Epstein‐Barr Virus (EBV): Infection, Propagation, Quantitation, and Storage

Lan, Ke; Verma, Subhash C.; Murakami, Masanao; Bajaj, Bharat; Robertson, Erle S.

doi:10.1002/9780471729259.mc14e02s6

Cited by 19 publications

(16 citation statements)

References 38 publications

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“…Primers for BZLF1 were 59-GCCACCTTTGCTATCTTTG-CT-39 (forward) and 59-TTCCATTAGTAAACGAGGCGTG-39 (reverse). Primers for EBER and the BamHI W region were as described previously (Lan et al, 2007;Choy et al, 2008a). qRT-PCR was performed using a SYBR Premix Ex Taq system (TaKaRa) as described previously (Kew et al, 2013;Siu et al, 2014).…”

Section: Methodsmentioning

confidence: 99%

CRISPR/Cas9-mediated genome editing of Epstein–Barr virus in human cells

Yuen

Chan

Wong

et al. 2015

Journal of General Virology

156

114

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Section: Methodsmentioning

confidence: 99%

CRISPR/Cas9-mediated genome editing of Epstein–Barr virus in human cells

Yuen

Chan

Wong

et al. 2015

Journal of General Virology

156

114

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“…Akata (EBV-eGFP) and hybridoma cells were grown in RPMI medium 1640 supplemented with 5% (vol/vol) or 10% (vol/vol) FBS, respectively, in humidified 5% (vol/vol) CO 2 incubators at 37°C. EBV-eGFP cells were made as previously described (36,37). Briefly, EBV-eGFP cells were produced from Akata (EBV-eGFP) cells by cross-linking cell surface IgG proteins using 0.8% goat antihuman IgG.…”

Section: Methodsmentioning

confidence: 99%

Nonmuscle myosin heavy chain IIA mediates Epstein–Barr virus infection of nasopharyngeal epithelial cells

Xiong

Wang

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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EBV causes B lymphomas and undifferentiated nasopharyngeal carcinoma (NPC). Although the mechanisms by which EBV infects B lymphocytes have been extensively studied, investigation of the mechanisms by which EBV infects nasopharyngeal epithelial cells (NPECs) has only recently been enabled by the successful growth of B lymphoma Mo-MLV insertion region 1 homolog (BMI1)-immortalized NPECs in vitro and the discovery that neuropilin 1 expression positively affects EBV glycoprotein B (gB)-mediated infection and tyrosine kinase activations in enhancing EBV infection of BMI1-immortalized NPECs. We have now found that even though EBV infected NPECs grown as a monolayer at extremely low efficiency (<3%), close to 30% of NPECs grown as sphere-like cells (SLCs) were infected by EBV. We also identified nonmuscle myosin heavy chain IIA (NMHC-IIA) as another NPEC protein important for efficient EBV infection. EBV gH/gL specifically interacted with NMHC-IIA both in vitro and in vivo. NMHC-IIA densely aggregated on the surface of NPEC SLCs and colocalized with EBV. EBV infection of NPEC SLCs was significantly reduced by NMHC-IIA siRNA knock-down. NMHC-IIA antisera also efficiently blocked EBV infection. These data indicate that NMHC-IIA is an important factor for EBV NPEC infection. Epstein-Barr virusBV is a nearly ubiquitous human γ-herpesvirus that causes B-cell lymphomas and nasopharyngeal carcinoma (NPC), indicative of tropism for both cell types (1-3). Until recently, the molecular mechanisms of EBV infection of B lymphocytes were better understood than the mechanisms of epithelial cell infection (4). EBV attachment to the B-cell membrane is mediated by interactions between EBV glycoprotein 350 (gp350) and complement receptor type 2 (CR2 or CD21) (5) or CD35 (6). EBV gp42 binding to HLA class II triggers EBV fusion with B cells in the presence of EBV glycoprotein B (gB) and gH/gL (7,8). For epithelial cells, gH/gL and gB are important for EBV infection (4, 9, 10). Epithelial cells lack HLA class II expression; thus, gp42 cannot trigger EBV and cell fusion. Instead, gp42 inversely suppresses the infection (11), and an antibody against gp350 can enhance infections of CD21/CD35-negative epithelial cells (12). The gH/gL heterodimer is required for virus entry (4) and may be involved in binding (13), as well as fusion of EBV (14-17). However, the crystal structure of EBV gH/gL does not show any known fusion domain (18). It is now thought that gH/gL regulates the fusion function of gB (19). Binding of gH/gL to a subset of αv integrins (e.g., αvβ 5 , αvβ 6 , or αvβ 8 ) provides the initial trigger for gB-mediated fusion (16,20,21). However, E1D1(gH/gL) antibody or CL59(gH) antibody, with a different epitope, can impair epithelial cell infection (20,22). Thus, multiple gH/gL domains are critical to EBV infection, and gH/gL may interact with proteins in addition to integrins. Direct interaction of EBV gB amino acids 23-431 with neuropilin 1 (NRP1) and its associated tyrosine kinases is critical for EBV infection of nasopharyngeal ep...

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“…Both genetic changes in tumour suppressor genes as well as micro-environmental factors play important roles in dysregulated cell survival. There are pieces of evidence suggesting that viral infections can lead to lymphomagenesis, such as Epstein-Barr virus (EBV) in Burkitt's lymphoma [8] or human herpes virus-8 infection in primary effusion lymphoma [9]. Chronic inflammatory processes similarly activate B-cell divisions and the processes predisposing to translocations and lymphoma.…”

Section: Pathogenesis Of Nhlmentioning

confidence: 99%

Aspects of B‐Cell Non‐Hodgkin’s Lymphoma Development: A Transition from Immune‐Reactivity to Malignancy

et al. 2009

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The development of B‐cell lymphomas is an intricate interplay among various pathogenic factors, leading to a multi‐step process, encompassing various stages of B‐cell maturation. Besides genetic abnormalities, a variety of environmental and microbial factors, as well as disproportional immune‐regulatory processes lead to the malignant transformation. Yet, little is known about the exact chain of events, which lead from the physiological polyclonal B‐cell activation as a response to exogenous antigens through oligoclonality to a monoclonal, uncontrolled, malignant B‐cell proliferation. The aim of the present review was to summarize the potential harmful steps in the development of B‐cell lymphomas, according to conventional and novel theories, and to depict therapeutic regimens presently in use as well as to envision future drug developments, beneficial in the battle against this lymphoid malignancy.

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Epstein‐Barr Virus (EBV): Infection, Propagation, Quantitation, and Storage

Cited by 19 publications

References 38 publications

CRISPR/Cas9-mediated genome editing of Epstein–Barr virus in human cells

CRISPR/Cas9-mediated genome editing of Epstein–Barr virus in human cells

Nonmuscle myosin heavy chain IIA mediates Epstein–Barr virus infection of nasopharyngeal epithelial cells

Aspects of B‐Cell Non‐Hodgkin’s Lymphoma Development: A Transition from Immune‐Reactivity to Malignancy

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