All issues
Volume 57, Issue 1
Displaying 1-11 of 11 articles from this issue
- |<
- <
- 1
- >
- >|
Reviews
-
Takashi IRIE, Takemasa SAKAGUCHI2007 Volume 57 Issue 1 Pages 1-7
Published: 2007
Released on J-STAGE: November 27, 2007
JOURNAL FREE ACCESSOur knowledge about envelope virus budding has been dramatically increased, since L-domain motifs were identified within their matrix and retroviral Gag proteins which drive virus budding. These viral proteins have been shown to interact with host cellular proteins involved in endocytosis and/or multi-vesicular body (MVB) sorting via their L-domains. Since budding of many enveloped viruses have been reported to be dependent on the activity of cellular Vps4, which catalyzes the disassembly of ESCRT machinery in the final step of protein sorting, this cellular function is believed to be utilized for efficient virus budding. However, for many enveloped viruses, L-domain motifs have not yet been identified, and the involvement of MVB sorting machinery in virus budding is still unknown. In this review, we will focus on paramyxoviruses among such viruses, and discuss their budding with the latest information.View full abstractDownload PDF (481K) -
Akira ONO2007 Volume 57 Issue 1 Pages 9-18
Published: 2007
Released on J-STAGE: November 27, 2007
JOURNAL FREE ACCESSVirus particle formation of HIV-1 is driven by the viral structural protein Gag. In most cell types including T cells, Gag assembles into virus particles at the plasma membrane whereas, in HIV-1-infected macrophages, Gag and virus particles have been shown to accumulate in intracellular vesicles. At the moment, what causes this difference between cell types remains unknown. However, recent findings on the relationships between Gag and the cellular membrane system have substantially increased our understanding of the mechanisms by which sites of virus assembly are determined. I will review our current knowledge regarding the roles played by endosomal trafficking pathways, membrane microdomains, and plasma membrane lipids, and discuss the physiological significance of the interactions between Gag and specific membrane structures.View full abstractDownload PDF (280K)
Special Issue
-
Masayuki KUROOKA, Yasufumi KANEDA2007 Volume 57 Issue 1 Pages 19-27
Published: 2007
Released on J-STAGE: November 27, 2007
JOURNAL FREE ACCESSUltraviolet-inactivated, replication-defective Sendai virus particles (Hemagglutinating virus of Japan envelope, HVJ-E) injected into murine colon carcinoma (CT26) tumors growing in syngeneic Balb/c mice eradicated 60-80% of the tumors and obviously inhibited the growth of the remainder. Induced adaptive anti-tumor immune responses were dominant in the tumor eradication process because the effect was abrogated in severe combined immunodeficient (SCID) mice. Murine and human dendritic cells (DCs) underwent dose-dependent maturation by HVJ-E in vitro. Profiles of cytokines secreted by DCs after HVJ-E stimulation showed that the amount of IL-6 released was comparable to that elicited by live HVJ. Real-time RT-PCR and immunohistochemistory revealed that HVJ-E induced a remarkable infiltration of DCs, CD4+ and CD8+ T cells into tumors and CT26 specific cytotoxic T lymphocytes (CTL) were induced. On the other hand, conditioned medium from DCs stimulated by HVJ-E (H-DCCM) rescued CD4+CD25- effector T cell proliferation from Foxp3+CD4+CD25+ regulatory T cell (Treg) mediated suppression and IL-6 was presumably dominant for this phenomenon. We also confirmed such rescue in mice treated with HVJ-E in vivo. Moreover, anti-tumor effect of HVJ-E was significantly reduced by an in vivo blockade of IL-6 signaling. Depending on cancer cell types, it is also expected that HVJ-E eradicates tumor by its direct cytotoxity against cancer cells or activating NK cells. Because it can enhance anti-tumor immunity and simultaneously remove Treg mediated suppression, HVJ-E shows promise as a novel therapeutic for cancer immunotherapy.View full abstractDownload PDF (425K) -
Akihiro IIDA2007 Volume 57 Issue 1 Pages 29-36
Published: 2007
Released on J-STAGE: November 27, 2007
JOURNAL FREE ACCESSSendai virus (SeV) is an enveloped virus with a nonsegmented negative-strand RNA genome and a member of the paramyxovirus family. We have developed SeV vector which has shown a high efficiently of gene transfer and expression of foreign genes to a wide range of dividing and non-dividing mammalian cells and tissues. One of the characteristics of the vector is that the genome is located exclusively in the cytoplasm of infected cells and does not go through a DNA phase; thus there is no concern about unwanted integration of foreign sequences into chromosomal DNA. Therefore, this new class of "cytoplasmic RNA vector", an RNA vector with cytoplasmic expression, is expected to be a safer and more efficient viral vector than existing vectors for application to human therapy in various fields including gene therapy and vaccination. In this review, I describe development of Sendai virus vector, its application in the field of biotechnology and clinical application aiming to treat for a large number of diseases including cancer, cardiovascular disease, infectious diseases and neurologic disorders.View full abstractDownload PDF (597K) -
Saki KONDO, Miho TERASHIMA, Hiromitsu FUKUDA, Izumu SAITO, Yumi KANEGA ...2007 Volume 57 Issue 1 Pages 37-45
Published: 2007
Released on J-STAGE: November 27, 2007
JOURNAL FREE ACCESSThe adenovirus vector is very attractive tool not only for the gene therapy but also for the basic sciences. However, because a construction method of this vector had been complex, only limited scientists had constructed and enjoyed the benefits. Recently, various methods were developed and the researchers came to be able to choose an efficient method, which is the COS-TPC method, or a concise procedure, which is the intact-genome transfection method (in vitro ligation method). Here we described not only these methods but also new method to construct the various Ads simultaneously using the recombinase-mediated cassette exchange (RMCE) by the site-specific recombinase. And also we want to refer the possibility to the worth of the vector, especially the vector of the expression-switch.View full abstractDownload PDF (339K) -
Keiya OZAWA2007 Volume 57 Issue 1 Pages 47-55
Published: 2007
Released on J-STAGE: November 27, 2007
JOURNAL FREE ACCESSAAV (adeno-associated virus) vectors are considered to be promising gene-delivery vehicles for gene therapy, because they are derived from non-pathogenic virus, efficiently transduce non-dividing cells, and cause long-term gene expression. Appropriate AAV serotypes are utilized depending on the type of target cells. Among various neurological disorders, Parkinson's disease (PD) is one of the most promising candidates of gene therapy. PD is a progressive neurodegenerative disorder that predominantly affects dopaminergic neurons in the substantia nigra. One of the major approaches to gene therapy of PD is the intrastriatal expression of dopamine (DA)-synthesizing enzyme genes. As for the initial step of clinical application, AAV vector-mediated AADC (aromatic L-amino acid decarboxylase; the enzyme converting L-DOPA to DA) gene transfer in combination with oral administration of L-DOPA would be appropriate, since DA production can be regulated by adjusting the dose of L-DOPA. Second, intramuscular injection of AAV vectors is appropriate to protein-supplement gene therapy. Monogenic diseases such as hemophilia and Fabry disease are suitable candidates. Regarding cancer gene therapy, AAV vectors may be utilized to inhibit tumor angiogenesis, metastasis, and invasion. When long-term transgene expression in stem cells is needed, a therapeutic gene should be introduced with a minimal risk of insertional mutagenesis. To this end, site-specific integration into the AAVS1 locus on the chromosome 19 (19q13.4) by using the integration machinery of AAV would be particularly valuable.View full abstractDownload PDF (560K) -
Yukihiro NISHIYAMA, Fumi GOSHIMA2007 Volume 57 Issue 1 Pages 57-65
Published: 2007
Released on J-STAGE: November 27, 2007
JOURNAL FREE ACCESSOncolytic virotherapy using replication-competent viruses has attracted us as a new modality for cancer treatment. The fundamental concept of oncolytic virotherapy is that the viruses selectively replicate in and lyse tumor cells. Since 1997, numbers of clinical trials have been done in over 500 cancer patients. However, the results of those trials have been disappointing in most cases. We have isolated a spontaneously occurring herpes simplex virus type 1 mutant, designated HF10, which efficiently replicates and induces cell fusion in most transformed cells, but is highly attenuated in mice. HF10 has a number of deletions and insertions in the genome, resulting in the lack of the functional expression of UL43, UL49.5, UL55, UL56 and latency-associated transcripts. We have found that HF10 can be used as an oncolytic virus for treatment of malignant tumors in various animal models. Clinical trials have shown that intratumoral injection of HF10 can induce extensive tumor cell death in patients with recurrent breast cancer and head and neck squamous cell carcinoma without significant adverse effects. HF10 is a promising agent for use in oncolytic virotherapy in non-central nervous system malignancies.View full abstractDownload PDF (349K)
SUGIURA Memorial Incentive Award for Young Virologist, The Japanese Society for Virology, 2006
-
Jun SASAKI2007 Volume 57 Issue 1 Pages 67-74
Published: 2007
Released on J-STAGE: November 27, 2007
JOURNAL FREE ACCESSAichi virus is a member of the Family Picornaviridae. This virus was first isolated in 1989 from a stool specimen from a patient with oyster-associated gastroenteritis in Aichi, Japan. We analyzed the function of the 5' terminal region of the genome and the leader protein in virus replication. The results indicate that both the 5' terminal region of the genome and the leader protein are involved in viral RNA replication and encapsidation.View full abstractDownload PDF (263K) -
Masayuki SHIMOJIMA2007 Volume 57 Issue 1 Pages 75-82
Published: 2007
Released on J-STAGE: November 27, 2007
JOURNAL FREE ACCESSFeline immunodeficiency virus (FIV) induces a disease similar to acquired immunodeficiency syndrome (AIDS) in cats, yet in contrast to human immunodeficiency virus (HIV), CD4 is not the viral receptor. We identified a primary receptor for FIV as CD134 (OX40), a T cell activation antigen and costimulatory molecule. CD134 expression promotes viral binding and renders cells permissive for viral entry, productive infection, and syncytium formation. Infection is CXCR4-dependent, analogous to infection with X4 strains of HIV. Thus, despite the evolutionary divergence of the feline and human lentiviruses, both viruses use receptors that target the virus to a subset of cells that are pivotal to the acquired immune response. Further, we applied the new method for FIV receptor to Ebola virus entry factors with some modifications, and identified receptor-type tyrosine kinases, Axl and Dtk (members of Tyro3 family). Distribution of the molecules matches well with the Ebola virus tropism.View full abstractDownload PDF (283K) -
Makoto TAKEDA2007 Volume 57 Issue 1 Pages 83-90
Published: 2007
Released on J-STAGE: November 27, 2007
JOURNAL FREE ACCESSIn 1990 Kobune et al. succeeded in isolating pathogenic wild-type strains of measles virus (MV) using a marmoset B-lymphoblastoid cell line B95a. Their data indicated that MV strains that have been used in laboratories are attenuated strains through the adaptation to grow in a variety of cultured cells. We have established a very efficient reverse genetics system that allows us to engineer the genome of a wild-type MV strain at will by site-directed mutagenesis or recombination. Using the system it was shown that (1) the H protein determines tropism of MV, (2) the M protein regulates mode of MV spread, (3) the C protein inhibits host innate immune responses, and (4) the long untranslated regions in the M and F genes function to moderate cytopathogenicity by MV. These data advanced our understanding of molecular bases for MV pathogenicity and mechanisms of MV adaptation to grow in cultured cells.View full abstractDownload PDF (520K)
Comment
-
Takahiko NIKAIDO, Kaoru TAKEUCHI2007 Volume 57 Issue 1 Pages 91-100
Published: 2007
Released on J-STAGE: November 27, 2007
JOURNAL FREE ACCESSCartagena Protocol on Biosafety to the Convention on Biological Diversity seeks to protect biological diversity from potential risks posed by living modified organisms (LMOs) resulting from modern biotechnology. This protocol was ratified in Japan after establishing domestic law and regulations for the protocol. In the domestic law, use of LMOs is classified into type 1 use (use without containment measures) and type 2 use (use with containment measures). According to the domestic law, most of experiments using recombinant viruses are required for the approval of the Minister. In this article, we will explain Cartagena Protocol and the Japanese domestic low and indicate an example of application form for the approval of the Minister.View full abstractDownload PDF (483K)
- |<
- <
- 1
- >
- >|