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An Efficient and Simple Method to Establish NK and T Cell Lines from Patients with Chronic Active Epstein-Barr Virus Infection
Published on: March 30, 2018
Fas/FasL and Complement Activation are Associated with Chronic Active Epstein-Barr Virus Hepatitis
Jing Lin1, Miao-Fang Su1, Jiao-Long Zheng1
1Department of Hepatobiliary Medicine, Fuzong Clinical Medical College of Fujian Medical University, 900TH Hospital of the Joint Logistic Support Force, PLA, Fuzhou, Fujian, China.
Insights
Chronic active Epstein-Barr virus hepatitis (CAEBVH) is a severe liver disease. Our study reveals immune cell dysfunction and complement system activation are key pathogenic mechanisms in CAEBVH.
Area of Science:
- Hepatology
- Virology
- Immunology
Background:
- Chronic active Epstein-Barr virus hepatitis (CAEBVH) is a rare, lethal condition causing liver inflammation and enlargement.
- Understanding its clinicopathological features and disease mechanisms is crucial for patient outcomes.
Purpose of the Study:
- To investigate the clinicopathological characteristics of CAEBVH.
- To elucidate the pathogenic mechanisms underlying CAEBVH.
Main Methods:
- Analysis of clinicopathological data from ten CAEBVH patients.
- Flow cytometry for immune cell phenotyping.
- Whole exome sequencing and immunohistochemistry for genetic and molecular mechanisms.
Main Results:
- Patients presented with fever, hepatosplenomegaly, abnormal liver function, and CD8+ T cell lymphopenia.
- Liver biopsies showed lymphocytic infiltration and Epstein-Barr virus-encoded small RNA (EBER) positivity.
- Enhanced expression of cytotoxic T lymphocyte markers, apoptosis-related proteins (Fas/FasL, Caspase-8), and complement components (C1q, C3d) was observed.
Conclusions:
- CAEBVH is characterized by fever, hepatosplenomegaly, and lymphadenopathy.
- Histopathology reveals lymphocytic infiltration and EBER positivity.
- Fas/FasL pathway and complement activation are implicated in CAEBVH pathogenesis.
Background And Aims:
Chronic active Epstein-Barr virus hepatitis (CAEBVH) is a rare and highly lethal disease characterized by hepatitis and hepatomegaly. This study aimed to investigate the clinicopathological features and pathogenic mechanisms of CAEBVH.
Methods:
Ten patients with confirmed Epstein-Barr virus hepatitis infection were enrolled. The clinicopathological characteristics of these patients were summarized and analyzed. Flow cytometry was utilized to detect peripheral blood immune cell phenotypes and whole exome sequencing was used to explore pathogenic genetic mechanisms. Lastly, immunohistochemical staining was employed to verify pathogenic mechanisms.
Results:
Clinical features observed in all Epstein-Barr virus hepatitis patients included fever (7/10), splenomegaly (10/10), hepatomegaly (9/10), abnormal liver function (8/10), and CD8+ T cell lymphopenia (6/7). Hematoxylin and eosin staining revealed lymphocytic infiltration in the liver. Positive Epstein-Barr virus-encoded small RNA in-situ hybridization (EBER-ISH) of lymphocytes of liver tissues was noted. Whole exome sequencing indicated that cytotoxic T lymphocytes and the complement system were involved. The expression of CD8, Fas, FasL, and Caspase-8 expression as well as apoptotic markers was enhanced in the Epstein-Barr virus hepatitis group relative to the controls (p<0.05). Lastly, Complement 1q and complement 3d expression, were higher in CAEBVH patients relative to controls (p<0.05).
Conclusions:
CAEBVH patients developed fever, hepatosplenomegaly, and lymphadenopathy. Histopathological changes were a diffuse lymphocytic sinusoidal infiltrate with EBER-ISH positivity. Fas/FasL and complement activation were involved in CAEBVH patients.
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