phenotypic and molecular quaIities to those associated with HIV and SIV infections. The evidence availabIe supports an indirect raIe for FIV in tumour development. FlV induces activation of lymphoid tissue, polyclonaI B-ceIl activation and increased serum cytokine

1ymphosarcomas. Callanan et aL. (1992) found normal responses of lymphocytes to mitogens in one case, and Poli et al. (1994) detected a marked reduction in circulating CD4+ T-Iymphocytes in another case. ln a series of eight FIV -infected cats (two experimental and six naturaI) with lymphosarcoma, seven of the tumours were high-grade B-cell Iymphomas of the centroblastic or immunoblastic subtypes. The remaining case was a T -cell tumour associated with concurrent FeL V infection (Callanan et aL., 1996). Lymphosarcomas in experimental infection described by English et al. (1994) and Poli et al. (1994) were aIso of B-cell origin, based on immunoglobulin expression. However, the single neopIasm described by Poli et al. (1994) was low-grade. Four of the tumours reported by CaIlanan et aL. (1996) were examined with moIecular probes to establish tumour ceIl lineage and to screen for integrated viral sequences (Terry et aL., 1995). Confirmation of a B-cell origin was supported by the identification of monoclonal or oligoclonai immunoglobulin heavy-chain gene rearrangements and the 1ack of rearrangements of T -cell receptor ß-chain genes in aIl four cases. Rearrangement of the c-myc locus, which occurs in many FeL V Iymphosarcomas, was not found in any of the FIV -associated tumours and none of the tumours showed evidence of integrated FlV sequences by Southern blot hybridization. Poli et al. (1994) identified DNA of the FIV gag gene in many tissues including tumour tissue of an experimentaIly FIV -infected cat. However, in this tumour tissue, it could not be determined whether the infection was of neopIastic ceIls. Thus lymphosarcomas in FlV -infected cats share similar morphologicaI, immunophenotypic and molecular quaIities to those associated with HIV and SIV infections. The evidence availabIe supports an indirect raIe for FIV in tumour development. FlV induces activation of lymphoid tissue, polyclonaI B-ceIl activation and increased serum cytokine levels, aIl of which may facilitate malignant transformation of B cells (Lawrence et aL., 1992; Rideout et al., 1992; CaIlanan et aL., 1993; Flynn et aL., 1994).