‘miR2Disease’, a manually curated database, aims at providing a comprehensive resource of microRNA deregulation in various human diseases. The current version of miR2Disease documents 1939 curated relationships between 299 human microRNAs and 94 human diseases by reviewing more than 600 published papers. Around one-seventh of the microRNA–disease relationships represent the pathogenic roles of deregulated microRNA in human disease. Each entry in the miR2Disease contains detailed information on a microRNA–disease relationship, including a microRNA ID, the disease name, a brief description of the microRNA–disease relationship, an expression pattern of the microRNA, the detection method for microRNA expression, experimentally verified target gene(s) of the microRNA and a literature reference. miR2Disease provides a user-friendly interface for a convenient retrieval of each entry by microRNA ID, disease name, or target gene. In addition, miR2Disease offers a submission page that allows researchers to submit established microRNA–disease relationships that are not documented. Once approved by the submission review committee, the submitted records will be included in the database. miR2Disease is freely available at http://www.miR2Disease.org.

BackgroundThe identification of disease-related microRNAs is vital for understanding the pathogenesis of diseases at the molecular level, and is critical for designing specific molecular tools for diagnosis, treatment and prevention. Experimental identification of disease-related microRNAs poses considerable difficulties. Computational analysis of microRNA-disease associations is an important complementary means for prioritizing microRNAs for further experimental examination.ResultsHerein, we devised a computational model to infer potential microRNA-disease associations by prioritizing the entire human microRNAome for diseases of interest. We tested the model on 270 known experimentally verified microRNA-disease associations and achieved an area under the ROC curve of 75.80%. Moreover, we demonstrated that the model is applicable to diseases with which no known microRNAs are associated. The microRNAome-wide prioritization of microRNAs for 1,599 disease phenotypes is publicly released to facilitate future identification of disease-related microRNAs.ConclusionsWe presented a network-based approach that can infer potential microRNA-disease associations and drive testable hypotheses for the experimental efforts to identify the roles of microRNAs in human diseases.

ciated viruses are dependoviruses. The autonomous parvoviruses, which replicate in the absence of other viruses, are common animal pathogens; feline panleucopenia virus, Aleutian mink disease virus, minute virus of mice, and Kilham rat virus are examples of members of this genus. Despite differences in their biological behavior, both types of parvovirus have similar genetic organizations. The coding potential of the short genome is increased by utilization of overlapping transcripts and multiple reading frames. Structurally, their DNA is characterized by the presence of terminal hairpin structures that serve as initiation sites for replication through double-stranded intermediate forms. Two or three structurally similar capsid proteins are encoded by the right side of the genome by separate but overlapping RNA species. One to three noncapsid proteins that are thought to provide replicative functions are encoded by the left side. In the parvoviruses studied so far, separate promoters drive transcription from the left side and the middle of the genome. The pathogenic B19 human virus is, for a member of the Parvoviridae family, remarkable in its highly restricted tissue range. The molecular basis of this unusual biologic behavior remains uncertain. In erythroid bone marrow cells cultured in vitro, the pattern of B19 DNA replication resembles that of other parvoviruses (26). The protein species that compose the capsid and the noncapsid proteins also are analogous in number and size to those of other parvoviruses (13, 27). As we report here, however, the B19 transcription map differs in several fundamental aspects from that of other Parvoviridae. MATERIALS AND METHODS Cell culture. B19 parvovirus was propagated in human erythroid bone marrow cells that were obtained from patients with sickle cell disease after informed consent and 2395