Grützmeier Sven, Porwit Anna, Schmitt Corinna, Sandström Eric, Åkerlund Börje, Ernberg Ingemar
Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institute, Box 280, Stockholm, SE- 17177 Sweden ; Department of Infectious diseases/Venhälsan, Stockholm South General Hospital, Sjukhusbacken 14, SE-11883 Stockholm, Sweden.
Department of Oncology/Pathology, Karolinska Institutet, SE- 17177 Stockholm, Sweden ; Present address: Department of Laboratory Hematology, Laboratory Medicine Program, University Health Network, Toronto, ON Canada.
Infect Agent Cancer. 2016 Aug 22;11:46. doi: 10.1186/s13027-016-0094-5. eCollection 2016.
Most malignant lymphomas in HIV-patients are caused by reactivation of EBV-infection. Some lymphomas have a very rapid fulminant course. HHV-8 has also been reported to be a cause of lymphoma. The role of CMV in the development of lymphoma is not clear, though both CMV and HHV-8 have been reported in tissues adjacent to the tumour in Burkitt lymphoma patients. Here we present a patient with asymptomatic HIV infection, that contracted a primary cytomegalovirus (CMV) infection and human herpes virus 8 (HHV-8) infection. Three weeks before onset of symptoms the patient had unprotected sex which could be possible source of his CMV and also HHV-8 infection He deteriorated rapidly and died with a generalized anaplastic large cell lymphoma (ALCL).
A Caucasian homosexual male with asymptomatic human immunodeficiency virus (HIV) infection contracted a primary cytomegalovirus (CMV) infection and human herpes virus 8 (HHV-8) infection. He deteriorated rapidly and died with a generalized anaplastic large cell lymphoma (ALCL). Clinical and laboratory records were compiled. Immunohistochemistry was performed on lymphoid tissues, a liver biopsy, a bone marrow aspirate and the spleen during the illness and at autopsy. Serology and PCR for HIV, CMV, EBV, HHV-1-3 and 6-8 was performed on blood drawn during the course of disease.
The patient presented with an acute primary CMV infection. Biopsies taken 2 weeks before death showed a small focus of ALCL in one lymph node of the neck. Autopsy demonstrated a massive infiltration of ALCL in lymph nodes, liver, spleen and bone marrow. Blood samples confirmed primary CMV- infection, a HHV-8 infection together with reactivation of Epstein- Barr-virus (EBV).
Primary CMV-infection and concomitant HHV-8 infection correlated with reactivation of EBV. We propose that these two viruses influenced the development and progression of the lymphoma. Quantitative PCR blood analysis for EBV, CMV and HHV-8 could be valuable in diagnosis and treatment of this type of very rapidly developing lymphoma. It is also a reminder of the importance of prevention and prophylaxis of several infections by having protected sex.
大多数HIV患者的恶性淋巴瘤是由EB病毒感染重新激活所致。一些淋巴瘤病程发展非常迅速且呈暴发性。据报道,HHV - 8也是淋巴瘤的一个病因。尽管在伯基特淋巴瘤患者肿瘤邻近组织中已报道有CMV和HHV - 8,但CMV在淋巴瘤发生发展中的作用尚不清楚。在此,我们报告一名无症状HIV感染患者,其感染了原发性巨细胞病毒(CMV)和人类疱疹病毒8型(HHV - 8)。在症状出现前三周,该患者有过无保护性行为,这可能是其CMV及HHV - 8感染的潜在来源。他病情迅速恶化,最终死于弥漫性间变性大细胞淋巴瘤(ALCL)。
一名无症状人类免疫缺陷病毒(HIV)感染的白人同性恋男性感染了原发性巨细胞病毒(CMV)和人类疱疹病毒8型(HHV - 8)。他病情迅速恶化,最终死于弥漫性间变性大细胞淋巴瘤(ALCL)。收集了临床和实验室记录。在患病期间及尸检时,对淋巴组织、肝活检组织、骨髓穿刺物及脾脏进行了免疫组织化学检查。在病程中采集的血液样本进行了HIV、CMV、EBV、HHV - 1 - 3及6 - 8的血清学检测和PCR检测。
该患者表现为急性原发性CMV感染。死亡前两周所取活检显示颈部一个淋巴结有小灶性ALCL。尸检显示ALCL大量浸润于淋巴结、肝脏、脾脏及骨髓。血液样本证实存在原发性CMV感染、HHV - 8感染以及爱泼斯坦 - 巴尔病毒(EBV)重新激活。
原发性CMV感染及合并的HHV - 8感染与EBV重新激活相关。我们认为这两种病毒影响了淋巴瘤的发生发展及进程。对EBV、CMV和HHV - 8进行定量PCR血液分析可能对诊断和治疗这种快速发展的淋巴瘤有价值。这也提醒人们通过采取安全性行为预防和预防多种感染的重要性。