Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from A549 cells infected by adenovirus not carrying virus associated sequences in the genome.

ABSTRACT: Non-coding small RNAs are involved in viral life cycles. Adenovirus-encoding small RNAs, virus-associated RNAs (VA RNAs), are transcribed throughout the replication process, and the transcript levels depend on the copy numbers of the viral genome. Although the VA RNA transcription starts immediate early phase, little is known about the function in the early phase. Here we applied replication-deficient adenovirus vectors (AdVs) and novel VA-RNA deleted AdVs to analyze expression change of cellular gene mediated by VA RNAs. Human lung cell, A549, were infected by VA(+) or VA(-) adenoviral vectors. After the designed preiod of infection, cells were harvested and RNA was extacted, followed by DNA microarray analysis.

ORGANISM(S): Homo sapiens

SUBMITTER: Kenji Yoshida

PROVIDER: E-GEOD-58605 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Replicating viruses have broad applications in biomedicine, notably in cancer virotherapy and in the design of attenuated vaccines, however uncontrolled virus replication in vulnerable tissues can give pathology and often restricts the use of potent strains. Increased knowledge of tissue-selective microRNA expression now affords the possibility of engineering replicating viruses that are attenuated at the RNA level in sites of potential pathology, but retain wild type replication activity at sites not expressing the relevant microRNA. To assess the usefulness of this approach for the DNA virus, adenovirus, we have engineered a hepatocyte-safe wild type adenovirus 5 (Ad5), which normally mediates significant toxicity and is potentially lethal in mice. To do this we have included binding sites for hepatocyte-selective microRNA122a within the 3' UTR of the E1A transcription cassette. Imaging versions of these viruses, produced by fusing E1A with luciferase, showed that inclusion of microRNA122a binding sites caused up to 80 fold decreased hepatic expression of E1A following intravenous delivery to mice. Animals administered a ten-times lethal dose of wild type Ad5 (5 x 1010 viral particles/mouse) showed substantial hepatic genome replication and extensive liver pathology, while inclusion of 4 microRNA binding sites decreased replication 50-fold and virtually abrogated liver toxicity. This modified wild type virus retained full activity within cancer cells and provides a potent, liver-safe oncolytic virus. In addition to providing many potent new viruses for cancer virotherapy, microRNA-control of virus replication should provide a new strategy for designing safe attenuated vaccines applied across a broad range of viral diseases. four groups which we had were: WT: RNA extracted from livers of mice treated with wild type Ad5, 3 Replicates miR: RNA extracted from livers of mice treated with wild type Ad5 bearing mir122-binding sites in the 3'UTR of E1A (3 Replicates) Luc: RNA extracted from livers of mice treated with non-replicating Ad5 (3 Replicates) PBS: RNA extracted from livers of mice treated with PBS only (3 Replicates)

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Expression data from A549 cells infected by adenovirus not carrying virus associated sequences in the genome.

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