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1 Respiratory and Enterovirus Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, MS-G17, 1600 Clifton Road, Atlanta, GA 30333, USA
2 Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil
3 Maternal and Child Health Hospital of Shaanxi Province, Xi'an, People's Republic of China
To evaluate the genetic variability of human parvovirus B19, the complete coding region of the VP1/VP2 structural proteins of 29 B19 isolates obtained from 25 infected patients were sequenced and compared with each other and with two previously published B19 isolates. The VP1/VP2 gene was amplified by PCR using B19-specific oligonucleotide primers and the amplification products were sequenced directly. Overall, the average nucleotide and predicted amino acid identity among B19 isolates was high. Sequential virus isolates from the same cases and isolates obtained from two cases linked by transmission in the same household were essentially identical. Sequence variation was minimal among isolates obtained from a single community-wide B19 outbreak, ranging between 0 and 10 (0.4%) base substitutions, although there appeared to be more than one genetic lineage circulating in the outbreak. A comparison with 18 additional isolates from distinct epidemiological settings found greater variability. These isolates differed from each other by between 11 (0.5%) and 112 (4.8%) base substitutions. B19 isolates from Xi'an, China, were significantly different from other isolates at both the nucleotide and amino acid levels, and were more closely related to a single isolate from Japan, obtained 10 years earlier, than to isolates from other countries. Isolates examined in this study included distinct genotypes from patients with similar clinical presentations and similar genotypes from patients with diverse clinical presentations. These data suggest that geographically defined genetic lineages of B19 may exist and that no particular B19 genotype was associated with a particular clinical outcome.
Received 22 April 1996;
accepted 27 June 1996.
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