HHV-8: a newly recognized pathogen in transplantation.

Abstract

Outcome of Kidney Transplant Recipients with Previous Human Herpesvirus-8 Infection. Transplantation 2000; 69: 1776. Francès C, Mouquet C, Marcelin AG, Barete S, Agher R, Charron D, Benalia H, Dupin N, Piette JC, Bitker MO, and Calvez V. As perioperative mortality is becoming low, a major life-threatening complication of solid organ transplantation is infection in the transplant recipient taking long-term immunosuppressive therapy. Infectious agents include a broad variety of pathogens, ranging from latent viruses to pathogens of both community and hospital origin (1). After organ transplantation, patients have an increased risk for neoplasms, including epithelial skin tumors, posttransplantation lymphoproliferative diseases (PTLD), and Kaposi’s sarcoma (KS). The immunomodulating viruses of the herpes family not only have been shown to play a direct pathogenic role, but also have been linked to allograft injury and rejection, to infection with opportunistic pathogens, and to the development of cancer in organ transplant recipients. PTLD is strongly linked to Epstein Barr virus (EBV) and KS to the recently discovered human herpes virus-8 (HHV-8), also called Kaposi’s sarcoma-associated herpesvirus (KSHV). HHV-8 has been identified as the causative agent of all forms of Kaposi’s sarcoma (KS), including transplantation-associated KS. In this issue of Transplantation, Francès and colleagues provide new data concerning the risk of patients infected with HHV-8 for KS after solid organ transplantation. In their retrospective study of sera obtained from 400 renal transplant patients, sera of 32 (8%) patients were shown to be positive for HHV-8 at the time of transplantation. In the 3-year follow-up period, 9 (28%) of these 32 patients developed KS but none of the remaining 368 patients. Patient and graft survival rates for HHV-8 positive patients were lower than those for the remaining patients, and severe bacterial and/or or Pneumocystis carinii infections were factors associated with KS. The authors propose a systematic screening of transplant recipients for HHV-8 and a close monitoring of HHV-8-positive patients to severe infections. Primary CMV infection is associated with a higher risk of symptomatic disease in transplant patients than reactivation of latent infection. Similarly, primary EBV infection in a seronegative recipient is the most important risk factor for PTLD. We and others have shown that HHV-8 is transmitted through renal transplantation (23). The data presented by Francès and colleagues are therefore surprising, as one would expect primary HHV-8 infection as a main risk factor for KS. In our cohort of 220 transplant patients, KS developed in 2 (8%) of 25 patients with primary HHV-8 infection after renal transplantation but in none of 14 patients who were HHV-8 positive at the time of transplantation. In the study by Parravicini, 1 (9%) of 11 patients with posttransplant KS had a primary HHV-8 infection, whereas the other 10 patients were positive for HHV-8 at the time of transplantation. These data are partly controversial, but regional variations in HHV-8 epidemiologic features and type of immunosuppressive regimen are additional factors to consider. However, we may assume that KS is primarily associated with HHV-8 reactivation under immunosuppressive therapy, and that seropositivity for HHV-8 before transplantation is more important than viral transmission through the transplant as risk for KS. Nevertheless, it seems advisable to screen not only transplant recipients for HHV-8, as proposed by Francès and colleagues, but also organ donors when possible. Whether a potentially infected organ should then be used for transplantation remains to be discussed, considering the extreme shortage of available organs. Whatsoever, we believe a close monitoring of recipients of organs potentially infected with HHV-8 is warranted.