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Journal of Virology, December 2000, p. 11153-11161, Vol. 74, No. 23
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Molecular Evolution of a Type 1 Wild-Vaccine Poliovirus
Recombinant during Widespread Circulation in China
Hong-Mei
Liu,1,2,*
Du-Ping
Zheng,1,
Li-Bi
Zhang,3
M. Steven
Oberste,1
Mark A.
Pallansch,1 and
Olen
M.
Kew1
Division of Viral and Rickettsial Diseases,
National Center for Infectious Diseases, Centers for Disease Control
and Prevention, Atlanta, Georgia 30333,1 and
National Vaccine and Serum Institute, Beijing
100024,2 and National Poliovirus
Reference Center, Institute of Virology, Chinese Academy of
Preventive Medicine, Beijing 100052,3 People's
Republic of China
Received 24 July 2000/Accepted 13 September 2000
Type 1 wild-vaccine recombinant polioviruses were isolated from
poliomyelitis patients in China from 1991 to 1993. We compared the
sequences of 34 recombinant isolates over the 1,353-nucleotide (nt)
genomic interval (nt 2480 to 3832) encoding the major capsid protein,
VP1, and the protease, 2A. All recombinants had a 367-nt block of
sequence (nt 3271 to 3637) derived from the Sabin 1 oral poliovirus
vaccine strain spanning the 3'-terminal sequences of VP1 (115 nt) and the 5' half of 2A (252 nt). The remaining VP1 sequences were
closely (up to 99.5%) related to those of a major genotype of wild
type 1 poliovirus endemic to China up to 1994. In contrast, the
non-vaccine-derived sequences at the 3' half of 2A were more distantly
related (<90% nucleotide sequence match) to those of other
contemporary wild polioviruses from China. The vaccine-derived
sequences of the earliest (April 1991) isolates completely matched
those of Sabin 1. Later isolates diverged from the early isolates
primarily by accumulation of synonymous base substitutions (at a rate
of ~3.7 × 10
2 substitutions per synonymous site
per year) over the entire VP1-2A interval. Distinct evolutionary
lineages were found in different Chinese provinces. From the combined
epidemiologic and evolutionary analyses, we propose that the
recombinant virus arose during mixed infection of a single individual
in northern China in early 1991 and that its progeny spread by multiple
independent chains of transmission into some of the most populous areas
of China within a year of the initiating infection.
*
Corresponding author. Mailing address: Respiratory and
Enterovirus Branch, G-17, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30333. Phone: (404) 639-2762. Fax: (404)
639-4011. E-mail: hdl1{at}cdc.gov.

Present address: Department of Biology, Georgia State University,
Atlanta, GA
30303.
Journal of Virology, December 2000, p. 11153-11161, Vol. 74, No. 23
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
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