Pathogenic Role of Epstein–Barr Virus in Lung Cancers

Becnel, David; Abdelghani, Ramsy; Nanbo, Asuka; Janardhan, Avilala; Kahn, Jacob; Li, Li; Lin, Zhen

doi:10.3390/v13050877

Cited by 17 publications

(19 citation statements)

References 112 publications

(153 reference statements)

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“…The fact that tobacco smoke components can provide such alterations, including p16 loss [163] and cyclin D1 overexpression [164], suggests that EBV latency establishment may be favored in the lung cells of smoker subjects. This possibility is compatible with the model established by Becnel et al, who proposed that pro-tumor signals such as chronic inflammation result in dysplastic lesions, supporting EBV infection and maintenance of type II latency in the lung epithelia [22]. Considering that tobacco smoke is a frequent cause of the chronic obstructive pulmonary disease (COPD) that is caused by chronic inflammation [165], we suggest that tobacco smoke is a factor potentially leading to EBV latency establishment in lung cells.…”

Section: Epidemiology Of Ebv In Lung Cancersupporting

confidence: 91%

“…Viral infections have been proposed to be involved in LC, namely, high-risk human papillomaviruses (HR-HPVs) [18], Merkel cell polyomavirus (MCPyV) [19], Jaagsiekte Sheep Retrovirus (JSRV) [20], John Cunningham Virus (JCV) [21], and Epstein-Barr virus (EBV) [22]. EBV is an exclusive human virus (without an animal reservoir) present in ~95% of the human population and establishing persistent infections during the lifetime [23].…”

Section: Introductionmentioning

confidence: 99%

“…EBV preferentially infects both B cells and epithelial cells [24] and is characterized as a class I carcinogen [25]. Epidemiological evidence suggests that EBV is present in a relatively small subset of LCs [22], with demographic variations, though an etiological relationship remains inconclusive. In this review, we address the epidemiological and mechanistic evidence regarding a potential role of EBV in this malignancy.…”

Section: Introductionmentioning

confidence: 99%

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Epstein–Barr Virus Infection in Lung Cancer: Insights and Perspectives

et al. 2022

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Lung cancer (LC) is the leading cause of cancer death worldwide. Tobacco smoke is the most frequent risk factor etiologically associated with LC, although exposures to other environmental factors such as arsenic, radon or asbestos are also involved. Additionally, the involvement of some viral infections such as high-risk human papillomaviruses (HR-HPVs), Merkel cell polyomavirus (MCPyV), Jaagsiekte Sheep Retrovirus (JSRV), John Cunningham Virus (JCV), and Epstein–Barr virus (EBV) has been suggested in LC, though an etiological relationship has not yet been established. EBV is a ubiquitous gamma herpesvirus causing persistent infections and some lymphoid and epithelial tumors. Since EBV is heterogeneously detected in LCs from different parts of the world, in this review we address the epidemiological and experimental evidence of a potential role of EBV. Considering this evidence, we propose mechanisms potentially involved in EBV-associated lung carcinogenesis. Additional studies are warranted to dissect the role of EBV in this very frequent malignancy.

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Section: Epidemiology Of Ebv In Lung Cancersupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Epstein–Barr Virus Infection in Lung Cancer: Insights and Perspectives

et al. 2022

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“…However, immunosuppression accompanying acquired immune deficiency syndrome (AIDS) or transplantation treatment favors EBV-driven fatal lymphoproliferative disease [21,25]. Moreover, EBV may contribute to the development of several malignancies, such as B cell lymphomas (i.e., Burkitt's lymphoma (BL) [27][28][29][30][31], Hodgkin's lymphoma (HL) [32,33], and diffuse large B-cell lymphoma (DLBCL) [34][35][36]), lung carcinoma (LC) [37][38][39], gastric cancer (GC) [40][41][42], nasopharyngeal carcinoma (NPC) [43][44][45], T cell lymphoma [46], T/NK cell lymphoma (NKTL) [47,48], and AIDS-related primary central nervous system lymphoma (AR-PCNSL) [49]. EBV has also been detected in the saliva of patients with systemic lupus erythematosus (SLE), and found to be associated with one of its symptoms (i.e., oral lesions) [50].…”

Section: Ebv and Its Pathogenicitymentioning

confidence: 99%

Virus-Mediated Inhibition of Apoptosis in the Context of EBV-Associated Diseases: Molecular Mechanisms and Therapeutic Perspectives

Wyżewski

Mielcarska

Gregorczyk-Zboroch

et al. 2022

IJMS

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Epstein-Barr virus (EBV), the representative of the Herpesviridae family, is a pathogen extensively distributed in the human population. One of its most characteristic features is the capability to establish latent infection in the host. The infected cells serve as a sanctuary for the dormant virus, and therefore their desensitization to apoptotic stimuli is part of the viral strategy for long-term survival. For this reason, EBV encodes a set of anti-apoptotic products. They may increase the viability of infected cells and enhance their resistance to chemotherapy, thereby contributing to the development of EBV-associated diseases, including Burkitt’s lymphoma (BL), Hodgkin’s lymphoma (HL), gastric cancer (GC), nasopharyngeal carcinoma (NPC) and several other malignancies. In this paper, we have described the molecular mechanism of anti-apoptotic actions of a set of EBV proteins. Moreover, we have reviewed the pro-survival role of non-coding viral transcripts: EBV-encoded small RNAs (EBERs) and microRNAs (miRNAs), in EBV-carrying malignant cells. The influence of EBV on the expression, activity and/or intracellular distribution of B-cell lymphoma 2 (Bcl-2) protein family members, has been presented. Finally, we have also discussed therapeutic perspectives of targeting viral anti-apoptotic products or their molecular partners.

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“…Epidemiologically, EBV infects 95% of individuals worldwide, and currently, the extent of the pathological burden is highest, with EBV causally linked to 200,000 cases of cancer each year and approximately 1.8% of total cancer-related deaths annually. 1 2 3 However, these numbers—although already impressive in themselves—define only a minimal part of the risks that might associate with EBV infection. Indeed, EBV is ubiquitous in the human population, mainly as an asymptomatic, harmless, latent infection, with only occasional reactivation, which is the harbinger of the EBV-related diseases.…”

Section: Introductionmentioning

confidence: 99%

The Role of Codon Usage, tRNA Availability, and Cell Proliferation in EBV Latency and (Re)Activation

Kanduc

2022

Glob Med Genet

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Epstein–Barr nuclear antigen 1 (EBNA1) protein synthesis is inhibited during Epstein–Barr virus (EBV) latency and is resumed in EBV (re)activation. In analyzing the molecular mechanisms underpinning the translation of EBNA1 in the human host, this article deals with two orders of data. First, it shows that the heavily biased codon usage of the EBNA1 open reading frame cannot be translated due to its noncompliance with the human codon usage pattern and the corresponding tRNA pool. The EBNA1 codon bias resides in the sequence composed exclusively of glycine and alanine, i.e., the Gly-Ala repeat (GAR). Removal of the nucleotide sequence coding for GAR results in an EBNA1 codon usage pattern with a lower codon bias, thus conferring translatability to EBNA1. Second, the data bring cell proliferation to the fore as a conditio sine qua non for qualitatively and quantitatively modifying the host's tRNA pool as required by the translational needs of EBNA1, thus enabling viral reactivation. Taken together, the present work provides a biochemical mechanism for the pathogen's shift from latency to (re)activation and confirms the role of human codon usage as a first-line tool of innate immunity in inhibiting pathogens' expression. Immunologically, this study cautions against using codon optimization and proliferation-inducing substances such as glucocorticoids and adjuvants, which can (re)activate the otherwise quiescent, asymptomatic, and innocuous EBV infection. Lastly, the data pose the question whether the causal pathogenic role attributed to EBV should instead be ascribed to the carcinogenesis-associated cellular proliferation.

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Pathogenic Role of Epstein–Barr Virus in Lung Cancers

Cited by 17 publications

References 112 publications

Epstein–Barr Virus Infection in Lung Cancer: Insights and Perspectives

Epstein–Barr Virus Infection in Lung Cancer: Insights and Perspectives

Virus-Mediated Inhibition of Apoptosis in the Context of EBV-Associated Diseases: Molecular Mechanisms and Therapeutic Perspectives

The Role of Codon Usage, tRNA Availability, and Cell Proliferation in EBV Latency and (Re)Activation

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