• Tung-Ying Chen, Horng-Woei Yang, Dar-Shong Lin, Zo-Darr Huang, and Lung Chang.
• Department of Pathology, MacKay Memorial Hospital, Taipei, Taiwan.
• Medicine (Baltimore). 2022 Oct 28; 101 (43): e31310e31310.

AbstractKaposi sarcoma (KS) is a malignant vascular neoplasm caused by KS-associated herpesvirus (KSHV) infection. HIV plays a major role in KS pathogenesis. KS in HIV usually produces more malignant features than classic KS. Despite the close KS-HIV relationship, no study has reported the existence of HIV in KS tissue. We used ddPCR to detect HIV and KSHV in HIV+ KS samples and classic KS control. We verified KS cell types through immunohistochemistry and applied hypersensitive in situ hybridization (ISH) to detect HIV and KSHV in tumor cells. Furthermore, we co-stained samples with ISH and immunohistochemistry to identify HIV and KSHV in specific cell types. Regarding pathological stages, the KS were nodular (58.3%), plaque (33.3%), and patch (8.3%) tumors. Moreover, ddPCR revealed HIV in 58.3% of the KS samples. ISH revealed positive Pol/Gag mRNA signals in CD34 + tumor cells from HIV + patients (95.8%). HIV signals were absent in macrophages and other inflammatory cells. Most HIV + KS cells showed scattered reactive particles of HIV and KSHV. We demonstrated that HIV could infect CD34 + tumor cells and coexist with KSHV in KS, constituting a novel finding. We hypothesized that the direct KSHV-HIV interaction at the cellular level contributes to KS oncogenesis.Copyright © 2022 the Author(s). Published by Wolters Kluwer Health, Inc.

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