Progress in clinical diagnosis and treatment of chronic active Epstein-Barr virus infection
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关键词:
- 慢性活动性EB病毒感染 /
- 诊断 /
- 治疗
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Key words:
- chronic active EBV infection /
- diagnosis /
- treatment
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表 1 CAEBV的三步疗法[21]
步骤 方案 第一步 目的:抑制活化的T、NK和巨噬细胞
方案:泼尼松龙0.5~2 mg/(kg·d)×7 d/周
依托泊苷150 mg/m2×1 d/周
环孢素3 mg/kg×2/d×7 d/周第二步 目的:尽可能消除EBV感染的T/NK细胞
一线方案:改良CHOP方案
长春新碱1.5 mg/m2
环磷酰胺750 mg/m2
吡柔比星25 mg/(m2·d)×2 d
泼尼松龙50 mg/(m2·d)×5 d
二线方案:ESCAP方案
依托泊苷150 mg/m2
阿糖胞苷1.5 g/m2×8次
左旋天冬酰胺酶6000 U/(m2·d)×5 d
甲泼尼龙62.5 mg/m2×2/d
泼尼松龙30 mg/(m2·d)×4 d第三步 HSCT -
[1] Kawamoto K, Miyoshi H, Suzuki T, et al. A distinct subtype of Epstein-Barr virus-positive T/NK-cell lymphoproliferative disorder: adult patients with chronic active Epstein-Barr virus infection-like features[J]. Haematologica, 2018, 103(6): 1018-1028. doi: 10.3324/haematol.2017.174177
[2] Nowalk A, Green M. Epstein-Barr Virus[J]. Microbiol Spectr, 2016, 4(3). doi:10.1128/microbiolspec.DMIH2-0011-2015.
[3] Taylor GS, Long HM, Brooks JM, et al. The immunology of Epstein-Barr virus-induced disease[J]. Annu Rev Immunol, 2015, 33: 787-821. doi: 10.1146/annurev-immunol-032414-112326
[4] Kimura H, Cohen JI. Chronic Active Epstein-Barr Virus Disease[J]. Front Immunol, 2017, 8: 1867. doi: 10.3389/fimmu.2017.01867
[5] Jiang L, Gu ZH, Yan ZX, et al. Exome sequencing identifies somatic mutations of DDX3X in natural killer/T-cell lymphoma[J]. Nat Genet, 2015, 47(9): 1061-1066. doi: 10.1038/ng.3358
[6] Jones JF, Shurin S, Abramowsky C, et al. T-cell lymphomas containing Epstein-Barr viral DNA in patients with chronic Epstein-Barr virus infections[J]. N Engl J Med, 1988, 318(12): 733-741. doi: 10.1056/NEJM198803243181203
[7] Okano M, Kawa K, Kimura H, et al. Proposed guidelines for diagnosing chronic active Epstein-Barr virus infection[J]. Am J Hematol, 2005, 80(1): 64-69. doi: 10.1002/ajh.20398
[8] 杨小舟, 杨清銮, 陈宇明, 等. 成人EB病毒感染相关性疾病的临床特征及预后分析[J]. 中华传染病杂志, 2021, 39(3): 163-167.
[9] Kimura H, Ito Y, Kawabe S, et al. EBV-associated T/NK-cell lymphoproliferative diseases in nonimmunocompromised hosts: prospective analysis of 108 cases[J]. Blood, 2012, 119(3): 673-686. doi: 10.1182/blood-2011-10-381921
[10] Collins PJ, Fox CP, George L, et al. Characterizing EBV-associated lymphoproliferative diseases and the role of myeloid-derived suppressor cells[J]. Blood, 2021, 137(2): 203-215. doi: 10.1182/blood.2020005611
[11] Swerdlow SH, Campo E, Pileri SA, et al. The 2016 revision of the World Health Organization classification of lymphoid neoplasms[J]. Blood, 2016, 127(20): 2375-2390. doi: 10.1182/blood-2016-01-643569
[12] Yonese I, Sakashita C, Imadome KI, et al. Nationwide survey of systemic chronic active EBV infection in Japan in accordance with the new WHO classification[J]. Blood Adv, 2020, 4(13): 2918-2926. doi: 10.1182/bloodadvances.2020001451
[13] Fryer JF, Heath AB, Wilkinson DE, et al. A collaborative study to establish the 1st WHO International Standard for Epstein-Barr virus for nucleic acid amplification techniques[J]. Biologicals, 2016, 44(5): 423-433. doi: 10.1016/j.biologicals.2016.04.010
[14] Yu S, Yang Q, Wu J, et al. Clinical application of Epstein-Barr virus DNA loads in Epstein-Barr virus-associated diseases: A cohort study[J]. J Infect, 2021, 82(1): 105-111. doi: 10.1016/j.jinf.2020.11.027
[15] Fournier B, Boutboul D, Bruneau J, et al. Rapid identification and characterization of infected cells in blood during chronic active Epstein-Barr virus infection[J]. J Exp Med, 2020, 217(11): e20192262. doi: 10.1084/jem.20192262
[16] Ghosh S, Köstel Bal S, Edwards ESJ, et al. Extended clinical and immunological phenotype and transplant outcome in CD27 and CD70 deficiency[J]. Blood, 2020, 136(23): 2638-2655. doi: 10.1182/blood.2020006738
[17] Kawa K, Sawada A, Sato M, et al. Excellent outcome of allogeneic hematopoietic SCT with reduced-intensity conditioning for the treatment of chronic active EBV infection[J]. Bone Marrow Transplant, 2011, 46(1): 77-83. doi: 10.1038/bmt.2010.122
[18] Dojcinov SD, Fend F, Quintanilla-Martinez L. EBV-Positive Lymphoproliferations of B- T- and NK-Cell Derivation in Non-Immunocompromised Hosts[J]. Pathogens, 2018, 7(1): 28. doi: 10.3390/pathogens7010028
[19] Arai A. Chronic Active Epstein-Barr Virus Infection: The Elucidation of the Pathophysiology and the Development of Therapeutic Methods[J]. Microorganisms, 2021, 9(1): 180. doi: 10.3390/microorganisms9010180
[20] Sawada A, Inoue M. Hematopoietic Stem Cell Transplantation for the Treatment of Epstein-Barr Virus-Associated T- or NK-Cell Lymphoproliferative Diseases and Associated Disorders[J]. Front Pediatr, 2018, 6: 334. doi: 10.3389/fped.2018.00334
[21] Sawada A, Inoue M, Kawa K. How we treat chronic active Epstein-Barr virus infection[J]. Int J Hematol, 2017, 105(4): 406-418. doi: 10.1007/s12185-017-2192-6
[22] Bollard CM, Cohen JI. How I treat T-cell chronic active Epstein-Barr virus disease[J]. Blood, 2018, 131(26): 2899-2905. doi: 10.1182/blood-2018-03-785931
[23] Cohen JI, Jaffe ES, Dale JK, et al. Characterization and treatment of chronic active Epstein-Barr virus disease: a 28-year experience in the United States[J]. Blood, 2011, 117(22): 5835-5849. doi: 10.1182/blood-2010-11-316745
[24] Savoldo B, Huls MH, Liu Z, et al. Autologous Epstein-Barr virus(EBV)-specific cytotoxic T cells for the treatment of persistent active EBV infection[J]. Blood, 2002, 100(12): 4059-4066. doi: 10.1182/blood-2002-01-0039
[25] Onozawa E, Shibayama H, Takada H, et al. STAT3 is constitutively activated in chronic active Epstein-Barr virus infection and can be a therapeutic target[J]. Oncotarget, 2018, 9(57): 31077-31089. doi: 10.18632/oncotarget.25780
[26] Albeituni S, Verbist KC, Tedrick PE, et al. Mechanisms of action of ruxolitinib in murine models of hemophagocytic lymphohistiocytosis[J]. Blood, 2019, 134(2): 147-159. doi: 10.1182/blood.2019000761
[27] Jin Z, Wang Y, Wang J, et al. Long-term survival benefit of ruxolitinib in a patient with relapsed refractory chronic active Epstein-Barr virus[J]. Ann Hematol, 2019, 98(8): 2003-2004. doi: 10.1007/s00277-019-03647-5
[28] Song Y, Wang J, Wang Y, et al. Ruxolitinib in Patients With Chronic Active Epstein-Barr Virus Infection: A Retrospective, Single-Center Study[J]. Front Pharmacol, 2021, 12: 710400. doi: 10.3389/fphar.2021.710400
[29] Bi XW, Wang H, Zhang WW, et al. PD-L1 is upregulated by EBV-driven LMP1 through NF-κB pathway and correlates with poor prognosis in natural killer/T-cell lymphoma[J]. J Hematol Oncol, 2016, 9(1): 109. doi: 10.1186/s13045-016-0341-7
[30] Kwong YL, Chan TSY, Tan D, et al. PD1 blockade with pembrolizumab is highly effective in relapsed or refractory NK/T-cell lymphoma failing l-asparaginase[J]. Blood, 2017, 129(17): 2437-2442. doi: 10.1182/blood-2016-12-756841
[31] Liu P, Pan X, Chen C, et al. Nivolumab treatment of relapsed/refractory Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis in adults[J]. Blood, 2020, 135(11): 826-833. doi: 10.1182/blood.2019003886
[32] Kanazawa T, Hiramatsu Y, Iwata S, et al. Anti-CCR4 monoclonal antibody mogamulizumab for the treatment of EBV-associated T- and NK-cell lymphoproliferative diseases[J]. Clin Cancer Res, 2014, 20(19): 5075-5084. doi: 10.1158/1078-0432.CCR-14-0580
[33] Xue W, Zhang M. Updating targets for natural killer/T-cell lymphoma immunotherapy[J]. Cancer Biol Med, 2021, 18(1): 52-62. doi: 10.20892/j.issn.2095-3941.2020.0400