Chronic Epstein-Barr viral load carriage after pediatric organ transplantation

Masaki Yamada1, Sharon F Chen2, Michael Green3

  • 1National Center for Child Health and Development (NCCHD), Tokyo, Japan.

Frontiers in Pediatrics
|February 15, 2024
PubMed

Insights

Pediatric solid organ transplant recipients can develop chronic high Epstein-Barr virus (EBV) load, a condition that may precede EBV-associated post-transplant lymphoproliferative disorder (EBV/PTLD). This review explores current knowledge and expert-recommended management strategies for EBV CHL.

Area of Science:

  • Virology
  • Immunology
  • Transplant Medicine

Background:

  • Epstein-Barr virus (EBV) infection is a significant risk factor for post-transplant lymphoproliferative disorder (PTLD) in pediatric solid organ transplant (SOT) recipients.
  • Serial EBV monitoring in SOT patients has revealed a subset with chronic high EBV load (CHL), more prevalent in pediatric recipients.
  • The biological underpinnings and optimal clinical management of CHL remain poorly understood.

Purpose of the Study:

  • To review current knowledge regarding chronic high EBV load (CHL) in pediatric SOT recipients.
  • To discuss the potential progression of CHL to EBV-associated PTLD (EBV/PTLD).
  • To present expert-adopted clinical approaches for managing CHL.

Main Methods:

  • Literature review of EBV monitoring and CHL in SOT recipients.
  • Synthesis of current evidence on EBV biology and CHL.
  • Compilation of expert-recommended clinical management strategies.

Main Results:

  • Chronic high EBV load (CHL) is observed in a subset of pediatric SOT recipients.
  • CHL is more common in pediatric versus adult transplant recipients.
  • While some CHL cases may progress to EBV/PTLD, the exact risk and underlying mechanisms require further investigation.

Conclusions:

  • Understanding the biology of CHL is crucial for preventing EBV/PTLD in pediatric SOT recipients.
  • Standardized clinical approaches for CHL management are needed.
  • Further research is warranted to elucidate CHL pathogenesis and optimize therapeutic strategies.