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Volume 64, Issue 1
Displaying 1-12 of 12 articles from this issue
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Reviews
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Kazuhiro ISHIBASHI, Masayuki ISHIKAWA2014 Volume 64 Issue 1 Pages 3-10
Published: June 25, 2014
Released on J-STAGE: March 10, 2015
JOURNAL FREE ACCESSReplication proteins of eukaryotic positive-strand RNA viruses specifically recognize the genomic RNA as replication template, recruit them to the surfaces of intracellular membranes, and form replication complexes. We recently revealed that tobacco mosaic virus (TMV) replication protein cotranslationally binds 5' untranslated region (UTR) of the genomic RNA, and that a full-length replication protein cannot posttranslationally bind TMV RNA in trans. This result provides a mechanistic explanation for the previously reported property of TMV replication protein that it selects replication template preferentially in cis. We also found that the binding of the replication protein to the 5' UTR prevents further translation of the genomic RNA. Fatal collision between translating ribosomes and negative-strand RNA-synthesizing polymerases on the genomic RNA is thus avoided.View full abstractDownload PDF (787K) -
Nobuhiro SUZUKI2014 Volume 64 Issue 1 Pages 11-24
Published: June 25, 2014
Released on J-STAGE: March 10, 2015
JOURNAL FREE ACCESSThere appear to be over a million of fungal species including those that have been unidentified and unreported, where a variety of viruses make a world as well. Studies on a very small number of them conducted during the last two decades demonstrated the infectivity of fungal viruses that had previously been assumed to be inheritable, indigenus and non-infectious. Also, great technical advances were achieved. The chest blight fungus (Cryphonectria parasitica), a phytopathogenic ascomycetous fungus, has emerged as a model filamentous fungus for fungal virology. The genome sequence with annotations, albeit not thorough, many useful research tools, and gene manipulation technologies are available for this fungus. Importantly, C. parasitica can support replication of homologous viruses naturally infecting it, in addition to heterologous viruses infecting another plant pathogenic fungus, Rosellinia necatrix taxonomically belonging to a different order. In this article, I overview general properties of fungal viruses and advantages of the chestnut blight fungus as a mycovirus host. Furthermore, I introduce two recent studies carried out using this fungal host:''Defective interfering RNA and RNA silencing that regulate the replication of a partitivirus'' and'' RNA silencing and RNA recombination''View full abstractDownload PDF (1590K) -
Hirofumi SAWA, Shintaro KOBAYASHI, Tadaki SUZUKI, Yasuko ORBA2014 Volume 64 Issue 1 Pages 25-34
Published: June 25, 2014
Released on J-STAGE: March 10, 2015
JOURNAL FREE ACCESSRecently, the family Polyomaviridae was classified as 3 genera, such as Orthopolyomavirus, Wukipolyomavirus which contain mammalian polyomaviruses and Avipolyomavirus which only contain avian polyomaviruses. We have recently isolated novel polyomaviruses, including Mastomys Polyoamvirus (MasPyV) and Vervet monkey Polyoamvirus-1 (VmPyV-1) by epidemiological activities and examined functions of their encoding proteins. In addition, we have been investigating the mechanisms of replication of human polyomavirus, JC polyomavirus (JCPyV). We recently obtained the results of function of JCVPyV-encoding proteins, including early protein (Large T antigen) and late proteins (VP1 and Agno). In this review, we summarized the data of our basic research activities.View full abstractDownload PDF (1840K)
Special Issue: Oncogenic virus - Reports on Symposium 1 in the 61th Annual JSV Meeting
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Kei KAWANA2014 Volume 64 Issue 1 Pages 35-42
Published: June 25, 2014
Released on J-STAGE: March 10, 2015
JOURNAL FREE ACCESSHigh-risk HPV E6 and E7 oncogenes are an ideal targeting gene for treatment of cervical cancer. In this paper, we introduce researches on cancer-immunotherapy targeting HPV E7 through mucosal immunity and E6/E7-targeting siRNA therapy using PEGylated polymeric micelles. Therapeutic HPV vaccine has also attracted attention as a cancer immunotherapy agent. We have found homing of Integrin β7-positive intestinal mucosal lymphocyte on the cervical mucosa. In this study, we generated a novel therapeutic vaccine; an HPV E7-expressing Lactobacillus casei (LacE7) to induce anti-HPV cellular immunity directly to intestinal mucosa. Cervical lymphocytes (CxLs) and peripheral blood mononuclear cells (PBMCs) were counted E7 specific INFγ-producing cells (E7 cell-mediated immune responses: E7-CMI) by ELISPOT assay. We confirmed induction of anti-E7 IFNγ-producing cells in the cervix lymphocytes obtained from these patients. E6/E7 siRNA therapy requires a delivery system for its systemic intravenous administration. We here demonstrated that intravenous injection of HPV16 or 18 E6/E7 siRNA polymeric micelles suppressed excellently an increase in size of subcutaneous tumor formed by SiHa or HeLa cell, respectively. Our drug-delivery technology using polymeric micelles enabled the successful systemic administration of siRNA to exhibit anti-tumor effect.View full abstractDownload PDF (1064K) -
Ai KOTANI2014 Volume 64 Issue 1 Pages 43-48
Published: June 25, 2014
Released on J-STAGE: March 10, 2015
JOURNAL FREE ACCESSEB virus (EBV) is associated with heterogeneous lymphomas. In these lymphomas EBV+ lymphoma cells are embedded in non-neoplastic bystanders: B and T cells, macrophages. Without these bystander cells, the lymphoma cells are incapable of being engrafted in immunodeficient mice. In this context, the bystanders are tumor-supportive "inflammatory niche". Recently, EBV-infected cells produce exosomes that contain EBV specifically encoded miRNAs (EBV-miRNAs). Accordingly, we hypothesized that exosomal EBV-miRNAs might redirect tumor surrounding immune cells from tumor reactive into tumor-supportive "inflammatory niche”.
The EBV-miRNAs in the exosome secreted from EBV positive lymphoma cells significantly influenced on monocyte/macrophage Mo/Mf in inducing CD69, IL-10, and TNF, suggesting that EBV-miRNAs might polarize Mo/Mf into tumor associated Mf (TAM). EBV-miRNAs were required to develop lymphoproliferative disease (LPD) in vivo mouse model. Moreover, when Mfs were depleted by clodronate liposome, EBV positive tumor cells disappeared. These results suggest that lymphoma-derived secretary EBV-miRNAs regulate Mo/Mf to support the lymphoma survival or development. Most importantly, exosomal EBV-miRNAs derived from the lymphoma cells were transferred to Mf in human EBV+ lymphoma samples, which showed correlation with prognosis.View full abstractDownload PDF (1418K) -
Dai IWAKIRI2014 Volume 64 Issue 1 Pages 49-56
Published: June 25, 2014
Released on J-STAGE: March 10, 2015
JOURNAL FREE ACCESSEpstein-Barr virus (EBV), a ubiquitous human double stranded DNA virus, is associated with a variety of malignancies including Burkitt's lymphoma, Hodgkin's lymphoma, nasopharyngeal carcinoma (NPC) and gastric carcinoma (GC). These EBV-associated cancers are characterized by the proliferation of monoclonal EBV-infected cells, and viral gene expression in these cells is limited to a subset of latent genes, indicating that EBV latent genes contribute to carcinogenesis. Here I describe the mechanisms of carcinogenesis by EBV, focusing on the function of two EBV latent gens, latent membrane protein 2A (LMP2A) and EBV-encoded small RNA (EBER). LMP2A, which is known to mimic the B cell receptor (BCR) signaling, has been reported to contribute to malignant lymphoma development through the modulation of immune signals. Also, it has been demonstrated that LMP2A-mediated intracellular signaling plays significant roles in epithelial carcinogenesis. On the other hand, it has been demonstrated that EBER, which is expected to form double stranded RNA (dsRNA) structure, triggers a signal transduction from host viral RNA sensors RIG-I and TLR3. Activation of innate immune signals by EBER has been reported to contribute to the pathogenesis of EBV-associated disseases, including cancers.View full abstractDownload PDF (918K) -
Tomomi NAKAHARA, Tohru KIYONO2014 Volume 64 Issue 1 Pages 57-66
Published: June 25, 2014
Released on J-STAGE: March 10, 2015
JOURNAL FREE ACCESSHigh-risk human papillomavirus (HR-HPV) infections account for more than 5% of all cancers (11% in women) such as cervical cancer worldwide. HPVs infect to basal cells of the stratified squamous epithelium and establish persistent infection within the basal compartment. HR-HPV infections can persist more than a decade, leading to development of cancers. The life cycle of HPVs is tightly associated with the differentiation processes of the stratified squamous epithelium; the replication of the viral genome and the expression of the viral genes are strictly regulated depending on differentiation of the host keratinocytes. The viral genome is transiently amplified immediately following infection and then maintained at constant copy numbers in the basal cells. In terminally differentiating keratinocytes, the viral genome is drastically amplified. However, molecular mechanisms underlying switching these three stages of viral genome replication in the viral life cycle are poorly understood. Recently, it has become evident that DNA damage response pathways are involved in the regulation of HPV genome replication. In this review, we would like to introduce recent findings describing the associations of DNA damage response with HPV genome replication.View full abstractDownload PDF (1704K) -
~ target cells of infection, and disease ~Shouichi OHGA2014 Volume 64 Issue 1 Pages 67-74
Published: June 25, 2014
Released on J-STAGE: March 10, 2015
JOURNAL FREE ACCESSHalf a century has passed since Epstein-Barr virus (EBV) particles were isolated from the cultured lymphoblasts of Burkitt lymphoma. During the period, molecular biology, hematology/immunology, and transplantation medicine made amazing progress, that clarified the mode of infection and pathophysiology of the virus in human diseases. Research strategies on the relationship between EBV and human have expanded to the epidemiology, structures and functions of both genomes, regulatory genes including microRNA, and the nature of epigenetics. Although no animal models of EBV infection long hampered the completion of in vivo experiments, humanized mice have broken through a barrier of in vitro study on EBV-infected cell lines. Our understanding of the life cycle of EBV has continued to deepen about the infection via the CD21 receptor expressed on B cells, the latency, reactivation/reinfection, and transformation, and also the dynamics of T-cell immune response and the intracellular immunosurveillance beyond acquired and innate immunity. On the other hand, the disease entity of life-threatening lymphoproliferative disease of EBV-infected T cells or NK cells is on controversial. The other parts of this special issue include the recent topics of the basic and clinical researches of EBV as the oncogenic virus. Then, we herewith overview the research history of EBV with special reference to the infected cells and host immune responses in EBV-associated diseases.View full abstractDownload PDF (417K)
Topics
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Takashi YAMAMOTO, Naoaki SAKAMOTO, Tetsushi SAKUMA2014 Volume 64 Issue 1 Pages 75-82
Published: June 25, 2014
Released on J-STAGE: March 10, 2015
JOURNAL FREE ACCESSGenome editing is a cutting-edge technology that enables to modify the target gene using programmable site-specific nucleases, such as TALENs and CRISPR/Cas9. Currently, cell and animal models of human diseases have been competitively created throughout the world, because genome editing technology paved the way for genetic modifications even in cells and organisms that had been difficult to manipulate the genome. In this review, we introduce the basic principles and current situations of genome editing with programmable nucleases.View full abstractDownload PDF (1875K) -
Takayuki ABE2014 Volume 64 Issue 1 Pages 83-94
Published: June 25, 2014
Released on J-STAGE: March 10, 2015
JOURNAL FREE ACCESSHow the cells triggers the induction of innate immune genes in response to nucleic acids derived from microbes, such as DNA viruses, intracellular bacteria, and parasites, or self DNA, has not been elucidated fully. We have previously shown that an endoplasmic reticulum (ER)-associated multiple transmembrane protein, so-called STING (stimulator of interferon genes), functions as an essential molecules for triggering DNA-mediated gene induction. STING may directly associate with stimulatory ligands, which include DNA, as well as with cyclic dinucleotides (CDNs), which are secreted by intracellular bacteria. After DNA or CDN stimulation, STING traffics with kinase TBK1 in an autophagic signaling complex, from ER to perinuclear endosomal compartments harboring IRF3 and NF-κB. STING may involve in autoinflammatory disease manifested by aberrant self-DNA. Understanding of STING function may conceivably lead to the development of potent adjuvants for vaccine development or conversely therapeutics that could control inflammation aggravated disease.View full abstractDownload PDF (1866K)
SUGIURA Memorial Incentive Award for Young Virologist,The Japanese Society for Virology, 2013
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Takayuki MURATA2014 Volume 64 Issue 1 Pages 95-104
Published: June 25, 2014
Released on J-STAGE: March 10, 2015
JOURNAL FREE ACCESSEpstein-Barr virus (EBV) is a member of gamma-herpesvirus, which can cause various types of tumor. Coexisting with the host for a long period of time, it has evolved unique and sophisticated strategy for survival by taking complicated, tactical modes of infection. Such modes include latent and lytic infections, and latent state is further categorized into four types. Differences and transitions in such lifestyles are significantly associated not only with virus amplification, but also with pathology and advancement of the disorders. I here review oncogenesis and pathogenesis of EBV-related disorders, especially focusing on our recent results on the modes of EBV infection.View full abstractDownload PDF (2736K) -
Misako YONEDA2014 Volume 64 Issue 1 Pages 105-112
Published: June 25, 2014
Released on J-STAGE: March 10, 2015
JOURNAL FREE ACCESSNipah virus (NiV), a paramyxovirus, was first discovered in Malaysia in 1998 in an outbreak of infection in pigs and humans, and incurred a high fatality rate in humans. We established a system that enabled the rescue of replicating NiVs from a cloned DNA. Using the system, we analyzed the functions of accessory proteins in infected cells and the implications in in vivo pathogenicity. Further, we have developed a recombinant measles virus (rMV) vaccine expressing NiV envelope glycoproteins, which appeared to be an appropriate to NiV vaccine candidate for use in humans.View full abstractDownload PDF (2375K)
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