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Upregulation of the Chemokine Receptor CCR2B in Epstein‒Barr Virus-Positive Burkitt Lymphoma Cell Lines with the Latency III Program

1
August Kirchenstein Institute of Microbiology and Virology, Riga Stradins University, 5 Ratsupites Str, 1067 Riga, Latvia
2
Latvian Biomedical Research and Study Centre, 1 Ratsupites Str k-1, 1067 Riga, Latvia
3
Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institutet, 16 Nobelsväg, Box 280, 171 77 Stockholm, Sweden
4
R.E. Kavetsky Institute of Experimental Pathology, Oncology, and Radiobiology, NASU, 45 Vasylkivska str, 03022 Kyiv, Ukraine
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Viruses 2018, 10(5), 239; https://doi.org/10.3390/v10050239
Received: 9 April 2018 / Revised: 28 April 2018 / Accepted: 29 April 2018 / Published: 3 May 2018
(This article belongs to the Section Animal Viruses)
CCR2 is the cognate receptor to the chemokine CCL2. CCR2–CCL2 signaling mediates cancer progression and metastasis dissemination. However, the role of CCR2–CCL2 signaling in pathogenesis of B-cell malignancies is not clear. Previously, we showed that CCR2B was upregulated in ex vivo peripheral blood B cells upon Epstein‒Barr virus (EBV) infection and in established lymphoblastoid cell lines with the EBV latency III program. EBV latency III is associated with B-cell lymphomas in immunosuppressed patients. The majority of EBV-positive Burkitt lymphoma (BL) tumors are characterized by latency I, but the BL cell lines drift towards latency III during in vitro culture. In this study, the CCR2A and CCR2B expression was assessed in the isogenic EBV-positive BL cell lines with latency I and III using RT-PCR, immunoblotting, and immunostaining analyses. We found that CCR2B is upregulated in the EBV-positive BL cells with latency III. Consequently, we detected the migration of latency III cells toward CCL2. Notably, the G190A mutation, corresponding to SNP CCR2-V64I, was found in one latency III cell line with a reduced migratory response to CCL2. The upregulation of CCR2B may contribute to the enhanced migration of malignant B cells into CCL2-rich compartments. View Full-Text
Keywords: CCR2; EBV; latency III; Burkitt lymphoma cell lines; B-cell lymphoma CCR2; EBV; latency III; Burkitt lymphoma cell lines; B-cell lymphoma
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Kozireva, S.; Rudevica, Z.; Baryshev, M.; Leonciks, A.; Kashuba, E.; Kholodnyuk, I. Upregulation of the Chemokine Receptor CCR2B in Epstein‒Barr Virus-Positive Burkitt Lymphoma Cell Lines with the Latency III Program. Viruses 2018, 10, 239.

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