Characterization of the humoral immune response to the EBV proteome in extranodal NK/T-cell lymphoma

Liu, Zhiwei; Sarathkumara, Yomani D.; Chan, John K.; Kwong, Yok–Lam; Lam, Tai Hing; Ip, Dennis Kai Ming; Chiu, Brian C.‐H.; Xu, Jun; Su, Yu-Chieh; Proietti, Carla; Cooper, Martha M; Yu, Kelly J.; Bassig, Bryan A.; Liang, Raymond; Hu, Wei; Ji, Bu‐Tian; Coghill, Anna E.; Pfeiffer, Ruth M.; Hildesheim, Allan; Rothman, Nathaniel; Doolan, Denise L.; Lan, Qing

doi:10.1038/s41598-021-02788-w

Cited by 6 publications

(9 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast with other EBV-associated tumors, anti-EBNA-1 IgG were not elevated in cases of ENKTL [ 108 , 109 ]. A high level of antibodies against EBNA-3A, BZLF-1, and BPLF-1 antigens was detected in ENKTL patients using a multiplex strategy exploring the entire EBV proteome [ 109 ]. High anti-EA IgA and anti-VCA IgA levels could thus be related to an adverse ENKTL profile and correlated with poor treatment response, early relapse, and poor prognosis in this population [ 108 ].…”

Section: Ebv-associated Malignanciesmentioning

confidence: 95%

“…The humoral immune response against EBV in ENKTL patients has been poorly explored to date. Studies revealed high antibody levels against VCA and EA antigens in patients with ENKTL [ 108 , 109 ]. In contrast with other EBV-associated tumors, anti-EBNA-1 IgG were not elevated in cases of ENKTL [ 108 , 109 ].…”

Section: Ebv-associated Malignanciesmentioning

confidence: 99%

“…Studies revealed high antibody levels against VCA and EA antigens in patients with ENKTL [ 108 , 109 ]. In contrast with other EBV-associated tumors, anti-EBNA-1 IgG were not elevated in cases of ENKTL [ 108 , 109 ]. A high level of antibodies against EBNA-3A, BZLF-1, and BPLF-1 antigens was detected in ENKTL patients using a multiplex strategy exploring the entire EBV proteome [ 109 ].…”

Section: Ebv-associated Malignanciesmentioning

confidence: 99%

See 2 more Smart Citations

Virological Markers in Epstein–Barr Virus-Associated Diseases

Lupo

Truffot

Andréani

et al. 2023

Viruses

View full text Add to dashboard Cite

Epstein–Barr virus (EBV) is an oncogenic virus infecting more than 95% of the world’s population. After primary infection—responsible for infectious mononucleosis in young adults—the virus persists lifelong in the infected host, especially in memory B cells. Viral persistence is usually without clinical consequences, although it can lead to EBV-associated cancers such as lymphoma or carcinoma. Recent reports also suggest a link between EBV infection and multiple sclerosis. In the absence of vaccines, research efforts have focused on virological markers applicable in clinical practice for the management of patients with EBV-associated diseases. Nasopharyngeal carcinoma is an EBV-associated malignancy for which serological and molecular markers are widely used in clinical practice. Measuring blood EBV DNA load is additionally, useful for preventing lymphoproliferative disorders in transplant patients, with this marker also being explored in various other EBV-associated lymphomas. New technologies based on next-generation sequencing offer the opportunity to explore other biomarkers such as the EBV DNA methylome, strain diversity, or viral miRNA. Here, we review the clinical utility of different virological markers in EBV-associated diseases. Indeed, evaluating existing or new markers in EBV-associated malignancies or immune-mediated inflammatory diseases triggered by EBV infection continues to be a challenge.

show abstract

Section: Ebv-associated Malignanciesmentioning

confidence: 95%

Section: Ebv-associated Malignanciesmentioning

confidence: 99%

Section: Ebv-associated Malignanciesmentioning

confidence: 99%

See 1 more Smart Citation

Virological Markers in Epstein–Barr Virus-Associated Diseases

Lupo

Truffot

Andréani

et al. 2023

Viruses

View full text Add to dashboard Cite

show abstract

“…Interestingly, high level of antibodies against the proteins EBNA3A, BZLF1, BALF2, BMRF1, BVRF and BPLF1 (but not against EBNA1) have been detected in patients with ENKTCL ( 119 ), suggesting some degree of viral replication in these patients. The usefulness of these findings in the clinical management of ENKTCL is not yet established.…”

Section: A Possible Role Of Ebv In the Oncogenesis Of Enktcl And Nktclmentioning

confidence: 99%

Contribution of the Epstein-Barr virus to the oncogenesis of mature T-cell lymphoproliferative neoplasms

Barros,

Alves

2023

Front. Oncol.

View full text Add to dashboard Cite

EBV is a lymphotropic virus, member of the Herpesviridae family that asymptomatically infects more than 90% of the human population, establishing a latent infection in memory B cells. EBV exhibits complex survival and persistence dynamics, replicating its genome through the proliferation of infected B cells or production of the lytic virions. Many studies have documented the infection of T/NK cells by EBV in healthy individuals during and after primary infection. This feature has been confirmed in humanized mouse models. Together these results have challenged the hypothesis that the infection of T/NK cells per se by EBV could be a triggering event for lymphomagenesis. Extranodal NK/T-cell lymphoma (ENKTCL) and Epstein-Barr virus (EBV)-positive nodal T- and NK-cell lymphoma (NKTCL) are two EBV-associated lymphomas of T/NK cells. These two lymphomas display different clinical, histological and molecular features. However, they share two intriguing characteristics: the association with EBV and a geographical prevalence in East Asia and Latin America. In this review we will discuss the genetic characteristics of EBV in order to understand the possible role of this virus in the oncogenesis of ENKTCL and NKTCL. In addition, the main immunohistological, molecular, cytogenetic and epigenetic differences between ENKTCL and NKTCL will be discussed, as well as EBV differences in latency patterns and other viral molecular characteristics.

show abstract

“…The first human oncovirus to be described was EBV, following the discovery of viral particles in cultured lymphoblasts from Burkitt lymphoma (BL) in 1964 6 . Since then, EBV has been linked to a wide array of both hematological and solid tumors, including Hodgkin lymphoma (HL) (20-50% of cases 7 ), other B and T cell lymphomas (such as plasmablastic lymphoma [PBL], extranodal NK T-cell lymphomas [NKTCL], and primary central nervous system lymphoma [PCNSL] in immune-suppressed patients, each in 70-100% of cases 8–10 ), gastric cancer (GC) (8.7% of cases 11 ), and nasopharyngeal carcinoma (NPC) (100% of cases 12 ), summing to approximately 1% of all cancers 3 . It has also been suggested that EBV may be associated to B-cell lymphomagenesis more widely than currently acknowledged, possibly via a “hit and run” mechanism 13 .…”

Section: Introductionmentioning

confidence: 99%

Genomic landscape of virus-associated cancers

Gómez

Schiavoni

Nam

et al. 2023

Preprint

View full text Add to dashboard Cite

It has been estimated that 15%-20% of human cancers are attributable to infections, mostly by carcinogenic viruses. The incidence varies worldwide, with a majority affecting developing countries. Here, we present a comparative analysis of virus-positive and virus-negative tumors in nine cancers linked to five viruses. We find that virus-positive tumors occur more frequently in males and show geographical disparities in incidence. Genomic analysis of 1,658 tumors reveals virus-positive tumors exhibit distinct mutation signatures and driver gene mutations and possess a lower somatic mutation burden compared to virus-negative tumors of the same cancer type. For example, compared to the respective virus-negative counterparts, virus-positive cases across different cancer histologies had less often mutations of TP53 and deletions of 9p21.3/CDKN2A-CDKN1A; Epstein-Barr virus-positive (EBV+) gastric cancer had more frequent mutations of EIF4A1 and ARID1A and less marked mismatch repair deficiency signatures; and EBV-positive cHL had fewer somatic genetic lesions of JAK-STAT, NF-κB, PI3K-AKT and HLA-I genes and a less pronounced activity of the aberrant somatic hypermutation signature. In cHL, we also identify germline homozygosity in HLA class I as a potential risk factor for the development of EBV-positive Hodgkin lymphoma. Finally, an analysis of clinical trials of PD-(L)1 inhibitors in four virus-associated cancers suggested an association of viral infection with higher response rate in patients receiving such treatments, which was particularly evident in gastric cancer and head and neck squamous cell carcinoma. These results illustrate the epidemiological, genetic, prognostic, and therapeutic trends across virus-associated malignancies.

show abstract

Characterization of the humoral immune response to the EBV proteome in extranodal NK/T-cell lymphoma

Cited by 6 publications

References 38 publications

Virological Markers in Epstein–Barr Virus-Associated Diseases

Virological Markers in Epstein–Barr Virus-Associated Diseases

Contribution of the Epstein-Barr virus to the oncogenesis of mature T-cell lymphoproliferative neoplasms

Genomic landscape of virus-associated cancers

Contact Info

Product

Resources

About