Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. == Contributor Information == Adrienne L. VA45-54(2E) is lymphomagenic in hamsters, that hamster lymphoid cells of histiocytic origin can be transformed in vivo and established in culture, and that reagents to hamster leukocyte differentiation molecules are now available. Keywords:SV40, T-antigen, Polyomavirus, Hamsters, Lymphomas, Viral strains, Anti-hamster lymphocyte antibodies, Tumorigenicity, Phagocytosis == Introduction == Polyomavirus simian virus 40 (SV40) is an oncogenic DNA virus that was an inadvertent contaminant of early poliovirus vaccines that were prepared using cultures of primary monkey kidney cells (Butel and Lednicky, 1999;Stratton et al., 2003). It is estimated that millions of people in the US and worldwide received one or more doses of contaminated vaccines between RO5126766 (CH5126766) 1955 and 1963. Exposures may have occurred beyond that time period, as the USSR oral poliovirus vaccine may have been contaminated as late as 1978 (Cutrone et al., 2005). SV40 has been found to be associated with selected human cancers at varying RO5126766 (CH5126766) frequencies, including non-Hodgkins lymphoma (NHL) (Amara et al., 2007;Butel, 2008;Butel and Lednicky, 1999;Gazdar et al., 2002;Shivapurkar et al., 2002;Vilchez et al., 2002b;Zekri et al., 2007); however, other studies have failed to detect an association (Butel, 2008;MacKenzie et al., 2003;Schler et al., 2006;Sui et al., 2005). The pathogenesis of SV40 infections in humans has not been characterized, but lymphoid cells are thought to play an important role. The Syrian golden hamster is the animal model for SV40-mediated oncogenesis because these rodents are highly susceptible to SV40-induced tumors (Butel et al., 1972;Butel and Lednicky, 1999;Carbone et al., 1989;Cicala et al., 1993;Diamandopoulos, 1972,1973;Girardi et al., 1962). The types of neoplasms that develop in hamsters are influenced by the route of inoculation. The spectrum of tumors found to be SV40-positive in humans is the same as that observed in hamsters following SV40 inoculation (Gazdar et al., 2002;Vilchez and Butel, 2004). It has been shown that biological differences exist among SV40 strains. The distinction of genetic strains is based on sequence differences in the C-terminal region of the large tumor antigen (T-ag) gene, which result in amino acid changes in T-ag, the viral replication protein and the major oncogenic protein (Butel and Lednicky, 1999;Forsman et al., 2004;Stewart et al., 1996,1998). In addition, virus variants can be distinguished by rearrangements in the viral regulatory region (Lednicky and Butel, 2001). Recent results showed that SV40 isolates differ in oncogenic potential in hamsters Rabbit Polyclonal to SGK (phospho-Ser422) following intraperitoneal (i.p.) inoculation (Sroller et al., 2008;Vilchez et al., 2004). The viral regulatory region was found to exert a major influence on tumorigenicity, as a significantly larger number of animals developed tumors following inoculation of viruses with simple (1E) regulatory regions than those exposed to viruses with complex (2E) regulatory regions (Sroller et al., 2008). The influence of T-ag strain differences was less pronounced, although the SVCPC T-ag was more oncogenic than either the 776 or VA45-54 T-ag domains. Together these studies suggest that virus-specific factors influence the oncogenic outcome in an SV40-infected host. Intraperitoneal inoculation of weanling hamsters often results in mesotheliomas (Cicala et al., 1993). In contrast, intravenous (i.v.) inoculation of weanling hamsters reportedly induces leukemias, lymphomas, and osteosarcomas, as well as undifferentiated sarcomas (Diamandopoulos, 1972,1973;Carbone et al., 1989;Cicala et al., 1992). The lymphomas have been characterized as being of B cell or histiocytic and macrophage origin (Carbone et al., 1989;Cicala et al., 1992;Coe and Green, 1975). An evaluation of the oncogenicity of different SV40 strains administered via i.v. inoculation has not previously been performed. Characterization of SV40-mediated lymphomagenesis in hamsters RO5126766 (CH5126766) may elucidate viral effects on lymphoid cells that will provide insights into a possible RO5126766 (CH5126766) role of SV40 in human lymphoid tumors. Additionally, this model will allow for studies of a role that infected lymphoid cells may play in disseminating virus in a host. This report describes tumor induction in hamsters following i.v. inoculation of SV40, the development of monoclonal antibodies useful to characterize surface markers of hamster lymphoid cells, and the derivation and characterization of SV40 lymphoma tumor cell lines. We focused on SV40 strains SVCPC, highly oncogenic by.