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Epstein-Barr virus and persistent graft dysfunction after liver transplantation.
A Telenti1, T F Smith, J Ludwig
1Division of Infectious Diseases, Mayo Clinic, Rochester, Minnesota 55905.
Hepatology (Baltimore, Md.)
|August 1, 1991
Summary
Epstein-Barr virus (EBV) primary infection in liver transplant recipients receiving EBV-positive grafts can cause prolonged graft dysfunction. Treatment with acyclovir and azathioprine withdrawal reduced EBV DNA levels and improved graft function.
Area of Science:
- Hepatology
- Virology
- Immunology
Background:
- Epstein-Barr virus (EBV) infections present diverse clinical outcomes based on host immune status.
- Liver transplantation involves managing immunosuppression, which can impact EBV reactivation or primary infection.
Observation:
- Two liver transplant recipients developed primary EBV infection from EBV-seropositive donors, leading to sustained liver graft dysfunction.
- Histological analysis revealed mononuclear infiltration and immunoblastic changes, indicative of evolving lymphoma.
- In situ hybridization and PCR confirmed EBV genome presence in liver biopsies, correlating with hepatitis severity.
Findings:
- High levels of Epstein-Barr virus DNA were detected in liver biopsies during acute hepatitis post-seroconversion.
- EBV DNA levels correlated with the progression of lymphocytic infiltrates in the liver parenchyma.
- One patient also showed high EBV DNA in a cervical lymph node biopsy.
- Discontinuation of azathioprine and initiation of acyclovir treatment led to a significant decrease in EBV DNA levels.
Implications:
- These cases highlight the critical role of immune regulation in managing EBV infection post-transplant.
- Chronic liver allograft dysfunction can be directly linked to Epstein-Barr viral infection dynamics.
- Antiviral therapy and immunosuppression adjustment are crucial for managing EBV-related complications in transplant patients.