Nineteen CVA9 isolates were obtained between 2010 and 2019 from six provinces of mainland China, using the HFMD surveillance network established in China. Nucleotide sequencing revealed that the full-length VP1 of 19 CVA9 isolates was 906 bases encoding 302 amino acids. The combination of the thresholds of the phylogenetic tree and nucleotide divergence of different genotypes within the same serotype led to a value of 15–25%, and enabled CVA9 worldwide to be categorized into ten genotypes: A–J. The phylogenetic tree showed that the prototype strain was included in genotype A, and that the B, C, D, E, H, and J genotypes disappeared during virus evolution, whereas the F, I, and G genotypes showed co-circulation. Lineage G was the dominant genotype of CVA9 and included most of the strains from nine countries in Asia, North America, Oceania, and Europe. Most Chinese strains belonged to the G genotype, suggesting that the molecular epidemiology of China is consistent with that observed worldwide. The 165 partial VP1 strains (723 nt) showed a mean substitution rate of 3.27 × 10−3 substitution/site/year (95% HPD range 2.93–3.6 × 10−3), dating the tMRCA of CVA9 back to approximately 1922 (1911–1932). The spatiotemporal dynamics of CVA9 showed the spread of CVA9 obviously increased in recent years. Most CVA9 isolates originated in USA, but the epidemic areas of CVA9 are now concentrated in the Asia–Pacific region, European countries, and North America. Recombination analysis within the enterovirus B specie (59 serotypes) revealed eight recombination patterns in China at present, CVB4, CVB5, E30, CVB2, E11, HEV106, HEV85, and HEV75. E14, and E6 may act as recombinant donors in multiple regions. Comparison of temperature sensitivity revealed that temperature-insensitive strains have more amino acid substitutions in the RGD motif of the VP1 region, and the sites T283S, V284M, and R288K in the VP1 region may be related to the temperature tolerance of CVA9.

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Echovirus 30 (E30) infection causes a wide spectrum of diseases with mild symptoms, such as hand, foot, and mouth disease (HFMD), acute flaccid paralysis, and aseptic meningitis and other diseases, especially one of the most common pathogens causing aseptic meningitis outbreaks. We established a novel mouse model of E30 infection by inoculating neonatal mice with clinical isolates of E30 and observed the pathological changes induced by E30.

Background China implemented the globally synchronized switch from trivalent oral poliovirus vaccine (tOPV) to bivalent OPV (bOPV) on May 1, 2016. During April 2018 to May 2019, the first outbreak caused by type 2 circulating vaccine-derived poliovirus (cVDPV2) after the switch occurred in Xinjiang and Sichuan, China. Methods. We performed sequence analysis of VP1 and the whole genome to determine the genomic characteristics of type 2 cVDPVs, and carried out coverage surveys to assess the risk of viral propagation. Surveillance for environment and acute flaccid paralysis was intensified to enhance case ascertainment. Results. Comparison of the complete genomes between early (Xinjiang strain) and late strains (Sichuan strains) revealed that recombination pattern and reverse mutation of attenuation sites had been fixed early, but the mutations of the neutralizing antigenic sites were introduced over the circulation. The Markov Chain Monte Carlo tree showed that the cVDPV2 initial infection was April 2016, earlier than the switch. So, we speculated that the cVDPV2 was originated from tOPV recipients and spread among children with a low level of immunity against the type 2. Conclusions The detection of this outbreak combined acute flaccid paralysis (AFP) surveillance with environmental surveillance (ES) indicates that ES should be expanded geographically to further complement AFP surveillance.