Molecular epidemiological analysis of coxsackievirus A16 strains causing neurologic complications
10.3760/cma.j.issn.0254-5101.2018.04.006
- VernacularTitle:引起神经症状的柯萨奇A组16型病毒分子流行病学分析
- Author:
Hongxia MA
1
;
Jingjing PAN
;
Yi LI
;
Haiyan WEI
;
Yanhua DU
;
Xingle LI
;
Xueyong HUANG
;
Bianli XU
Author Information
1. 450016郑州,河南省疾病预防控制中心,河南省传染病病原生物重点实验室
- Keywords:
Viral encephalitis;
CA16;
Phylogenetic analysis
- From:
Chinese Journal of Microbiology and Immunology
2018;38(4):274-279
- CountryChina
- Language:Chinese
-
Abstract:
Objective To analyze the VP1 sequences of coxsackievirus A16(CA16) causing neu-rologic complications. Methods Clinical samples and epidemiological information were collected from pa-tients with viral encephalitis. Coxsackievirus A16 in these samples were first detected with real time RT-PCR and then isolated. RT-PCR was performed to amplify VP1 sequences and the amplified products were se-quenced. DNAStar 5.0 and Mega 5 were used for sequence analysis. All data was analyzed with SPSS statis-tical software. Results Fifteen samples were collected from 12 patients with hand, foot and mouth disease (HFMD) complicated by neurologic complications. Eight patients had the symptoms of fever, skin rash, signs of meningeal irritation and neck rigidity. No typical cluster was associated with clinical features or the time of onset. Both pharyngeal/anal swab and serum samples were collected from three patients (patient′s number:01111,01169 and 01130). The two samples collected from both 01111 and 01130 patients shared 100% similarity in nucleotide and amino acid based on VP1 sequences,while those from 01169 patient dif-fered in only one base. The 15 CA16 isolates were highly similar in VP1 gene, sharing 94.5%-100% ho-mology in nucleotide sequences and 98.0%-100% homology in amino acid sequences. These 15 isolates showed 68.5%-70.5% identities in nucleotide sequences and 90.5%-91.9% identities in amino acid se-quences with the CA16 prototype strain G10. Phylogenetic analysis revealed that based upon VP1 sequences, all of the 15 CA16 isolates grouped into genotype B subtype 1b (B1b), which was further classified into three clusters. Conclusion All of the 15 CA16 isolates causing neurologic complications belonged to B1b sub-genotype. Understanding the molecular epidemiology of CA16 would be essential for controlling morbidi-ty rates of HFMD and vaccine research.
