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Journal of Virology, July 2008, p. 6427-6433, Vol. 82, No. 13
0022-538X/08/$08.00+0     doi:10.1128/JVI.00471-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Rapid Sequence Change and Geographical Spread of Human Parvovirus B19: Comparison of B19 Virus Evolution in Acute and Persistent Infections{triangledown} ,{dagger}

Päivi Norja,1,3 Anna Maria Eis-Hübinger,2 Maria Söderlund-Venermo,3 Klaus Hedman,3 and Peter Simmonds1*

Centre for Infectious Diseases, University of Edinburgh, Summerhall, Edinburgh EH9 1QH, United Kingdom,1 Institute of Virology, University of Bonn, Sigmund-Freud-Strasse 25, D-53105 Bonn, Germany,2 Department of Virology, University of Helsinki, and Helsinki University Hospital Laboratory Division, Haartmaninkatu 3, FI-00290 Helsinki, Finland3

Received 4 March 2008/ Accepted 7 April 2008

Parvovirus B19 is a common human pathogen maintained by horizontal transmission between acutely infected individuals. However, B19 virus can also be detected in tissues throughout the life of the host, although little is understood about the nature of such persistence. In the current study, we created large VP1/2 sequence data sets of plasma- and tissue (autopsy)-derived variants of B19 virus with known sample dates to compare the rates of sequence change in exogenous virus populations with those in persistently infected individuals. By using linear regression and likelihood-based methods (such as the BEAST program), we found that plasma-derived B19 virus showed a substitution rate of 4 x 10–4 and an unconstrained (synonymous)-substitution rate of 18 x 10–4 per site per year, several times higher than previously estimated and within the range of values for mammalian RNA viruses. The underlying high mutation frequency implied by these substitution rates may enable rapid adaptive changes that are more commonly ascribed to RNA virus populations. These revised estimates predict that the last common ancestor for currently circulating genotype 1 variants of B19 virus existed around 1956 to 1959, fitting well with previous analyses of the B19 virus "bioportfolio" that support a complete cessation of genotype 2 infections and their replacement by genotype 1 infections in the 1960s. In contrast, the evolution of B19 virus amplified from tissue samples was best modeled by using estimated dates of primary infection rather than sample dates, consistent with slow or absent sequence change during persistence. Determining what epidemiological or biological factors led to such a complete and geographically extensive population replacement over this short period is central to further understanding the nature of parvovirus evolution.

* Corresponding author. Mailing address: Center for Infectious Diseases, University of Edinburgh, Summerhall, Edinburgh EH9 1QH, United Kingdom. Phone: 44 131 650 7927. Fax: 44 131 650 6511. E-mail: peter.simmonds{at}ed.ac.uk

{triangledown} Published ahead of print on 16 April 2008.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

Journal of Virology, July 2008, p. 6427-6433, Vol. 82, No. 13
0022-538X/08/$08.00+0     doi:10.1128/JVI.00471-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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