دورية أكاديمية
أعرض في EDS

Targeting latent viral infection in EBV-associated lymphomas.

التفاصيل البيبلوغرافية
العنوان: Targeting latent viral infection in EBV-associated lymphomas.
المؤلفون: Kong IY; Weill Cornell Medical College, New York, NY, United States., Giulino-Roth L; Weill Cornell Medical College, New York, NY, United States.
المصدر: Frontiers in immunology [Front Immunol] 2024 Feb 23; Vol. 15, pp. 1342455. Date of Electronic Publication: 2024 Feb 23 (Print Publication: 2024).
نوع المنشور: Journal Article; Review; Research Support, Non-U.S. Gov't; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: Frontiers Research Foundation] Country of Publication: Switzerland NLM ID: 101560960 Publication Model: eCollection Cited Medium: Internet ISSN: 1664-3224 (Electronic) Linking ISSN: 16643224 NLM ISO Abbreviation: Front Immunol Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [Lausanne : Frontiers Research Foundation]
مواضيع طبية MeSH: Epstein-Barr Virus Infections*/complications , Burkitt Lymphoma*/pathology , Lymphoma, Large B-Cell, Diffuse*/pathology , Latent Infection*, Humans ; Herpesvirus 4, Human ; Virus Latency ; Viral Proteins/genetics
مستخلص: Epstein-Barr virus (EBV) contributes to the development of a significant subset of human lymphomas. As a herpes virus, EBV can transition between a lytic state which is required to establish infection and a latent state where a limited number of viral antigens are expressed which allows infected cells to escape immune surveillance. Three broad latency programs have been described which are defined by the expression of viral proteins RNA, with latency I being the most restrictive expressing only EBV nuclear antigen 1 (EBNA1) and EBV-encoded small RNAs (EBERs) and latency III expressing the full panel of latent viral genes including the latent membrane proteins 1 and 2 (LMP1/2), and EBNA 2, 3, and leader protein (LP) which induce a robust T-cell response. The therapeutic use of EBV-specific T-cells has advanced the treatment of EBV-associated lymphoma, however this approach is only effective against EBV-associated lymphomas that express the latency II or III program. Latency I tumors such as Burkitt lymphoma (BL) and a subset of diffuse large B-cell lymphomas (DLBCL) evade the host immune response to EBV and are resistant to EBV-specific T-cell therapies. Thus, strategies for inducing a switch from the latency I to the latency II or III program in EBV+ tumors are being investigated as mechanisms to sensitize tumors to T-cell mediated killing. Here, we review what is known about the establishment and regulation of latency in EBV infected B-cells, the role of EBV-specific T-cells in lymphoma, and strategies to convert latency I tumors to latency II/III.
Competing Interests: LG-R: consultant for Merck, Roche; research funds from Seagen. The remaining author declare that the research was conducted in the absence of any commercial or financial relationships that could be constructed as a potential conflict of interest.
(Copyright © 2024 Kong and Giulino-Roth.)
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معلومات مُعتمدة: R37 CA262517 United States CA NCI NIH HHS; U01 CA275301 United States CA NCI NIH HHS
فهرسة مساهمة: Keywords: EBNA2; EBNA3; LMP1; T-cell; ebv; latency; lymphoma
المشرفين على المادة: 0 (Viral Proteins)
تواريخ الأحداث: Date Created: 20240311 Date Completed: 20240312 Latest Revision: 20240515
رمز التحديث: 20240515
مُعرف محوري في PubMed: PMC10920267
DOI: 10.3389/fimmu.2024.1342455
PMID: 38464537
قاعدة البيانات: MEDLINE
الوصف
تدمد:1664-3224
DOI:10.3389/fimmu.2024.1342455