CD68(+) CELLS OF MONOCYTE MACROPHAGE LINEAGE IN THE ENVIRONMENT OF AIDS-ASSOCIATED AND CLASSIC-SPORADIC KAPOSI-SARCOMA ARE SINGLY OR DOUBLYINFECTED WITH HUMAN HERPESVIRUSES-7 AND 6B/

Earlier studies have shown that Kaposi sarcomas contain cells infected with human herpesvirus (HHV) 6B, and in current studies we report tha t both AIDS-associated and classic-sporadic Kaposi sarcoma contain HHV -7 genome sequences detectable by PCR. To determine the distribution o f HHV-7-infected cells relative to those infected with HHV-6, sections from paraffin-embedded tissues were allowed to react with antibodies to HHV-7 virion tegument phosphoprotein pp85 and to HHV-6B protein p10 1. The antibodies are specific for HHV-7 and HHV-6B, respectively, and they retained reactivity for antigens contained in formalin-fixed, pa raffin-embedded tissue samples. We report that (i) HHV-7 pp85 was pres ent in 9 of 32 AIDS-associated Kaposi sarcomas, and in 1 of 7 classica l-sporadic HIV-negative Kaposi sarcomas; (ii) HHV-7 pp85 was detected primarily in cells bearing the CD68 marker characteristic of the monoc yte/macrophage lineage present in or surrounding the Kaposi sarcoma le sions; and (iii) in a number of Kaposi sarcoma specimens, tumor-associ ated CD68(+) monocytes/macrophages expressed simultaneously antigens f rom both HHV-7 and HHV-6B, and therefore appeared to be doubly infecte d with the two viruses. CD68(+) monocytes/macrophages infected with HH V-7 were readily detectable in Kaposi sarcoma, but virtually absent fr om other normal or pathological tissues that harbor macrophages. Becau se all of the available data indicate that HHV-7 infects CD4(+) T lymp hocytes, these results suggest that the environment of the Kaposi sarc oma (i) attracts circulating peripheral lymphocytes and monocytes, tri ggers the replication of latent viruses, and thereby increases the loc al concentration of viruses, (ii) renders CD68(+) monocytes/macrophage s susceptible to infection with HHV-7, and (iii) the combination of bo th events enables double infections of cells with both HHV-6B and HHV- 7.