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Narita, Yohei

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Narita

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Yohei

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Narita, Yohei

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2017 - 20182

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Author's Publications: search.filters.isAuthorOfPublication.baa1b311-36f5-4045-9f45-dfdd9ff8ff29

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    BGLF2 Increases Infectivity of Epstein-Barr Virus by Activating AP-1 upon De Novo Infection
    (American Society for Microbiology, 2018) Konishi, Natsuno; Narita, Yohei; Hijioka, Fumiya; Masud, H. M. Abdullah Al; Sato, Yoshitaka; Kimura, Hiroshi; Murata, Takayuki
    ABSTRACT Epstein-Barr virus (EBV) is a human gammaherpesvirus that causes infectious mononucleosis and several malignancies, such as endemic Burkitt lymphoma and nasopharyngeal carcinoma. Herpesviruses carry genes that can modify cell functions, including transcription and ubiquitination, thereby facilitating viral growth and survival in infected cells. Using a reporter screening system, we revealed the involvement of several EBV gene products in such processes. Of these, BGLF2 activated the AP-1 signaling pathway through phosphorylation of p38 and c-Jun N-terminal kinase (JNK). Knockout of the BGLF2 gene did not affect viral gene expression and viral genome DNA replication, but resulted in marked reduction of progeny titer. We also found that the BGLF2 disruption resulted in significant loss of infectivity upon de novo infection. Interestingly, expression of a binding partner, BKRF4, repressed the activation of AP-1 by BGLF2. These results shed light on the physiological role of the tegument protein BGLF2. IMPORTANCE: Epstein-Barr virus (EBV), an oncogenic gammaherpesvirus, carries ~80 genes. While several genes have been investigated extensively, most lytic genes remain largely unexplored. Therefore, we cloned 71 EBV lytic genes into an expression vector and used reporter assays to screen for factors that activate signal transduction pathways, viral and cellular promoters. BGLF2 activated the AP-1 signaling pathway, likely by interacting with p38 and c-Jun N-terminal kinase (JNK), and increased infectivity of the virus. We also revealed that BKRF4 can negatively regulate AP-1 activity. Therefore, it is suggested that EBV exploits and modifies the AP-1 signaling pathway for its replication and survival.
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    A Temporal Proteomic Map of Epstein-Barr Virus Lytic Replication in B Cells
    (Cell Press, 2017) Ersing, Ina; Nobre, Luis; Wang, Liang Wei; Soday, Lior; Ma, Yijie; Paulo, Joao; Narita, Yohei; Ashbaugh, Camille W.; Jiang, Chang; Grayson, Nicholas E.; Kieff, Elliott; Gygi, Steven; Weekes, Michael P.; Gewurz, Benjamin
    Summary Epstein-Barr virus (EBV) replication contributes to multiple human diseases, including infectious mononucleosis, nasopharyngeal carcinoma, B cell lymphomas, and oral hairy leukoplakia. We performed systematic quantitative analyses of temporal changes in host and EBV proteins during lytic replication to gain insights into virus-host interactions, using conditional Burkitt lymphoma models of type I and II EBV infection. We quantified profiles of >8,000 cellular and 69 EBV proteins, including >500 plasma membrane proteins, providing temporal views of the lytic B cell proteome and EBV virome. Our approach revealed EBV-induced remodeling of cell cycle, innate and adaptive immune pathways, including upregulation of the complement cascade and proteasomal degradation of the B cell receptor complex, conserved between EBV types I and II. Cross-comparison with proteomic analyses of human cytomegalovirus infection and of a Kaposi-sarcoma-associated herpesvirus immunoevasin identified host factors targeted by multiple herpesviruses. Our results provide an important resource for studies of EBV replication.