Human herpesvirus 8 (HHV-8) infection has been linked to the development of Kaposi's sarcoma and to rare lymphoproliferative disorders. We used molecular methods, serologic methods, in situ hybridization, and immunohistochemical analyses to study HHV-8 infection in association with nonmalignant illnesses in three patients after transplantation. Primary HHV-8 infections developed in two patients four months after each received a kidney from the same HHV-8–seropositive cadaveric donor. Seroconversion and viremia occurred coincidentally with disseminated Kaposi's sarcoma in one patient and with an acute syndrome of fever, splenomegaly, cytopenia, and marrow failure with plasmacytosis in the other patient. HHV-8 latent nuclear antigen was present in immature progenitor cells from the aplastic marrow of the latter patient. Identification of the highly variable K1 gene sequence of the HHV-8 genome in both the donor's peripheral-blood cells and the recipients' serum confirmed that transmission had occurred. HHV-8 viremia also occurred after autologous peripheral-blood stem-cell transplantation in an HHV-8–seropositive patient with non-Hodgkin's lymphoma. Reactivation of the infection was associated with the development of fever and marrow aplasia with plasmacytosis; there was no evidence of other infections. HHV-8 transcripts and latent nuclear antigen were expressed in the aplastic marrow but not in two normal marrow samples obtained before transplantation. Primary HHV-8 infection and reactivation of infection may be associated with nonneoplastic complications in immunosuppressed patients.

Independent epidemiologic studies have shown a strong association between Kaposi's sarcoma (KS) and infection with human herpesvirus 8 (HHV-8 or KSHV). HHV-8 genomic sequences have been found in all forms (1–5) and all histologic stages (6) of KS, with viral DNA being localized to tumor endothelial cells and spindle cells (7,8). Detection of HHV-8 DNA sequences in the peripheral blood of patients who are seropositive for human immunodeficiency virus 1 (HIV) is a strong predictor of progression to KS (9,10). The vast majority of patients with KS have antibodies against HHV-8 (11–14), with seroconversion before clinical disease (15). HHV-8 infection is apparently not common in the general population of the U.K. and the United States, but it is common in groups at high risk for KS (11–14). In addition, HHV-8 seroprevalence is higher in HIV-positive homosexual men than in HIV-positive patients with hemophilia (13), just as acquired immunodeficiency syndrome (AIDS)-related KS occurs far more commonly in homosexual men than in patients with hemophilia. HHV-8 infection is common in the general population of Uganda, which has a high incidence of endemic KS (11,13,14).

Mucorales-specific T cells were investigated in 28 hematologic patients during the course of their treatment. Three developed proven invasive mucormycosis (IM), 17 had infections of known origin but other than IM, and 8 never had fever during the period of observation. Mucorales-specific T cells could be detected only in patients with IM, both at diagnosis and throughout the entire course of the IM, but neither before nor for long after resolution of the infection. Such T cells predominantly produced IL-4, IFN-γ, IL-10, and to a lesser extent IL-17 and belonged to either CD4⁺ or CD8⁺ subsets. The specific T cells that produced IFN-γ were able to directly induce damage to Mucorales hyphae. None of the 25 patients without IM had Mucorales-specific T cells. Specific T cells contribute to human immune responses against fungi of the order Mucorales and could be evaluated as a surrogate diagnostic marker of IM.