Luppi et al. reply
We would like to thank Parravicini et al. for their interest in our work. In their correspondence, they argue that the majority of transplant Kaposi sarcoma cases are due to reactivation of a pre-existing infection with KSHV, rather than caused by transmission of the virus or virus-infected cells from the organ donor to the recipient, as described in our paper. Parravicini et al. stress that in the case of a reactivated viral infection, our suggestion to use KSHV-specific T cells for adoptive therapy would obviously have to be based on recipient-derived, rather than donor-derived, T cells.
We agree entirely with Parravicini et al. that the majority of transplant Kaposi sarcoma cases may be the consequence of a reactivated viral infection. This was, however, not the point of our paper, which described transmission of a KSHV-infected cell from donor to recipient that could subsequently lead to the development of a Kaposi sarcoma lesion. As for the frequency of donor-derived versus recipient-derived KSHV in the pathogenesis of transplant Kaposi sarcoma, we have recently reviewed the published literature on this issue5. It appears that of 50 well-documented and published cases of transplant Kaposi sarcoma, 16 (32%) could have been caused by donor-derived virus. Therefore, donor-derived virus may be responsible for the development of transplant Kaposi sarcoma more frequently than suggested by Parravicini et al., and this figure may depend on local prevalence of KSHV. Serologic testing for KSHV before and after transplantation may indeed be helpful, as mentioned by Parravicini et al. In addition, in order to substantiate the origin of KSHV in a transplant patient with Kaposi sarcoma, peripheral blood DNA from the donor should be stored at the time of transplantation. This would allow the comparison of KSHV strains in the donor and the recipient by sequencing of the hypervariable K1 gene or by restriction fragment–length polymorphism analysis6,7.
See “KSHV reactivation in post-transplant Kaposi sarcoma” by Parravicini et al.
References
Barozzi, P. et al. Post-transplant Kaposi sarcoma originates from the seeding of donor-derived progenitors. Nat. Med. 9, 554–561 (2003).
Parravicini, C. et al. Risk of Kaposi's sarcoma-associated herpesvirus transmission from donor allografts among Italian posttransplant Kaposi's sarcoma patients. Blood 90, 2826–2829 (1997).
Farge, D. et al. Human herpes virus-8 and other risk factors for Kaposi's sarcoma in kidney transplant recipients. Groupe Coopératif de Transplantation d'Ile de France (GCIF). Transplantation 67, 1236–1242 (1999).
Euvrard, S. et al. Skin cancers after organ transplantation. N. Engl. J. Med. 348, 1681–1691 (2003).
Luppi, M. et al. Human herpes virus-8 (HHV-8) associated diseases in solid organ transplantation: importance of viral transmission from the donor. Clin. Infect. Dis., in press.
Luppi, M., et al. Bone marrow failure associated with human herpesvirus 8 infection after transplantation. New Engl J Med 343, 1378–1385 (2000).
Luppi, M., et al. Molecular evidence of organ-related transmission of Kaposi sarcoma-associated herpesvirus or human herpesvirus-8 in transplant patients. Blood 96, 3279–3281 (2000).
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Luppi, M., Barozzi, P., Facchetti, F. et al. Reply to “KSHV reactivation in post-transplant Kaposi sarcoma”. Nat Med 9, 986 (2003). https://doi.org/10.1038/nm0803-986b
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DOI: https://doi.org/10.1038/nm0803-986b