Novel microRNA-like viral small regulatory RNAs arising during human hepatitis A virus infection
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ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE54368
PROVIDER: PRJNA236334 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1141245.fastq.gz | Fastqsanger.gz | |||
| SRR1141246.fastq.gz | Fastqsanger.gz | |||
| SRR1141247.fastq.gz | Fastqsanger.gz |
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Project description:MicroRNAs (miRNAs), including host miRNAs and viral miRNAs, play vital roles in regulating host-virus interactions. DNA viruses encode miRNAs that regulate the viral life cycle. However, it is generally believed that cytoplasmic RNA viruses do not encode miRNAs, owing to inaccessible cellular miRNA processing machinery. Here, we provide a comprehensive genome-wide analysis and identification of miRNAs that were derived from hepatitis A virus (HAV; Hu/China/H2/1982), which is a typical cytoplasmic RNA virus. Using deep-sequencing and in silico approaches, we identified 2 novel virally encoded miRNAs, named hav-miR-1-5p and hav-miR-2-5p. Both of the novel virally encoded miRNAs were clearly detected in infected cells. Analysis of Dicer enzyme silencing demonstrated that HAV-derived miRNA biogenesis is Dicer dependent. Furthermore, we confirmed that HAV mature miRNAs were generated from viral miRNA precursors (pre-miRNAs) in host cells. Notably, naturally derived HAV miRNAs were biologically and functionally active and induced post-transcriptional gene silencing (PTGS). Genomic location analysis revealed novel miRNAs located in the coding region of the viral genome. Overall, our results show that HAV naturally generates functional miRNA-like small regulatory RNAs during infection. This is the first report of miRNAs derived from the coding region of genomic RNA of a cytoplasmic RNA virus. These observations demonstrate that a cytoplasmic RNA virus can naturally generate functional miRNAs, as DNA viruses do. These findings also contribute to improved understanding of host-RNA virus interactions mediated by RNA virus-derived miRNAs.
2014-01-24 | GSE54368 | GEO
Project description:Small, non-coding RNAs control gene expression post-transcriptionally and play important roles in virus-host interactions. Within the liver, the microRNA (miRNA) miR-122 is essential for replication of hepatitis C virus (HCV), while repression of miR-148a by hepatitis B virus (HBV) may enhance tumorigenesis. Despite their importance to the outcome of these infections, few previous studies have described unbiased profiling of small RNAs in the liver during chronic viral hepatitis. Here, we sequenced small (14-40 nts) RNAs in liver from subjects with chronic hepatitis B and C. We found that small RNAs derived from tRNAs, specifically 5’ tRNA-halves (“5’ tRHs”, ~31-34 nts), are abundant in liver and significantly increased during chronic viral infection in humans and also chimpanzees. In most infected livers, 5’ tRH abundance exceeded that of miRNAs. In contrast, in hepatocellular carcinoma (HCC) tissue from these subjects, tRH abundance was reduced concomitant with decreased expression of the tRNA-cleaving ribonuclease, angiogenin. Although tRHs have been identified in mice, our results show they are abundantly expressed in human tissue, increased in chronic viral infection, and decreased in liver cancer. Our findings highlight the potential biological and clinical relevance of these small non-coding RNAs. Small RNA-seq of liver samples from control subjects (n=4), subjects with chronic hepatitis B (n=4) and hepatitis B associated hepatocellular carcinoma (n=4, 3 out of 4 matched with non-tumor tissue) and subjects with chronic hepatitis C (n=4) and tissue from hepatocellular carcinoma of the same patients. Also, small RNA-seq of AGO2 and IgG pulldown in FT3-7 cells. Sequenced AGO2 pulldown (n=3), IgG pulldown (n=2) and total small RNA from FT3-7 cells (n=3). This dataset is part of the TransQST collection.
2014-12-18 | E-GEOD-57381 | biostudies-arrayexpress
Project description:Small, non-coding RNAs control gene expression post-transcriptionally and play important roles in virus-host interactions. Within the liver, the microRNA (miRNA) miR-122 is essential for replication of hepatitis C virus (HCV), while repression of miR-148a by hepatitis B virus (HBV) may enhance tumorigenesis. Despite their importance to the outcome of these infections, few previous studies have described unbiased profiling of small RNAs in the liver during chronic viral hepatitis. Here, we sequenced small (14-40 nts) RNAs in liver from subjects with chronic hepatitis B and C. We found that small RNAs derived from tRNAs, specifically 5’ tRNA-halves (“5’ tRHs”, ~31-34 nts), are abundant in liver and significantly increased during chronic viral infection in humans and also chimpanzees. In most infected livers, 5’ tRH abundance exceeded that of miRNAs. In contrast, in hepatocellular carcinoma (HCC) tissue from these subjects, tRH abundance was reduced concomitant with decreased expression of the tRNA-cleaving ribonuclease, angiogenin. Although tRHs have been identified in mice, our results show they are abundantly expressed in human tissue, increased in chronic viral infection, and decreased in liver cancer. Our findings highlight the potential biological and clinical relevance of these small non-coding RNAs.
2014-12-18 | GSE57381 | GEO
Project description:Cell Mediated Immunity in Viral Hepatitis
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Project description:The natural history of chronic hepatitis B virus (HBV) infection could be divided in different phases by transaminase and HBV replication levels. However, it remains unknown how the intrahepatic transcriptomes in patients are correlated with the clinical phases. Here, we determined the intrahepatic transcriptomes of chronic hepatitis B patients and examined the role of specific groups of genes, including immune-related genes, in the control of hepatitis B virus infection. The transcriptomes of 83 chronic hepatitis B patients (22 immune tolerant, 50 immune clearance, and 11 inactive carrier state) were analyzed by performing microarray analysis of liver biopsies.KEGG pathway analysis showed that immune response genes and interferon-stimulated genes were up-regulated in the immune clearance phase. Although immune tolerant patients and inactive state carriers had significantly different serum viral loads, the hepatic transcriptomes of the two groups were largely similar and only significantly differed in the expression of 109 genes (p < 0.01). Thus, we hypothesized that some of the 109 genes may be involved in HBV control and identified genes of interest by performing systematic screening using specific siRNAs. We showed that silencing candidate genes such as EVA1A resulted in significantly increased viral replication. Conversely, overexpression of candidate genes suppressed virus replication. Conclusions: The immune related pathways were up-regulated in the immune clearance phase but not in the inactive carrier phase. A number of host genes unrelated to immune pathways were expressed in the inactive carrier phase and these may participate in the control of hepatitis B virus replication, resulting in low viral replication. This dataset is part of the TransQST collection.
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