Uirusu
Online ISSN : 1884-3433
Print ISSN : 0042-6857
ISSN-L : 0042-6857
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Volume 73, Issue 2
Displaying 1-7 of 7 articles from this issue
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Reviews
  • Integrase and reversetranscriptase: New insights into the HIV genome replication system in line.
    Takao MASUDA, Gota KAWAI
    2023 Volume 73 Issue 2 Pages 139-146
    Published: 2023
    Released on J-STAGE: September 27, 2024
    DOIhttps://doi.org/10.2222/jsv.73.139
    JOURNAL FREE ACCESS
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    Reverse transcriptase (RT) and integrase (IN) are retrovirus enzymes to convert virus genomic RNA into provirus DNA state in host cells. The RT and IN encoded tandemly in the pol gene, are translated as a fused form and incorporated into the virus particles. Recently, we discovered the potential role of HIV-1 IN to regulate the reverse transcription through the fused state with RT (RT-IN). On the other hand, analysis of HIV-1 transcripts have revealed the variations in number of guanine residue at the 5' end (5'G) due to fluctuations in the transcription initiation point within HIV-1 provirus DNA. Importantly, the number of 5’G dictates the packaging of HIV genome RNA into virus particles serving as a template for the reverse transcription reaction. In this review, we provide new insights into the mechanism of HIV genome replication based on our recent findings of the structural-functional correlation of HIV enzymes (RT and IN) and virus genomic RNA.
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  • Epidemiological and mechanistic links between Epstein-Barr virus and multiple sclerosis
    Yoshitaka SATO
    2023 Volume 73 Issue 2 Pages 147-152
    Published: 2023
    Released on J-STAGE: September 27, 2024
    DOIhttps://doi.org/10.2222/jsv.73.147
    JOURNAL FREE ACCESS
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    Epstein-Barr virus (EBV) is a ubiquitous human lymphotropic herpesvirus that causes several malignancies. EBV infects approximately 90% of individuals worldwide. Recent studies have provided robust evidence for a causal role of EBV in multiple sclerosis. Multiple sclerosis is the most prevalent chronic inflammatory and degenerative disease of the central nerve system (CNS) that progresses over time to progressive neurodegeneration and disability. Here, I review how a ubiquitous virus can elicit autoreactive antibodies through molecular mimicry between viral and host CNS antigens, triggering multiple sclerosis.
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Special Issue: Countermeasures for Combating SARS-CoV-2 and Emerging Virus Infections
  • Neutralizing antibodies against SARS-CoV-2
    Saya MORIYAMA
    2023 Volume 73 Issue 2 Pages 153-162
    Published: 2023
    Released on J-STAGE: September 27, 2024
    DOIhttps://doi.org/10.2222/jsv.73.153
    JOURNAL FREE ACCESS
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    Severe acute respiratory syndrome (SARS) corona virus 2 (SARS-CoV-2) is a novel coronavirus that infects humans and causes respiratory symptoms, resulting in a global pandemic since its appearance in 2019. Neutralizing antibody production is an important immune response following SARS-CoV-2 infection, and a great deal of research has been performed regarding the immune response against SARS-CoV-2 infection. However, SARS-CoV-2 is constantly changing and multiple amino acid reconstitutions accumulated in the spike protein enabled viruses to escape from immune responses, especially from neutralizing antibodies. In this review, the antibody responses to SARS-CoV-2 and the emergence of escape variants, and the development of broadly neutralizing antibodies will be introduced.
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  • Development of an engineered ACE2 decoy for COVID-19 therapy.
    Toru OKAMOTO, Yumi ITOH, Tatsuya SUZUKI
    2023 Volume 73 Issue 2 Pages 163-172
    Published: 2023
    Released on J-STAGE: September 27, 2024
    DOIhttps://doi.org/10.2222/jsv.73.163
    JOURNAL FREE ACCESS
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    It has been passed four years since the pandemic caused by the severe acute respiratory syndrome-2 (SARS-CoV-2) that began in 2019. Since June 2020, we have been working on a project to develop a therapeutic drug using receptor decoys, even though we cannot predict how long the pandemic will last or how long our daily lives will be restricted. This receptor decoy utilizes Angiotensin-converting enzyme 2 (ACE2), which is the receptor for SARS-CoV-2, and involves introducing mutations that enhance its binding ability with the spike protein of SARS-CoV-2. This high-affinity ACE2, acting as a decoy protein, is a strategy to inhibit viral infection and to expect therapeutic effects by replacing the endogeneous ACE2 that SARS-CoV-2 binds to with ACE2 decoy. This paper introduces the development of ACE2 decoys that have progressed through collaborative research with many researchers outside the field of virology.
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  • SARS-CoV-2-specific T cell recognition toward emerging variants
    Chihiro MOTOZONO
    2023 Volume 73 Issue 2 Pages 173-182
    Published: 2023
    Released on J-STAGE: September 27, 2024
    DOIhttps://doi.org/10.2222/jsv.73.173
    JOURNAL FREE ACCESS
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    Cytotoxic T lymphocytes (CTLs) play an important role in the control of various viral infection. CTLs recognize a complex of HLA (human leukocyte antigen) class I molecule and epitope peptide derived from viral protein on the cell surface via T cell receptors and can destroy virally infected cells. It is becoming evident that SARS-CoV-2 specific T cells play a crucial role in the control of COVID-19. We characterized T cells specific for various SARS-CoV-2 variants and identified that a L452R mutation in the Delta spike protein evades HLA-A*24:02-restricted T cell responses and increases virus infectivity. In contrast, HLA-A*24:02-restricted T cells strongly suppresses Omicron BA.1 replication due to a G446S mutation, located just outside the N-terminus of the cognate epitope, in the Omicron BA.1 variant via enhanced antigen processing and presentation of the epitope. These data indicate that T cell specific for antigens derived from variable regions is highly susceptible for the mutation and its location. The detail analysis of antigen-specific T cell responses toward variants provides better insights for the rational design of vaccine antigens or immunotherapy to induce efficient cellular immunity against new emerging viruses/variants.
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