Affiliations of authors: M. L. Calabrò, P. Gasperini, M. Barbierato, L. Chieco-Bianchi, Department of Oncology and Surgical Sciences, Oncology Section, University of Padova, Italy; J. R. Fiore, G. Angarano, Clinic of Infectious Diseases, Policlinico Hospital, University of Bari, Italy.
Correspondence to: Maria Luisa Calabrò, BSc.D., Department of Oncology and Surgical Sciences, Oncology Section, University of Padova, via Gattamelata 64, I-35128 Padova, Italy (e-mail: lcalabro{at}ux1.unipd.it).
Human herpesvirus 8 (HHV8) infection is transmitted through sexual contacts among homosexual men in non-Kaposi's sarcoma (KS)-endemic areas, whereas nonsexual routes seem responsible for an age-related increase in HHV8 seroprevalence in children from endemic countries (14). To gain insights into heterosexual and nonsexual interpersonal contacts involved in HHV8 transmission, we measured HHV8 antibodies to the structural protein encoded by open reading frame 65 (ORF65) and a latency-associated nuclear antigen (LANA), as described previously (5), in plasma samples from a human immunodeficiency virus type 1 (HIV-1)-seropositive woman (designated W) who developed KS during a 10-year follow-up (from 1989 through 1999), from her HIV-1-seropositive sexual partners, designated P1 and P2, who were both intravenous drug users, and from her two children. Informed consent was obtained from study subjects, when possible. All of the subjects lived in southeast Italy, a KS-endemic area (6); W's only reported risk factor for HIV-1 infection was her relationship with P1.
W presented with several cutaneous KS lesions in 1995; massive oral and gastrointestinal involvement was found in April 1997, and highly active antiretroviral therapy (HAART) was started immediately. The drug combination was changed twice (June 1997 and March 1998). From June to December 1997, five cycles of doxorubicin, bleomycin, and vinblastine were administered, after which the cutaneous lesions progressively improved and gastric and oral involvement disappeared; HAART was suspended in January 1999. P1 presented with a few cutaneous KS lesions in June 1989 that did not change in the following 18 months; he died in December 1990 of a cerebral abscess. P1 and W had a son (designated C1) in 1985, who became HIV-1 seronegative at 9 months of age, as well as a daughter (designated C2) in 1988, who died of acquired immunodeficiency syndrome at 16 months of age. P2 had disseminated tuberculosis in 1991 and died in 1995 of cytomegalovirus-related pneumonia.
Long-term follow-up findings in W suggested that ORF65 antibody titers might be a possible marker of disease evolution. Indeed, while her LANA antibody titers were steady throughout follow-up, her ORF65 antibody titers were rather stable for only the first 4 years, rose 1 year before KS diagnosis and during disease progression, and then decreased concomitantly with KS regression (Fig. 1). Our previous data indicating that tumor burden is correlated with ORF65 antibody levels were confirmed (5) because P1, who had limited and stable KS, had lower ORF65 antibody titers than W, who developed an aggressive KS. The ORF65 antibody titers, therefore, reflected tumor burden and evolution and, thus, could be a useful parameter for monitoring KS therapy.
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Despite high ORF65 antibody titers in W's plasma samples, potentially indicative of active HHV8 replication, and unprotected sexual intercourse, she did not infect P2, who was persistently HHV8 seronegative (Fig. 1). Thus, with the evidence that HHV8 is rarely detected in cervicovaginal secretions (7), these data confirm that heterosexual transmission via female to male is not a preferential route for HHV8 dissemination.
NOTES
Supported by grants from the Istituto Superiore di Sanità (30A.0.12), the Italian Association for Cancer Research, the Italian Foundation for Cancer Research, and the European Concerted Action on the Pathogenesis of Kaposi's Sarcoma (BMH497-2302).
We thank P. Segato for English editing of the manuscript and P. Gallo for computer drawing of the figure.
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