With the model for Kaposi's sarcoma (KS), developed in our laboratory, we have been able to demonstrate that: 1) oncostatin M is a potent growth factor for KS-derived cells; 2) KS-derived cells secrete, among other factors, vascular permeability factor and interleukin 8 (IL-8), which may contribute to the pathology of the disease; 3) acquired immunodeficiency syndrome (AIDS)-KS cells have functional high affinity receptors for IL- 2, compatible with our model linking KS with immune stimulation and/or dysregulation; 4) a bacterial cell wall, sulfated polysaccharide- peptidoglycan compound, can inhibit the growth of KS-derived cells and the development of KS-like lesions, while disclosing a low toxicity; and 5) we have succeeded in growing a KS-derived mesenchymal cell line, that not only induces angiogenic lesions, but is also tumorigenic and metastatic in nude and scid mice. The study of T-cell colony formation by cells from human T lymphotropic virus type I (HTLV-I)-infected individuals, strongly suggests that the T- lymphocyte colony-forming cells (T-CFC) are infected by HTLV-I and may be an important reservoir for that retrovirus. We have isolated a herpesvirus, which is similar to the recently described human herpesvirus 7 (HHV-7). Molecular analysis shows that HHV- 7 is related to, but significantly different from HHV-6 and HCMV. We have developed molecular tools for the detection of HHV-7. A herpesvirus was detected in two B-lymphocyte cell lines were established from lymphomas from simian immunodeficiency virus (SIV), strain SMM3-infected cynomolgus monkeys. Since 40% of SIV-inoculated animals developed lymphoma and this herpesvirus was consistently detected in all these lymphomas, this animal model mimics the EBV+ B-cell lymphomas that develop frequently in AIDS patients and could become a useful model for the study of lymphomagenesis in general, and in AIDS in particular.
