Project description:With the purpose to elucidate the expression changes of host genes of SPF chickens infected with duck-origin H7N9 subtype avian influenza virus at 24 hours post-infection(hpi) and fowl adenovirus-4 at 48 dpi. The spleens of SPF chickens infected with duck-origin H7N9 subtype avian influenza virus and fowl adenovirus-4 were collected and high throughout sequenced. Compared with the control group, there were 2426 differentially expressed genes were obtained in the duck-origin H7N9 subtype avian influenza virus group, including 913 up-regulated genes and 1513 down-regulated genes, and there were 1534 differentially expressed genes were obtained in the fowl adenovirus-4 group, including 632 up-regulated genes and 902 down-regulated genes.
Project description:We infected HD11 macrophages with Salmonella Typhimurium, followed by chemical proteomic analysis of deubiquitinases by using ubiquitin-specific active-site probe.
Project description:Using next-generation sequencing, we sequenced transcriptomes of A. thaliana plants infected by the pathogenic and the symbiotic fungus and analyzed plant and fungal gene expression changes between pathogenic and symbiotic interactions. Infected plants were sampled at early infection stages, 12, 24, 48 and 96 HPI (hours post inoculation)
Project description:Background: Infection with Turkey Hemorrhagic Enteritis Virus (THEV) can cause hemorrhagic enteritis, which affects turkey poults. This disease is characterized by immunosuppression (IMS) and bloody droppings. The clinical disease usually lasts only a few days but secondary opportunistic infections due to THEV-induced IMS extend the duration of illness and mortality, which exacerbates economic losses. Although an avirulent THEV strain with only subclinical disease is used as a vaccine, some immunosuppressive properties remain in this prophylactic strain. To elucidate the mechanisms mediating THEV-induced IMS, we performed the first transcriptomic analysis of a THEV infection using bulk RNA-sequencing. Methods: After infecting a turkey B-cell line with the vaccine strain, samples in triplicates were collected at 4-, 12-, 24-, and 72-hours post-infection (hpi). Total RNA was extracted, and poly-Adenylated-tailed mRNAs were sequenced. Reads were mapped to the host turkey genome after trimming and gene expression was quantified with StringTie. Differential gene expression was performed with DESeq2 followed by functional enrichment analysis with gprofiler2 and DAVID from NCBI. RT-qPCR of select genes was performed to validate the RNA-sequencing data. Results: A total of 2,343 and 3,295 differentially expressed genes (DEGs) were identified at 12 hpi and 24 hpi, respectively. At 12 hpi, 1,079 genes were upregulated and 1,264 genes downregulated, whereas 1,512 genes were upregulated and 1,783 genes downregulated at 24 hpi. The DEGs contributed to multiple biological processes including apoptosis, ER unfolded protein response, and cell maintenance. Multiple pro-apoptotic genes, including APAF1, BNIP3L, BMF, BAK1, RIPK1, and FAS were upregulated. Genes that play a role in ER stress-induced unfolded protein response including VCP, UFD1, EDEM1, EDEM3, and ATF4 were also upregulated and may contribute to apoptosis. Conclusions: Our data suggest that several biological processes and pathways including apoptosis, immune response, ER response to stress, ubiquitin-dependent protein catabolic process, and repression of essential cellular maintenance are important aspects of the host cell response to THEV infection. It is possible that interplay between multiple processes may mediate apoptosis of infected B-cells, leading to IMS.
Project description:We sequenced the total mRNA from infected cells and detected differences in the expression of both host mRNA. We detected a small but significant suppression of T cell activation-related genes at 12 hpi. This suppression persisted and expanded by 24 hpi providing new possible markers of virus-induced T cell cytopathology. By 24 hpi the expression of over 50% of detectable host loci was also altered indicating widespread alteration of host processes including RNA processing, splicing, and transport to an extent not previously reported. In addition next-generation sequencing provided insights into the expression of non-coding RNAs including microRNA host genes.
Project description:In this work, we studied the impact of chikungunya virus (CHIKV) on the global proteome of functionally Dicer 2 active Aedes albopictus cells i.e. U4.4 cells at 12 hours post infection (hpi) and 60 hpi using mass spectrometry analysis. The non-radio labelling quantitative proteomics analysis of uninfected cells' proteome with that of 12 hpi and 60 hpi.
Project description:Human monocyte-derived macrophage cells were infected with Chikungunya virus (CHIKV) to identify and quantify intracellular transcriptional changes that contribute to the host response to infection with CHIKV. RNA was collected from these cells at 8 and 24 hours post-infection (hpi) and were compared to mock-infected cells. The RNAseq data was then analyzed to determine the genes, functions, and signaling pathways that were significantly affected in an effort to predict existing drugs that could be repurposed as potential therapeutics for CHIKV.
Project description:RNA-Seq was used to unveil the transcriptional profile of DF-1 cells at the early stage of cell-adapted Infectious Bursal Disease Virus (caIBDV) infection. Total RNAs were extracted from virus-infected cells at 0, 6 and 12 hpi. RNA-Seq datasets of respective samples mapped to 56.5 - 57.6% of isoforms in the reference genome Galgal4.73. At 6 hpi, 23 isoforms underwent an elevated expression, while 128 isoforms were up-regulated and 5 were down-regulated at 12 hpi in the virus-infected group. Besides, 10 isoforms were exclusively expressed in the virus-infected cells. Though no significant change was detected in cytokine and interferon expression levels at the first 12 hours of infection, modulations of the upstream regulators were observed. In addition to the reported regulatory factors including EIF2AK2, MX, OAS*A, GBP7 and IFIT, IBDV infection also triggered a IFIT5-IRF1/3-RSAD5 pathway in the DF-1 cells which potentially restricted the viral replication cycle in the early infection stage. Over-expression of LIPA and CH25H, together with the suppression of STARD4, LSS and AACS genes implied a modulation of membrane fluidity and lipid raft arrangement in the infected cells. Alternative splicing of the EFR3 homolog A gene was also through to be involved in the lipid membrane regulation, and these cumulative responses projected an inhibition of viral endocytosis. Recognition of viral RNA genomes and intermediates was presumably enhanced by the elevated levels of IFIH1, DHX58 and TRIM25 genes which possess properties on detecting viral dsRNA. On the other hand, the caIBDV arrested the host's apoptotic process by inducing the expression of apoptosis inhibitors including NFKBIA/Z, TNFAIP2/3 and ITA at the first 12 hours of infection. In conclusion, the differential expression landscape demonstrated with RNA-Seq provides a comprehensive picture on the molecular interactions between host cells and virus at the early stage of infection.
Project description:Differential expression was determined in Calu-3 cells between mock infected and infection with either Human coronavirus EMC and SARS coronavirus at different times post infection. Calu-3 2B4 cells were infected with Human Coronavirus EMC 2012 (HCoV-EMC) or mock infected. Samples were collected 0, 3, 7, 12, 18 and 24 hpi. There are 3 mock and 3 infected replicates for each time point, except for 12 hpi for which there are only 2 infected replicates (one replicate did not pass RNA quality check). There were no mock sampes at 18 hpi, and therefore infected samples at 18 hpi were compared with mocks at 24 hpi. For direct comparison with SARS-CoV infected cells, raw data from HCoV-EMC experiments were quantile normalized together with the SARS-CoV dataset (GEO Series accession number GSE33267).