J. the tumor people consisted of bed linens of densely loaded circular cells that totally effaced cells structures (Fig. ?(Fig.1A).1A). The neoplastic cells had been moderate to huge lymphoid cells with moderate pleomorphism. Mitotic cells with regions of hemorrhage and necrosis had been noticed regularly, indicating a higher cell turnover. A specific morphological feature was the current presence of a high amount of multinucleated huge cells fairly, around and inside the tumors usually. The huge cells had been also within Ancarolol regular areas of the lymph nodes, in the brain, Ancarolol in the lung (Fig. ?(Fig.1D),1D), in the tongue papillae, and in the palatine tonsils. These cells were SIVmac p27 antigen positive and are common in SIVmac infection in macaques; their presence supports a diagnosis of SIVsm-associated lymphoma in SM E041. Flow cytometry and immunohistochemistry (Fig. ?(Fig.1B)1B) confirmed that the neoplastic cells were CD3 negative and CD20 positive (B cells). Most were also Ki-67 positive, indicating a high cell turnover (data not shown). Based on these results, a diagnosis of immunoblastic B-cell lymphoma with plasmacytoid differentiation was made. In situ hybridization for EBV was negative for all tissues (data not shown). Open in a separate window FIG. 1. (A) HE-stained sections of lymphoma tissue. The tumor consisted of sheets of densely packed round cells that completely effaced the architecture of the mesenteric lymph nodes. Neoplastic cells were moderate- to large-sized lymphoid cells with moderate pleomorphism. (B) Immunophenotyping of neoplastic cells. The majority of large, atypical cells were CD20+ (B cells) as demonstrated by immunohistochemistry (stained brown). (C) HE stain of giant cells (arrows) in the connective tissue surrounding lung hilus. Inset, a giant cell that tested positive for SIV by immunohistochemistry (stained brown). (D) Lung showing multiple SIVp27+ giant cells (stained brown). Giant cell disease is also characteristic of AIDS seen in Ancarolol macaques infected with SIVsm. Immunohistochemistry was performed as described previously (44, 45). Natural history of SIVsm infection in the SM colony at TNPRC. SM E041 was a male born in January 1981 at the Yerkes National Primate Research Center (YNPRC) and transferred to the Tulane National Primate Research Center (TNPRC) in July 1983. According to TNPRC records, the TNPRC housed 86 SMs, 74 of which originated from the YNPRC mangabey colony in the 1980s. They were used for experimental leprosy infection (17, 18) because of their unique susceptibility to (16, 25, 46). A high prevalence of SIV infection has been reported for the YNPRC colony (10), and 90% of SMs were SIVsm infected when they were moved to TNPRC (29). SM A015 was naturally infected with and was the first donor of lesion from A022. In summary, A015 donated tissue to A022, and then A022 donated tissue to E041. No signs of leprosy were seen in E041 during the 18 years of observation. There was also no histological evidence of leprosy at necropsy (data not shown). Dynamics of anti-SIVsm by Western blot analysis. To determine when SIVsm infection began in the colony and whether SIVsm infection was inadvertently caused by intravenous inoculation, a retrospective analysis of the SIVsm infection status from SMs in the leprosy study was performed. Serial serum or plasma specimens obtained before and after inoculation were analyzed by Western blotting for anti-SIVsm antibody. A015 was anti-SIV antibody negative and anti-simian Rabbit Polyclonal to C1QC T-cell leukemia virus (STLV) positive, findings consistent with.