Uirusu
Online ISSN : 1884-3433
Print ISSN : 0042-6857
ISSN-L : 0042-6857
Search
Advanced search
OR
Browse
Search
Volume 69, Issue 1
Displaying 1-10 of 10 articles from this issue
Show all abstracts
    • |<
    • <
    • 1
    • >
    • >|
Reviews
  • Reverse genetics of rotaviruses: Generation of recombinant human rotaviruses from just 11 cDNAs encoding the rotavirus genome
    Satoshi KOMOTO, Saori FUKUDA
    2019 Volume 69 Issue 1 Pages 1-12
    Published: 2019
    Released on J-STAGE: September 16, 2020
    DOIhttps://doi.org/10.2222/jsv.69.1
    JOURNAL FREE ACCESS
    Show abstractHide abstract
    An entirely plasmid-based reverse genetics system for animal rotavirus was established very recently. We improved the reverse genetics system to generate recombinant rotavirus by transfecting only 11 T7 plasmids for its 11 genes under the condition of increasing the ratio (3- or 5-fold) of the cDNA plasmids for NSP2 and NSP5 genes (11-plasmid system). Utilizing this highly efficient system, we engineered the first infectious recombinant rotaviruses harboring fluorescent (EGFP and mCherry) protein genes. In addition to these recombinant animal viruses, the first infectious recombinant human rotavirus (strain KU (G1P[8])) was also generated with the 11-plasmid system with some modifications. The availability of recombinant human rotaviruses will provide a genetic platform for a better understanding of the replication, pathogenicity, and other biological characteristics of this medically important virus and enable the rational development of next-generation human rotavirus vaccines.
    View full abstract
    Download PDF (1534K)
  • EBV and Lymphomagenesis
    Hiroshi KIMURA, Yusuke OKUNO
    2019 Volume 69 Issue 1 Pages 13-22
    Published: 2019
    Released on J-STAGE: September 16, 2020
    DOIhttps://doi.org/10.2222/jsv.69.13
    JOURNAL FREE ACCESS
    Show abstractHide abstract
    Epstein–Barr virus (EBV) is a double stranded DNA virus of the family Herpesviridae. EBV is associated with a variety of lymphomas, and the mechanisms by which it promotes lymphomagenesis have been elucidated; this includes, for example, by translocation/activation of Myc in Burkitt lymphoma. However, the mechanisms by which it induces lymphoid tumors other than Burkitt lymphoma are unclear. Recently, we reported that the genome of EBV present in EBV-associated lymphomas harbors frequent intragenic deletions and that the deletion of a gene essential for virus replication promotes lymphomagenesis in a mouse model. Although intragenic deletions have been detected in other tumor viruses, little is known about the effects and importance of those of EBV, a large DNA virus whose genome encodes more than 70 genes. In this review, we summarize the role of EBV in lymphomagenesis with a focus on the impact of intragenic deletions.
    View full abstract
    Download PDF (2848K)
Special Issue: HTLV-1
  • The role of HTLV-1 provirus in clonal selection of the infected cells
    Misaki MATSUO, Paola MIYAZATO, Yorifumi SATOU
    2019 Volume 69 Issue 1 Pages 23-28
    Published: 2019
    Released on J-STAGE: September 16, 2020
    DOIhttps://doi.org/10.2222/jsv.69.23
    JOURNAL FREE ACCESS
    Show abstractHide abstract
    HTLV-1 inserts its viral genome into the host cellular DNA in the form of a provirus. The proviral DNA is a key to understand the persistence and pathogenesis of HTLV-1 infection. There has been a significant progress in proviral research due to technological advances on DNA sequencing.Next generation sequencing technology revolutionized our understanding of the human genome,showing how it is organized and regulated, not only by the nucleotide sequence itself but also by epigenetic features and higher-order chromatin structure. We will review recent findings regarding the role of HTLV-1 provirus in HTLV-1 infection.
    View full abstract
    Download PDF (1729K)
  • HTLV-1-associated myelopathy
    Yoshihisa YAMANO
    2019 Volume 69 Issue 1 Pages 29-36
    Published: 2019
    Released on J-STAGE: September 16, 2020
    DOIhttps://doi.org/10.2222/jsv.69.29
    JOURNAL FREE ACCESS
    Show abstractHide abstract
    Human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus that infects T lymphocytes. HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is an intractable neurodegenerative disease caused by HTLV-1 infection just like adult T cell leukemia/lymphoma (ATL) is, developing in a fraction of infected individuals. Here, we review the update information about the new drug development and therapeutic algorithm of HAM/TSP based on the resent research achievement in molecular pathogenesis and biomarkers.
    View full abstract
    Download PDF (754K)
  • Astute strategies of HTLV-1 with driven viral genes
    Kosuke TOYODA, Jun-ichirou YASUNAGA, Masao MATSUOKA
    2019 Volume 69 Issue 1 Pages 37-46
    Published: 2019
    Released on J-STAGE: September 16, 2020
    DOIhttps://doi.org/10.2222/jsv.69.37
    JOURNAL FREE ACCESS
    Show abstractHide abstract
    Human T-cell leukemia virus type 1 (HTLV-1) is the world’s first retrovirus with pathogenicity to cause adult T-cell leukemia-lymphoma (ATL) and chronic inflammatory diseases,such as HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP) and HTLV-1 uveitis. As the virological characteristic, HTLV-1 can transmit efficiently only through cell-to-cell contact. Spread of infection and viral persistence is ingeniously driven by several viral genes as exemplified by HTLV-1 bZIP factor (HBZ) and tax. After the infection, the virus promotes proliferation and immortalization of the infected cells with acculturating immunophenotype into effector/memory T cells. In addition, HBZ enhances expression of co-inhibitory receptors on the surface of infected cells, potentially leading to suppression of host immune responses. These viral strategies can also result in unforeseen by-product, the pathogenicity of HTLV-1-associated diseases. In this review, with recent progress of HTLV-1 researches, we focus on astute regulation systems of the viral genes developed by HTLV-1.
    View full abstract
    Download PDF (1595K)
Topics
  • Anti-viral responses in insect cells
    Motoko IKEDA
    2019 Volume 69 Issue 1 Pages 47-60
    Published: 2019
    Released on J-STAGE: September 16, 2020
    DOIhttps://doi.org/10.2222/jsv.69.47
    JOURNAL FREE ACCESS
    Download PDF (617K)
  • Protease-dependent virus tropism and pathogenicity: The role for TMPRSS2
    Makoto TAKEDA
    2019 Volume 69 Issue 1 Pages 61-72
    Published: 2019
    Released on J-STAGE: September 16, 2020
    DOIhttps://doi.org/10.2222/jsv.69.61
    JOURNAL FREE ACCESS
    Show abstractHide abstract
    The distribution pattern of host proteases and their cleavage specificity for viral fusion glycoproteins are key determinants for viral tissue tropism and pathogenicity. The discovery of this protease-dependent virus tropism and pathogenicity has been triggered by the leading studies of the host-induced or -controlled modification of viruses by Homma et al. in 1970s. With the introduction of advanced protein analysis method, the observations by Homma et al. have been clearly explained by the cleavage activation of viral fusion glycoproteins by proteases. The molecular biological features of viruses, which show distinct protease specificity or dependency, have been also revealed by newly introduced nucleotide and molecular analysis method. Highly pathogenic avian influenza viruses (HPAIVs) have multi-basic cleavage motif in the hemagglutinin (HA) protein and are activated proteolytically by furin. Furin is ubiquitously expressed in eukaryotic cells and thereby HPAIVs have the potential to cause a systemic infection in infected animals. On the other hand, the HA cleavage site of low pathogenic avian influenza viruses (LPAIVs) and seasonal human influenza viruses is mono-basic and thus not recognized by furin. They are likely cleaved by protease(s) localized in specific organs or tissues. However, the protease(s), which cleaves mono-basic HA in vivo, has long been undetermined, although many proteases have been shown as candidates. Finally, recent studies using gene knocked out mice revealed that TMPRSS2, a member of type II transmembrane serine proteases, is responsible for the cleavage of influenza viruses with a mono-basic HA in vivo. A subsequent study further demonstrated that TMPRSS2 contributes to replication and pathology of emerging SARS- and MERS coronaviruses in vivo.
    View full abstract
    Download PDF (2509K)
SUGIURA Memorial Incentive Award for Young Virologist, The Japanese Society for Virology, 2018
    • |<
    • <
    • 1
    • >
    • >|
feedback
 Top