Publications by authors named "Goshima F"

Herpes simplex virus type 1 (HSV-1) is a ubiquitous pathogen that causes various diseases in humans, ranging from common mucocutaneous lesions to severe life-threatening encephalitis. However, our understanding of the interaction between HSV-1 and human host factors remains incomplete. Here, to identify the host factors for HSV-1 infection, we performed a human genome-wide CRISPR screen using near-haploid HAP1 cells, in which gene knockout (KO) could be efficiently achieved.

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The necessity of image retakes is initially determined on a preview monitor equipped with an operating system; therefore, some image blurring is only noticed later, on a high-resolution monitor. The purpose of this study is to investigate blur detection performance on radiographs via a deep learning approach compared with human observers. A total of 99 radiographs (blurry 57, nonblurry 42) were independently observed and rated by six observers using preview and diagnostic liquid crystal displays (LCDs).

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Prognosis for advanced oral carcinoma remains poor. Oncolytic virotherapy uses replication-competent viruses to infect and kill only the tumor cells. However, it has been difficult to investigate the oncolytic activity of viruses against oral carcinomas in mouse models.

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Epstein-Barr virus (EBV) is a well-established tumor virus that has been implicated in a wide range of immunodeficiency-associated lymphoproliferative disorders (LPDs). Although rituximab, a CD20 mAb, has proven effective against EBV-associated LPDs, prolonged use of this drug could lead to resistance due to the selective expansion of CD20 cells. We have previously shown that cyclin-dependent kinase (CDK) inhibitors are able to specifically suppress the expression of viral late genes, particularly those encoding structural proteins; however, the therapeutic effect of CDK inhibitors against EBV-associated LPDs is not clear.

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Recent developments in therapeutic strategies have improved the prognosis of head and neck squamous cell carcinoma (HNSCC). Nevertheless, 5-year survival rate remains only 40%, necessitating new therapeutic agents. Oncolytic virotherapy entails use of replication-competent viruses to selectively kill cancer cells.

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Epstein⁻Barr virus (EBV) is a ubiquitous virus that causes infectious mononucleosis and several types of cancer, such as Burkitt lymphoma, T/NK-cell lymphoma, and nasopharyngeal carcinoma. As a herpesvirus, it encodes more than 80 genes, many of which have not been characterized. EBV HI S rightward reading frame 1 (BSRF1) encodes a tegument protein that, unlike its homologs herpes simplex virus unique long 51 (UL51) and human cytomegalovirus UL71, has not been extensively investigated.

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The Epstein-Barr virus (EBV) is a causative agent of infectious mononucleosis and several malignancies. Here, we focused on an EBV lytic protein, BOLF1, which is conserved throughout the herpesvirus family and is reported to be a virion tegument protein. We first constructed BOLF1-deficient viruses using the bacterial artificial chromosome (BAC) and CRISPR/Cas9 systems.

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In the version of this Letter originally published, in the sentence beginning "The major driver role of DDX3X mutations...

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Temporally controlled gene expression is necessary for the propagation of herpesviruses. To achieve this, herpesviruses encode several transcriptional regulators. In Epstein-Barr virus, BcRF1 associates with five viral proteins (BDLF4, BGLF3, BFRF2, BVLF1, and BDLF3.

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Epstein-Barr virus (EBV) infection is highly prevalent in humans and is implicated in various diseases, including cancer. Chronic active EBV infection (CAEBV) is an intractable disease classified as a lymphoproliferative disorder in the 2016 World Health Organization lymphoma classification. CAEBV is characterized by EBV-infected T/natural killer (NK) cells and recurrent/persistent infectious mononucleosis-like symptoms.

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Article Synopsis
  • Epigenetic modifications significantly influence how the Epstein-Barr virus (EBV) genes are expressed, particularly through the role of EZH2, a key enzyme in histone modification.
  • Research showed that knocking out the EZH2 gene in EBV-negative B cells led to slower cell growth post-infection and increased expression of viral genes during the lytic phase.
  • The findings highlight EZH2's importance in regulating both latent and lytic gene expression of EBV, suggesting it may serve as a form of innate immunity to control viral replication.
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Oncolytic virotherapy is a kind of antitumor therapy using viruses with natural or engineered tumor-selective replication to intentionally infect and kill tumor cells. An early clinical trial has been performed in the 1950s using wild-type and non-engineered in vitro-passaged virus strains and vaccine strains (first generation oncolytic viruses). Because of the advances in biotechnology and virology, the field of virotherapy has rapidly evolved over the past two decades and innovative recombinant selectivity-enhanced viruses (second generation oncolytic viruses).

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Latent membrane protein 1 (LMP1) is a major oncogene encoded by Epstein-Barr virus (EBV) and is essential for immortalization of B cells by the virus. Previous studies suggested that several transcription factors, such as PU.1, RBP-Jκ, NFκB, EBF1, AP-2 and STAT, are involved in LMP1 induction; however, the means by which the oncogene is negatively regulated remains unclear.

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Epstein-Barr virus (EBV), a member of human gammaherpesvirus, infects mainly B cells. EBV has two alternative life cycles, latent and lytic, and is reactivated occasionally from the latent stage to the lytic cycle. To combat EBV-associated disorders, understanding the molecular mechanisms of the EBV lytic replication cycle is also important.

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Article Synopsis
  • Advanced melanoma treatment has shifted from low-survival chemotherapy options like DTIC to more effective immunotherapies and targeted therapies, although high costs remain an issue.
  • This study explored the combined effect of HF10, a modified virus, with DTIC in mice to improve treatment outcomes, observing significant tumor growth inhibition and increased survivability compared to monotherapy.
  • Results indicated that the combination therapy not only showed enhanced cytotoxicity and tumor clearance but also stimulated a strong systemic immune response, evidenced by increased IFN-γ secretion from immune cells.
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The Epstein-Barr virus (EBV) is a gamma-herpesvirus associated with several malignancies. It establishes a latent infection in B lymphocytes and is occasionally reactivated to enter the lytic cycle. Here we examined the role of the EBV gene BRRF1, which is expressed in the lytic state.

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Epstein-Barr virus (EBV) latently infects malignant epithelial cells in approximately 10% of all gastric cancers. Latent membrane protein 1 (LMP1), an oncogenic protein, plays an important role in malignant transformation in EBV-associated nasopharyngeal carcinoma and B-cell lymphoma; however, its expression has not been detected in EBV-associated gastric cancer. To address why LMP1 has not been detected in EBV-positive gastric tumors, we focused on the interactions between LMP1-positive and -negative cells and stably expressed LMP1 in the gastric cancer cell line AGS.

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Epstein-Barr virus (EBV) is a human gammaherpesvirus associated with several malignancies. We reported previously that an EBV lytic gene product BRRF2 is involved in the maturation of progeny virus. To analyze the domain(s) needed for efficient production of progeny, we prepared a series of deletion mutants and found two functional domains in the N- and C-terminal regions by complementation assays.

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Epstein-Barr virus (EBV) infects not only B cells, but also T cells and natural killer (NK) cells, and is associated with T or NK cell lymphoma. These lymphoid malignancies are refractory to conventional chemotherapy. We examined the activation of the JAK3/STAT5 pathway in EBV-positive and -negative B, T and NK cell lines and in cell samples from patients with EBV-associated T cell lymphoma.

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Unlabelled: Latent membrane protein 1 (LMP1) is a major oncogene essential for primary B cell transformation by Epstein-Barr virus (EBV). Previous studies suggested that some transcription factors, such as PU.1, RBP-Jκ, NF-κB, and STAT, are involved in this expression, but the underlying mechanism is unclear.

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Epstein-Barr virus (EBV) is a gammaherpesvirus, associated with infectious mononucleosis and various types of malignancy. We focused here on the BDLF4 gene of EBV and identified it as a lytic gene, expressed with early kinetics. Viral late gene expression of the BDLF4 knockout strain was severely restricted; this could be restored by an exogenous supply of BDLF4.

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The Epstein-Barr virus (EBV) predominantly establishes a latent infection in B lymphocytes, and occasionally switches from the latent state to the lytic cycle. In this report, we identified and examined the role of a lytic gene, BRRF2. We first prepared an antibody against BRRF2 and identified the gene product as a viral lytic protein expressed in B95-8 cells with late kinetics.

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Article Synopsis
  • The Epstein-Barr virus (EBV) can switch from a latent state in B lymphocytes to a lytic cycle, where it actively replicates and produces new virus particles.
  • Researchers focused on the lytic gene BGLF3.5 and created mutants to study its function, discovering that a specific mutation led to a lack of BGLF4 protein and significantly hindered viral production.
  • Further experiments revealed that BGLF3.5 is not crucial for the processes of viral replication and progeny production in HEK293 cells, contrasting with its functionality in a related virus, MHV-68.
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