Project description:Coxsackievirus A16 (CA16) is one of the major pathogens associated with human hand, foot, and mouth disease (HFMD) and in some countries this pathogen is the leading cause of this disease. We previously found that CA16 could induce neurological disorders in young gerbils, which could serve as a good animal model for studying the neuropathogenesis of CA16 infection. In this study, we found that 1039 genes were up-regulated and 299 genes were down-regulated in CA16-infected gerbils compared with control. Differentially expressed genes were clustered into functional pathways and the top five pathways according to the enrich factor were viral myocarditis, type 1 diabetes mellitus, toxoplasmosis, toll-like receptor signaling pathway and TNF signaling pathway. Our results provide novel insight into the neuropathogenesis of HFMD induced by CA16 infection.
Project description:Enterovirus 71 (EV71) is one of the major pathogens associated with human hand, foot, and mouth disease (HFMD) and in some countries this pathogen is the leading cause of this disease. We previously found that CA16 could induce neurological disorders in young gerbils, which could serve as a good animal model for studying the neuropathogenesis of CA16 infection. In this study, we found that 1039 genes were up-regulated and 299 genes were down-regulated in CA16-infected gerbils compared with control. Differentially expressed genes were clustered into functional pathways and the top five pathways according to the enrich factor were viral myocarditis, type 1 diabetes mellitus, toxoplasmosis, toll-like receptor signaling pathway and TNF signaling pathway. Our results provide novel insight into the neuropathogenesis of HFMD induced by CA16 infection.
Project description:To investigate the transcriptional response of brainstem endothelial cells to mild respiratory infection, 12-month-old male C57Bl/6 mice were intranasally inoculated with SARS-CoV-2 MA10 strain or with saline.
Project description:Enterovirus 71 (EV71) and Coxsackievirus A16 (CA16) are the predominant etiological agents of hand, foot, and mouth disease (HFMD) and both belong to the human enterovirus A species of the Picornaviridae family. These viruses share similar genetic homology, although the clinical manifestations of HFMD caused by the two viruses have some discrepancies. Furthermore, the underlying mechanisms leading to these differences remain unclear. microRNAs (miRNAs) participate in numerous biological or pathological processes, including host responses to viral infections, by targeting messenger RNAs (mRNAs) for translational repression or degradation. Here, we focused on differences in miRNA expression patterns in peripheral blood mononuclear cells (PBMCs) of rhesus monkeys infected with EV71 or CA16 at different time points using high-throughput sequencing technology. For the first time, this study demonstrated that EV71 and CA16 infection result in specific miRNA expression patterns in PBMCs.
Project description:Enterovirus 71 (EV71) and coxsackievirus A16 (CA16) are major causative agents for hand, foot and mouth disease (HFMD). In China, more than 70,756 children were infected and 40 died from the disease in recent years. This study aimed to develop a protein chip that can simultaneously detect and differentiate the antibodies induced by EV71 and CA16 simultaneously. The structure protein vp1 and vp3 from the two viruses were purified and spotted onto an aldehyde groupmodified glass slide at 1mg/ml. After that, the protein chip was reacted with the corresponding positive serum against these viruses, hybridized with a Cy3-labeled secondary antibody and scanned using the popular GenePix 4000B Microarray Scanner. In this study, Both IgG and IgM serum antibody to EV71 and CA16 were detected using protein Chip. The results showed that this method could hybridize specifically with the corresponding antibodies with strong signals and without cross-hybridization. The data also confirmed the proposed method's specificity, sensitivity, and convenience. In conclusion, this protein chip can be used to differentiate the antibodies induced by the EV71and CA16.
Project description:We performed comprehensive miRNA profiling in EV71- and CA16-infected human umbilical vein endothelial cells (HUVECs) at multiple time points using high-throughput sequencing. The results showed that 135 known miRNAs exhibited remarkable differences in expression. Of these, 30differentially expressed miRNAs presented opposite trends in EV71- and CA16-infected samples. Subsequently, we mainly focused on the 30 key differentially expressed miRNAs through further screening to predict targets.Gene ontology (GO) and pathway analysis of the predicted targets showed the enrichment of 14 biological processes, 9 molecular functions, 8 cellular components, and 85 pathways. The regulatory networks of these miRNAs with predicted targets, GOs, pathways, and coexpression genes were determined, suggesting that miRNAs display intricate regulatory mechanisms during the infection phase. Consequently, we specifically analyzed the hierarchical GO categories of the predicted targets involved in biological adhesion. The results indicated that the distinct changes induced by EV71 and CA16 infection may be partly linked to the function of the blood-brain barrier. Taken together, this is the first report describing miRNA expression profiles in HUVECs with EV71 and CA16 infections using high-throughput sequencing. Our data provide useful insights that may help to elucidate the different host-pathogen interactions following EV71 and CA16 infection and offer novel therapeutic targets for these infections.
Project description:In this study, models of CA10, CA16 and EV71 infection were established in 7-day-old Institute of Cancer Research (ICR) mice by intraperitoneal injection to analyze the pathogenicity of these viruses. RNA sequencing analysis was used to screen the differentially expressed genes (DEGs) after CA10 infection, and innate immune-related pathways were activated in muscle. Compared with CA16 and EV71 infection, CA10 may have an inhibitory effect on Th cell differentiation and cell growth. Additionally, the common DEGs in the three viruses were most enriched in the immune system response, including the Toll-like receptor pathway and the nucleotide-binding and oligomerization domain (NOD)-like pathway. Our findings revealed a group of genes that coordinate in response to CA10 infection and are shared by the three viruses, which increases our understanding of the pathological mechanism of HFMD.