Objective: To reveal the genetic characteristic of Coxsackie virus A16 (CVA16) strains isolated during an epidemic of Hand-Foot-Mouth Disease (HFMD) in Shanghai in 2002.
Methods: CVA16 strains were isolated from the patients of HFMD during the epidemic in Shanghai in 2002. The VP1 coding gene of CVA16 strains was amplified by reverse transcription-polymerase chain reaction (RT-PCR) and sequenced. The homology and phylogenetic analyses were done between the 7 isolates and other CVA16 strains downloaded from Genbank, based on the sequence of VP1 gene.
Results: 7 CVA16 strains were isolated from the patients of HFMD in Shanghai, which belonged to different lineages of genotype B. Among them, except for SH-18-CHN02 strain in lineage 1, other CVA16 strains were all in lineage 2. The homology of nucleotide and amino acid of 7 CVA16 strains were 88.8%-99.7% and 99.3%-100% respectively.
Conclusions: 7 CVA16 strains in this study were all genotype B. There were some variations compared with the other CVA16 strains isolated in China before. It suggested that CVA16 strains might have spread for a long time in China, which belonged to several different transmissions. To reveal the genotype and genetic characteristic of CVA16 prevalent in China, the surveillance of CVA16 should be strengthened to get more molecular epidemiologic data.
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Sci Signal
January 2025
Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education), Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310000, China.
Activation of the stimulator of interferon genes (STING) pathway by cytosolic DNA leads to the activation of the transcription factors interferon regulatory factor 3 (IRF3) and nuclear factor κB (NF-κB). Although many viruses produce proteins that inhibit IRF3-dependent antiviral responses, some viruses produce proteins that inhibit STING-induced NF-κB activation without blocking IRF3 activation. Here, we found that STING-activated, NF-κB-dependent, and IRF3-independent innate immunity inhibited the replication of the DNA virus herpes simplex virus type 1 (HSV-1), the RNA virus coxsackievirus A16 (CV-A16), and the retrovirus HIV-1.
View Article and Find Full Text PDFmBio
January 2025
Shanghai Institute of Infectious Disease and Biosecurity, Fudan University, Shanghai, China.
Unlabelled: The KREMEN1 (KRM1) protein is a cellular receptor for multiple enteroviruses that cause hand, foot, and mouth disease (HFMD), including coxsackievirus CVA2, CVA3, CVA4, CVA5, CVA6, CVA10, and CVA12. The molecular basis for the broad recognition of these viruses by the KRM1 receptor remains unclear. Here, we report the indispensable role of the completely conserved VP2 capsid protein residue K140 (designated K2140) in mediating receptor recognition and infection by CVA10 and other KRM1-dependent enteroviruses.
View Article and Find Full Text PDFVirol J
December 2024
Wuhan Institute of Biological Products Co., Ltd.,, No.1 Huangjin Industrial Park Road, Jiangxia District, Wuhan, 430207, China.
Background: The hand, foot and mouth disease (HFMD) was caused by species of Enterovirus A and Enterovirus B in the Asian-Pacific region. Broad-spectrum monoclonal antibodies (mAb) that can bind multiple serotypes of enteroviruses have gradually become a research hotspot in the diagnosis, prevention and treatment of HFMD.
Methods: In this study, a mAb 1H4 was obtained using monoclonal antibody technology by immunizing purified virus particles of Coxsackievirus A5 (CV-A5).
Heliyon
October 2024
Institutes of Biomedical Sciences, Shanxi University, 92 Wucheng Road, Taiyuan, 030006, Shanxi province, China.
Vaccine X
October 2024
National Institute of Infectious Diseases and Vaccinology, National Health Research Institutes, Zhunan Town, Miaoli County, Taiwan.
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