Cytopathic effects induced by Epstein-Barr virus replication in epithelial nasopharyngeal carcinoma hybrid cells

Sato, Hiroshi; Takimoto, Toru; Tanaka, Saichiro; Ogura, Hisashi; Shiraishi, Kazunori; Tanaka, Junji

doi:10.1128/jvi.63.8.3555-3559.1989

Cited by 11 publications

(6 citation statements)

References 20 publications

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“…In addition, increased volume and pronounced multinucleation with cells counting more than 12 nuclei were reported in a nasal mucosal neoplasm infected with EBV ( 40 ). Furthermore, EBV replication in epithelial NPC hybrid cells induced the formation of multinucleated giant cells ( 41 ). B cell infection with an EBV strain isolated from a nasopharyngeal carcinoma, predisposed to polyploidy with cells displaying several micronuclei or containing a single large polyploid nucleus ( 42 ).…”

Section: Introductionmentioning

confidence: 99%

Polyploid Giant Cancer Cells, a Hallmark of Oncoviruses and a New Therapeutic Challenge

Herbein

Nehme

2020

Front. Oncol.

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Tumors are renowned as intricate systems that harbor heterogeneous cancer cells with distinctly diverse molecular signatures, sizes and genomic contents. Among those various genomic clonal populations within the complex tumoral architecture are the polyploid giant cancer cells (PGCC). Although described for over a century, PGCC are increasingly being recognized for their prominent role in tumorigenesis, metastasis, therapy resistance and tumor repopulation after therapy. A shared characteristic among all tumors triggered by oncoviruses is the presence of polyploidy. Those include Human Papillomaviruses (HPV), Epstein Barr Virus (EBV), Hepatitis B and C viruses (HBV and HCV, respectively), Human T-cell lymphotropic virus-1 (HTLV-1), Kaposi's sarcoma herpesvirus (KSHV) and Merkel polyomavirus (MCPyV). Distinct viral proteins, for instance Tax for HTLV-1 or HBx for HBV have demonstrated their etiologic role in favoring the appearance of PGCC. Different intriguing biological mechanisms employed by oncogenic viruses, in addition to viruses with high oncogenic potential such as human cytomegalovirus, could support the generation of PGCC, including induction of endoreplication, inactivation of tumor suppressors, development of hypoxia, activation of cellular senescence and others. Interestingly, chemoresistance and radioresistance have been reported in the context of oncovirus-induced cancers, for example KSHV and EBV-associated lymphomas and high-risk HPV-related cervical cancer. This points toward a potential linkage between the previously mentioned players and highlights PGCC as keystone cancer cells in virally-induced tumors. Subsequently, although new therapeutic approaches are actively needed to fight PGCC, attention should also be drawn to reveal the relationship between PGCC and oncoviruses, with the ultimate goal of establishing effective therapeutic platforms for treatment of virus-associated cancers. This review discusses the presence of PGCCs in tumors induced by oncoviruses, biological mechanisms potentially favoring their appearance, as well as their consequent implication at the clinical and therapeutic level.

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Section: Introductionmentioning

confidence: 99%

Polyploid Giant Cancer Cells, a Hallmark of Oncoviruses and a New Therapeutic Challenge

Herbein

Nehme

2020

Front. Oncol.

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“…EBV infects a variety of epithelial cells [32][33][34], and JCV infects renal tubular epithelial cells [3,35]. Epithelial cells, lytically infected with EBVl including nasopharyngeal cells, can fuse [36] The proximity of these cells to tonsillar cells harboring JCV [31,37] provides a potential mechanism for transfer of recombinant JCV among cell types. Nanbo and colleagues [34] have described cell-to-cell contact-mediated EBV transmission.…”

Section: Discussionmentioning

confidence: 99%

“…Under the right circumstances, EBV can mediate cell fusion and syncytium formation [36,40,41]. Glial cells transfected with an EBV-based CD4 expression vector have been observed to undergo fusion [42].…”

Section: Discussionmentioning

confidence: 99%

Opportunistic DNA Recombination With Epstein-Barr Virus at Sites of Control Region Rearrangements Mediating JC Virus Neurovirulence

et al. 2015

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We document a unique DNA recombination between polyomavirus JC (JC virus [JCV]) and Epstein-Barr virus (EBV) at sequences of JCV found infecting the brain. Archetype JCV is present in bone marrow and uroepithelial cells of most adults. During immunosuppression, JCV can infect the brain, causing a demyelinating disease, progressive multifocal leukoencephalopathy. Rearrangements in the archetype noncoding control region are necessary for neurovirulence. Two NCCR deletions and a duplication occur at sequences of homology with EBV, present latently in B cells, which may be coinfected with both viruses. Recombination between JCV and EBV occurs in B lymphoblasts at a sequence essential for JCV neurovirulence and in cerebrospinal fluid of immunosuppressed patients with multiple sclerosis, those susceptible to progressive multifocal leukoencephalopathy. Interviral recombination is a model for conferring advantages on JCV in the brain. It can alter a critical noncoding control region sequence and potentially facilitate use of EBV DNA abilities to transfer among different cell types.

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“…Desquamated epithelial cells, some of which are big and contain syncytial nuclei, are seen in the alveolar cavities of SARS-CoV-2 patients [ 11 ]. The cytopathogenic impact of viral replication in cells is mediated via the syncytial nuclei [ 12 ]. SARS-CoV-2 infection is thought to reduce ACE-2 receptor activation because viruses competitively bind to these receptors, rendering them less useful.…”

Section: Influence On Host Immunity Of Coinfection Of Covid-19 Along ...mentioning

confidence: 99%

Cellular Landscaping of COVID-19 and Gynaecological Cancers: An Infrequent Correlation

Bhattacharjee

Das

Bhadhuri

et al. 2022

Journal of Oncology

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COVID-19 resulted in a mortality rate of 3–6% caused by SARS-CoV-2 and its variant leading to unprecedented consequences of acute respiratory distress septic shock and multiorgan failure. In such a situation, evaluation, diagnosis, treatment, and care for cancer patients are difficult tasks faced by medical staff. Moreover, patients with gynaecological cancer appear to be more prone to severe infection and mortality from COVID-19 due to immunosuppression by chemotherapy and coexisting medical disorders. To deal with such a circumtances oncologists have been obliged to reconsider the entire diagnostic, treatment, and management approach. This review will provide and discuss the molecular link with gynaecological cancer under COVID-19 infection, providing a novel bilateral relationship between the two infections. Moreover, the authors have provided insights to discuss the pathobiology of COVID-19 in gynaecological cancer and their risks associated with such comorbidity. Furthermore, we have depicted the overall impact of host immunity along with guidelines for the treatment of patients with gynaecological cancer under COVID-19 infection. We have also discussed the feasible scope for the management of COVID-19 and gynaecological cancer.

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Cytopathic effects induced by Epstein-Barr virus replication in epithelial nasopharyngeal carcinoma hybrid cells

Cited by 11 publications

References 20 publications

Polyploid Giant Cancer Cells, a Hallmark of Oncoviruses and a New Therapeutic Challenge

Polyploid Giant Cancer Cells, a Hallmark of Oncoviruses and a New Therapeutic Challenge

Opportunistic DNA Recombination With Epstein-Barr Virus at Sites of Control Region Rearrangements Mediating JC Virus Neurovirulence

Cellular Landscaping of COVID-19 and Gynaecological Cancers: An Infrequent Correlation

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