Molecular Evolution of a Type 1 Wild-Vaccine Poliovirus Recombinant during Widespread Circulation in China

TLDR

The study aims to explain how a type 1 wild‑vaccine recombinant poliovirus emerged during a mixed infection in early 1991 and subsequently spread through multiple independent transmission chains across populous Chinese provinces within a year. Researchers isolated 34 recombinant type 1 polioviruses from patients (1991‑1993) and sequenced a 1,353‑nt VP1‑2A region to compare their genomes. All isolates carried a 367‑nt Sabin 1-derived block across VP1 and 2A; VP1 matched a dominant wild‑type genotype, whereas the 3′ half of 2A was more divergent; early strains matched Sabin 1 exactly, later strains accumulated synonymous substitutions at ~3.7 × 10⁻² per site per year, and distinct lineages appeared in different provinces.

Abstract

ABSTRACT 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.