Human Herpesvirus 8 Causes a Wide Spectrum of Disease in Liver Transplant Recipients and May be Donor Derived: Case Series and Systematic Review of an Emerging Challenge
Karen M. J. Waller, Sudarshan Arvind, Simone I. Strasser, Ken Liu, Geoff W. McCaughan, David G. Bowen, Madeleine Gill, Rebecca Davis, William Rawlinson, Sacha Stelzer‐Braid, Geoff Watson, Vinay Vanguru, Tina MarinelliABSTRACT
Background
Human herpesvirus 8 (HHV8), also known as Kaposi sarcoma (KS)‐associated herpesvirus, can cause severe disease in liver transplant (LT) recipients, be donor‐derived, and present variably. We describe HHV8 disease post‐LT.
Methods
HHV8 disease was identified post‐LT in New South Wales (NSW), 2017–2024, and from systematic review. Reports were compared by suspected donor‐derived infection (DDI) and disease manifestation, using chi‐square and t ‐tests. Survival was investigated with Cox proportional hazards.
Results
Of 188 records, 79 publications (131 cases) were included, plus four NSW cases ( n = 135). Median onset was 7 months posttransplant (IQR: 5–13), with 33% suspected DDI. After median 12 months of follow‐up, 68/125 had disease remission/regression; 59/135 died (49 HHV8‐related). In NSW, Case 1 was proven DDI: visceral KS, 6 months post‐LT; complete remission occurred with immunosuppression modification and chemotherapy. Case 2 was probable DDI: KS, multicentric Castleman's disease, and hemophagocytic lymphohistiocytosis, 3 months post‐LT; the patient died despite immunosuppression modification, hydrocortisone and rituximab. Case 3 was possible DDI: KS‐herpesvirus‐induced cytokine syndrome, 6 months post‐LT; died despite immunosuppression modification and ganciclovir. Case 4 was unlikely DDI: visceral KS, 5 months post‐LT; complete remission occurred with surgery and immunosuppression modification. Survival was worse with visceral KS and non‐KS disease (aHR 5.83 and 4.32, p = 0.002). Reduced immunosuppression, mTORi, and chemotherapy improved survival (aHRs 0.53, 0.36, 0.43; p = 0.006, 0.044, and 0.030). Treatment effects diverged by KS and non‐KS disease. Donor screening identified more KICS and DDI, with improved non‐KS disease survival.
Conclusion
Post‐LT HHV8 disease is heterogeneous, with high mortality. Targeted treatments and possibly donor screening improve survival.