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3 results on '"Hila Naaman"'

1. MiRNA-124 is a link between measles virus persistent infection and cell division of human neuroblastoma cells.

Author

Hila Naaman, Glenn Rall, Christine Matullo, Isana Veksler-Lublinsky, Yonat Shemer-Avni, and Jacob Gopas

Subjects
Medicine, Science
Abstract

Measles virus (MV) infects a variety of lymphoid and non-lymphoid peripheral organs. However, in rare cases, the virus can persistently infect cells within the central nervous system. Although some of the factors that allow MV to persist are known, the contribution of host cell-encoded microRNAs (miRNA) have not been described. MiRNAs are a class of noncoding RNAs transcribed from genomes of all multicellular organisms and some viruses, which regulate gene expression in a sequence-specific manner. We have studied the contribution of host cell-encoded miRNAs to the establishment of MV persistent infection in human neuroblastoma cells. Persistent MV infection was accompanied by differences in the expression profile and levels of several host cell-encoded microRNAs as compared to uninfected cells. MV persistence infection of a human neuroblastoma cell line (UKF-NB-MV), exhibit high miRNA-124 expression, and reduced expression of cyclin dependent kinase 6 (CDK6), a known target of miRNA-124, resulting in slower cell division but not cell death. By contrast, acute MV infection of UKF-NB cells did not result in increased miRNA-124 levels or CDK6 reduction. Ectopic overexpression of miRNA-124 affected cell viability only in UKF-NB-MV cells, causing cell death; implying that miRNA-124 over expression can sensitize cells to death only in the presence of MV persistent infection. To determine if miRNA-124 directly contributes to the establishment of MV persistence, UKF-NB cells overexpressing miRNA-124 were acutely infected, resulting in establishment of persistently infected colonies. We propose that miRNA-124 triggers a CDK6-dependent decrease in cell proliferation, which facilitates the establishment of MV persistence in neuroblastoma cells. To our knowledge, this is the first report to describe the role of a specific miRNA in MV persistence.

Published
2017
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2. Measles Virus Persistent Infection of Human Induced Pluripotent Stem Cells

Author

Solly Mizrahi, Rivka Ofir, Avi Yizhak, Bracha Rager, Ran Taube, Yacov Weinstein, Hila Naaman, Yonat Shemer Avni, Glenn F. Rall, Jacob Gopas, and Tatiana Rabinski

Subjects
0301 basic medicine, Cell type, Green Fluorescent Proteins, Induced Pluripotent Stem Cells, Cell, Mice, SCID, Germ layer, Cell Line, Membrane Cofactor Protein, Measles virus, Mice, 03 medical and health sciences, Signaling Lymphocytic Activation Molecule Family Member 1, Mice, Inbred NOD, medicine, Animals, Humans, Cell Lineage, Induced pluripotent stem cell, Receptor, biology, CD46, food and beverages, Cell Differentiation, Cell Biology, biology.organism_classification, Cell biology, MicroRNAs, 030104 developmental biology, medicine.anatomical_structure, Cell culture, Receptors, Virus, Brief Communications, Developmental Biology, Biotechnology
Abstract

In this study, we found that the measles virus (MV) can infect human-induced pluripotent stem cells (hiPSCs). Wild-type MV strains generally use human signaling lymphocyte activation molecule (SLAM; CD150) as a cellular receptor, while vaccine strains such as the Edmonston strain can use both CD150 and CD46 as receptors. It is not yet known how early in the embryonal differentiation stages these receptors are expressed. We established two hiPSCs (BGU-iPSCs and EMF-iPSCs) which express CD46 and CD150. Both cell types can be infected by MV to form persistent, noncytopathic cell lines that release infectious MV particles. Following MV persistent infection, BGU-iPSCs and EMF-iPSCs remain pluripotent and can differentiate in vitro into the three germ layers. This includes cells expressing the neuronal differentiation markers: NF68 and miRNA-124. Since the MV does not integrate into the cell's genome, it can be utilized as a vehicle to systematically introduce genes into iPSC, to dissect and to define factors regulating lineage differentiation.

Published
2018
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3. MicroRNA 146-5p, miR-let-7c-5p, miR-221 and miR-345-5p are differentially expressed in Respiratory Syncytial Virus (RSV) persistently infected HEp-2 cells

Author

G. Brkic, Glenn F. Rall, Jacob Gopas, Hila Naaman, B. Eilam-Frenkel, Yonat Shemer-Avni, and Isana Veksler-Lublinsky

Subjects
0301 basic medicine, Cancer Research, viruses, medicine.disease_cause, Genome, Virus, Cell Line, 03 medical and health sciences, Virology, Reference genes, microRNA, medicine, Humans, Gene, biology, Gene Expression Profiling, Respiratory Syncytial Viruses, MicroRNAs, 030104 developmental biology, Infectious Diseases, Respiratory syncytial virus (RSV), Cell culture, Host-Pathogen Interactions, biology.protein, Dicer
Abstract

Many viruses can establish non-cytolytic, chronic infections in host cells. Beyond the intrinsically interesting questions of how this long-term parasitism is achieved, persistently infected cells can be useful to study virus-host interactions. MicroRNAs (miRNAs) are a class of noncoding RNAs transcribed from the genomes of all multicellular organisms and some viruses. Individual miRNAs may regulate several hundred genes. In this research we have studied the expression of a selective group of host-cell encoded miRNAs, as expressed in a Respiratory Syncytial Virus (RSV) persistently infected HEp-2 cell line (HEp-2 + RSV-GFP). The RSV is a virus that does not encode miRNAs in its genome. Our study shows that Dicer is down regulated, miRNA’s 146a-5p is strongly up-regulated and miRNAs 345-5p, let-7c-5p and miRNA’s-221 are down-regulated in HEp-2 + RSV-GFP cells. Correspondingly, changes in the miRNA 146a-5p and he sequences of the reference genes are miRNA 345-5p respective miRNAs target proteins: HSP-70 and p21, were observed. Thus, RSV persistent viral infection induces unique patterns of miRNA’s expression with relevance to how the virus regulates the host cell response to infection.

Published
2017

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