rather, the results seem to imply that genetic drift is less dependent on immune pressure than on the rate of evolution and that the genetic drift of HCV is independent of the host immune pressure.

* Corresponding author. Mailing address: Division of Transfusion Medicine, East Anglia Blood Centre, Long Road, Cambridge, United Kingdom. Phone: 44 1223 548044. Fax: 44 1223 242044. E-mail: jpa1000{at}cam.ac.uk.

Journal of Virology, March 2000, p. 2541-2549, Vol. 74, No. 6
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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