Initial Characterization of the Epstein⁻Barr Virus BSRF1 Gene Product.

Yusuke Yanagi,Takayuki Murata,Hiroshi Kimura,Yoshitaka Sato,Fumi Goshima,H Masud,Takahiro Watanabe

doi:10.3390/v11030285

Yusuke Yanagi, Takayuki Murata + Show 5 more

Open Access

https://doi.org/10.3390/v11030285

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Journal: Viruses	Publication Date: Mar 21, 2019
Citations: 16	License type: CC BY 4.0

Affiliation: Fujita Health University, Nagoya University

Abstract

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 BamHI 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. To examine the role of BSRF1, we prepared knockout and revertant strains using the bacterial artificial chromosome system. Unexpectedly, the disruption of the gene had little or no effect on EBV lytic replication and the transformation of primary B cells. However, the knockdown of BSRF1 in B95-8 cells decreased progeny production. An immunofluorescence assay revealed that BSRF1 localized to the Golgi apparatus in the cytoplasm, as did its homologs. BSRF1 also associated with BamHI G leftward reading frame 3.5 (BGLF3.5), BamHI B rightward reading frame 2 (BBRF2), and BamHI A leftward reading frame 1 (BALF1), and BALF1 was incorporated into the tegument fraction with BSRF1. Taken together, our results indicate that BSRF1 plays a role in secondary envelopment or virion egress in the cytoplasm, as do its homolog genes.

Highlights

Epstein–Barr virus (EBV), a herpesvirus, infects more than 90% of the population
Because no BamHI S rightward reading frame 1 (BSRF1)-KO mutant of EBV has been reported, we knocked out the BSRF1 gene in the context of EBV-bacterial artificial chromosome (BAC) to analyze its role in the EBV lifecycle
We analyzed the role of BSRF1 protein by generating a KO virus using the BAC system

Summary

Introduction

Epstein–Barr virus (EBV), a herpesvirus, infects more than 90% of the population. EBV infection is associated with few or no symptoms, but it can cause infectious mononucleosis, following the primary infection of adolescents [1]. The virus establishes a latent infection in B cells and persists for life. EBV infection can induce carcinogenesis, including Burkitt lymphoma, Hodgkin lymphoma, T/NK-cell lymphoma, gastric carcinoma, and nasopharyngeal carcinoma [2]. EBV can establish a latent infection [3]. A limited number of viral genes, such as EBV nuclear antigen 1 (EBNA1) and latent membrane protein 1 (LMP1), are expressed. The virus genome is amplified simultaneously with that of the host in S phase and delivered to daughter cells in the M phase

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