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J Virol, July 1998, p. 6271-6276, Vol. 72, No. 7
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Evolution of Hypervariable Region 1 of Hepatitis C Virus in Primary Infection

Aldo Manzin,1,* Laura Solforosi,1 Enzo Petrelli,2 Giampiero Macarri,3 Grazia Tosone,4 Marcello Piazza,4 and Massimo Clementi5

Istituto di Microbiologia1 and Clinica di Gastroenterologia,3 Università di Ancona, Ancona, Divisione di Malattie Infettive, Ospedale S. Salvatore, Pesaro,2 Clinica di Malattie Infettive, Università di Napoli Federico II, Naples,4 and Dipartimento di Scienze Biomediche, Università di Trieste, Trieste,5 Italy

Received 12 December 1997/Accepted 25 March 1998

The hypervariable region 1 (HVR-1) of the putative envelope encoding E2 region of hepatitis C virus (HCV) RNA was analyzed in sequential samples from three patients with acute type C hepatitis infected from different sources to address (i) the dynamics of intrahost HCV variability during the primary infection and (ii) the role of host selective pressure in driving viral genetic evolution. HVR-1 sequences from 20 clones per each point in time were analyzed after amplification, cloning, and purification of plasmid DNA from single colonies of transformed cells. The intrasample evolutionary analysis (nonsynonymous mutations per nonsynonymous site [Ka], synonymous mutations per synonymous site [Ks], Ka/Ks ratio, and genetic distances [gd]) documented low gd in early samples (ranging from 2.11 to 7.79%) and a further decrease after seroconversion (from 0 to 4.80%), suggesting that primary HCV infection is an oligoclonal event, and found different levels and dynamics of host pressure in the three cases. The intersample analysis (pairwise comparisons of intrapatient sequences; rKa, rKs, rKa/rKs ratio, and gd) confirmed the individual features of HCV genetic evolution in the three subjects and pointed to the relative contribution of either neutral evolution or selective forces in driving viral variability, documenting that adaptation of HCV for persistence in vivo follows different routes, probably representing the molecular counterpart of the viral fitness for individual environments.

* Corresponding author. Mailing address: Institute of Microbiology, University of Ancona, via Pietro Ranieri, I-60100 Ancona, Italy. Phone: 39 71 596 4849. Fax: 39 71 596 4852. E-mail: manzin{at}popcsi.unian.it.

J Virol, July 1998, p. 6271-6276, Vol. 72, No. 7
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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