Recent advances in understanding Epstein-Barr virus

Stanfield, Brent; Luftig, Micah A.

doi:10.12688/f1000research.10591.1

Cited by 61 publications

(51 citation statements)

References 76 publications

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“…Epstein-Barr virus (EBV), also known as human herpesvirus 4, is a gammaherpesvirus that infects the majority of the world's population [1]. EBV is also associated with the development of certain malignancies, including African Burkitt lymphomas, B-cell lymphomas of immunocompromised patients, nasopharyngeal carcinomas, Hodgkin's disease, and occasionally with T-cell lymphomas and gastric cancers [2].…”

Section: Introductionmentioning

confidence: 99%

Characterization of the Nucleocytoplasmic Transport Mechanisms of Epstein-Barr Virus BFLF2

Chen

Zou

et al. 2018

Cell Physiol Biochem

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Background/Aims: Epstein-Barr virus (EBV) BFLF2, the homologue of herpes simplex virus 1 (HSV-1) UL31, is crucial for the efficient viral DNA packaging and primary egress across the nuclear membrane. However, we still do not know its subcellular transport mechanisms. Methods: Interspecies heterokaryon assays were utilized to detect the nucleocytoplasmic shuttling of BFLF2, and mutation analysis, plasmid transfection and fluorescence microscopy assays were performed to identify the functional nuclear localization sequence (NLS) and nuclear export sequence (NES) of BFLF2 in live cells. Furthermore, the nuclear import and export of BFLF2 were assessed by confocal microscopy, co-immunoprecipitation and immunoblot assays. Results: BFLF2 was confirmed to shuttle between the nucleus and cytoplasm. Two predicted NESs were shown to be nonfunctional, yet we proved that the nuclear export of BFLF2 was mediated through transporter associated with antigen processing (TAP), but not chromosomal region maintenance 1 (CRM1) dependent pathway. Furthermore, one functional NLS, ²²RRLMHPHHRNYTASKASAH⁴⁰, was identified, and the aa22-23, aa22-25, aa28-30 and aa37-40 had an important role in the nuclear localization of BFLF2. Besides, the nuclear import of BFLF2 was demonstrated through Ran-, importin α7-, importin β1- and transportin-1-dependent mechanism that does not require importin α1, α3 and α5. Conclusion: These works are of significance for the further study of the functions of BFLF2 during EBV infection, as well as for further insights into the design of new antiviral drug target and vaccine development against EBV.

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Section: Introductionmentioning

confidence: 99%

Characterization of the Nucleocytoplasmic Transport Mechanisms of Epstein-Barr Virus BFLF2

Chen

Zou

et al. 2018

Cell Physiol Biochem

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“…The immune regulation of EBV is mainly mediated by T cells. Once infected, antigen peptides combine with MHC1 molecules and are expressed on the surface of target cells [25]. Under auxiliary adhesion molecules, the antigen polypeptide can be recognized and combined by T cell receptor on the surface of CTLS, which gradually induces the production of toxic protein that ultimately kills the target cells.…”

Section: Discussionmentioning

confidence: 99%

Epstein Barr Virus Infection Affects Function of Cytotoxic T Lymphocytes in Patients with Severe Aplastic Anemia

Zhang

Liu

et al. 2018

BioMed Research International

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Severe aplastic anemia (SAA) is characterized by pancytopenia and failure of hematopoietic function and is caused by excessive functioning of cytotoxic T lymphocytes (CTLs). EBNA-1, a nucleoprotein of the Epstein Barr virus (EBV), can influence the proliferation and function of lymphocytes. We therefore tested the number of EBV copies in the CD8+ T cells of 27 patients with SAA and 10 healthy control subjects and observed the influences of EBNA-1 upon the CD8+ T cells of patients with SAA. The results showed that more EBV copies were found in the CD8+ T cells of patients with untreated SAA than in patients with SAA in remission or in the healthy control subjects. Their copy number was positively correlated with the expression of granzyme B and perforin, the secretion level of interferon-γ in CD8+ T cells, and the viability of CD8+ T cells, whereas no correlation was seen between the copy number and the interleukin 4 secretion level or the apoptosis rate. Meanwhile, the expression of granzyme B and perforin was reduced after EBNA-1 gene knockdown, whereas the interferon-γ secretion level and cell viability declined. Therefore, we infer that EBV infection may be a factor in the activation of CTLs and in damaging the bone marrow hematopoietic function of patients with SAA.

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“…While childhood infection with EBV is usually symptomless or indistinguishable from other mild, brief childhood illnesses, its manifestation during adolescence as infectious mononucleosis may present more severe and partly long-lasting symptoms. 85,86 EBV is also associated with specific forms of cancer, including both hematologic and epithelial malignancies, and it is estimated that worldwide over 200,000 cancer cases and up to 2% of cancer-related deaths per year may be attributed to infection with the virus. 87,88 EBV infection occurs by oral transfer of saliva, and genital secretions.…”

Section: Biological Background Of Ebv Infection In Gastrointestinal Cmentioning

confidence: 99%

Risk factors for esophageal cancer: emphasis on infectious agents

El‐Zimaity

Pilato

Ringressi

et al. 2018

Annals of the New York Academy of Sciences

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Risk factors for esophageal cancer include genetic factors (such as tylosis) and infectious agents. A variety of organisms have been implicated in esophageal carcinogenesis, either directly or indirectly. In this review, we explore the normal esophageal flora and how it may be controlled, and also the variety of organisms that may affect esophageal carcinogenesis, either directly or indirectly. The organisms with potential direct effects in squamous cell carcinoma include human papillomavirus (HPV), Epstein-Barr virus, and polyoma viruses. Interestingly, HPV is now implicated in esophageal adenocarcinoma (EAC), not in its initiation but in the development of dysplasia, in which HPV33 in particular has been associated. Indirectly, Helicobacter pylori has been associated with EAC by, initially, causing increased acid secretion that increases acid reflux, and by reducing lower esophageal sphincter pressure, which increases gastroesophageal reflux; the latter increases the risk of Barrett's esophagus, and hence EAC. Conversely, subsequent atrophic gastritis may normalize that risk.

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Recent advances in understanding Epstein-Barr virus

Cited by 61 publications

References 76 publications

Characterization of the Nucleocytoplasmic Transport Mechanisms of Epstein-Barr Virus BFLF2

Characterization of the Nucleocytoplasmic Transport Mechanisms of Epstein-Barr Virus BFLF2

Epstein Barr Virus Infection Affects Function of Cytotoxic T Lymphocytes in Patients with Severe Aplastic Anemia

Risk factors for esophageal cancer: emphasis on infectious agents

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