To the editor

In their article on post-transplant Kaposi sarcoma, Barozzi et al.1 elegantly show that in five of the eight Kaposi sarcoma patients investigated, tumor cells infected with Kaposi sarcoma–associated herpesvirus (KSHV) display phenotypic and genotypic features of donor origin. Based on these findings, the authors advocate the use of donor-derived, KSHV-specific T cells for the treatment of post-transplant Kaposi sarcoma.

The medical relevance and clinical implications of these findings need to be evaluated in the appropriate context, however. In particular, the seroepidemiological framework underlying the occurrence of post-transplant Kaposi sarcoma in different geographic areas must be considered.

We have previously shown that in northern Italy, where the seroprevalence of KSHV among organ donors and recipients is 4% and 6% respectively (C.P. et al., unpublished data), post-transplant Kaposi sarcoma has an incidence of 0.9%, and 90% of those cases occur in patients who were seropositive at the time of transplantation2. Our data are in agreement with other retrospective studies3,4. We can thus infer that KSHV reactivation is the most important pathogenetic event (>80% incidence) underlying postrenal transplant Kaposi sarcoma in the western world.

In this regard, it is noteworthy that in the only Kaposi sarcoma patient studied by Barozzi et al. with unequivocal serologic evidence of reactivation, the findings argue against a donor origin of Kaposi sarcoma tumor cells. We therefore advise that baseline serologic testing for KSHV be performed in all transplant donors and recipients to distinguish between viral transmission and reactivation in case of Kaposi sarcoma development. This should allow rational use of investigational immunotherapeutic strategies based on donor-derived, as opposed to recipient-derived, KSHV-specific T cells.

See Reply to “KSHV reactivation in post-transplant Kaposi sarcoma” by Luppi et al.