Bovine immunodeficiency virus (BIV) is prevalent in beef and dairy cattle, yet the mode(s) of BIV transmission are undefined. Using polymerase chain reaction, which specifically targeted a 235-bp, highly conserved region of the BIV pol gene, BIV-infected leukocytes were detected in the blood and milk of BIV-seropositive cows. These data confirm the presence of BIV in milk and identify the potential for lactogenic transmission of this virus.

We used monoclonal antibodies and immunohistologic examination of lymph nodes, to elucidate the pathogenesis of lymphosarcoma induced by, infection with bovine leukemia virus (BLV). The superficial cervical lymph nodes from 3 BLV-infected but apparently healthy sheep and 5 sheep with full-blown lymphosarcoma were examined. We also investigated the integration of bovine leukemia provirus by use of Southern blotting. In lymph nodes from sheep lacking clinical signs of infection, in which the provirus had been integrated at multiple sites in the genome, many large hypertrophic follicles were observed in the cortex. These follicles had germinal centers consisting of CD4+T cells and B cells that expressed surface IgM (sIgM) and major histocompatibility complex (MHC) class-II antigens, but not B cell-specific B2 molecule. The percentage of CD4+T cells in the cortex was significantly (P < 0.05) higher than that of the controls and sheep with lymphosarcoma. In all sheep with lymphosarcoma, the lymph nodes were completely destroyed by proliferating neoplastic cells, and in addition, small atrophic follicles, which consisted of normal B-cell marker-positive cells, were seen near the trabecula and the subcapsule. In these instances, neoplastic cells appeared to be a monoclonal population derived from a single CD5- B-cell lineage and to be classified as 2 types, CD5-CD4-CD8-B2+MHC class-II+sIgM+ and CD5-CD4-CD8-B2+MHC class-II+sIgM-. Moreover, CD8+T cells infiltrated diffusely throughout the tumorous lymph nodes apart from the atrophic follicles, and CD4+T cells were observed around atrophic follicles. Both types of T cells were small-size, normal lymphocytes with round and noncleaved nuclei, and were apparently non-neoplastic cells. In fact, after separation by use of a panning method, it seems that, in blood mononuclear cells from BLV-infected sheep without clinical signs of infection, but in lymphosarcomatous stages, the proviral genome was integrated only in B cells and not in T cells. Thus, we conclude that the host's immune response may be still maintained at a lymphosarcomatous stage.

The prevalence of feline leukemia virus (FeLV) antigen and DNA was assessed in formalin-fixed, paraffin-embedded tumor tissues from 70 cats with lymphosarcoma (LSA). Tissue sections were tested for FeLV gp70 antigen using avidinbiotin complex (ABC) immunohistochemistry (IHC); DNA was extracted and purified from the same tissue blocks for polymerase chain reaction (PCR) amplification of a 166 base pair region of the FeLV long terminal repeat (LTR). Results were related to antemortem FeLV enzyme-linked immunosorbent assay (ELISA) for serum p27 antigen, anatomic site of LSA, and patient age. Viral DNA was detected by PCR in 80% of cases and viral antigen by IHC in 57% of cases. Seventeen cases were PCR-positive and IHC-negative; one case was PCR-negative and IHC-positive. Clinical records included FeLV ELISA results for 30 of 70 cats. All 19 ELISA-positive cats were positive by PCR and IHC; of the 11 ELISA-negative cats that were negative by IHC, seven were positive by PCR. When evaluated according to anatomic site, FeLV DNA and antigen were detected less frequently in intestinal LSAs than in multicentric and mediastinal tumors. Lymphosarcoma tissues from cats < 7 yr were several fold more likely to be positive for FeLV antigen by IHC than were tumors from cats > or = 7 yr. However, there was no significant difference in PCR detection of FeLV provirus between LSAs from cats < 7 yr and those > or = 7 yr. These proviruspositive, antigen-negative cases may represent infection with latent or replication-defective FeLV.

Bovine immunodeficiency virus (BIV), a lentivirus, is prevalent in dairy and beef cattle in southeastern United States and may be associated with a lymphoproliferative disease. The mode(s) of BIV transmission are undefined. Because artificial insemination is a common practice in dairy production, contaminated stud semen could serve as an important source of infection if the virus is harbored in seminal fluids. To evaluate this possibility, we procured 11 cryopreserved semen specimens from a stud semen repository. Leukocytes were purified from the specimens, and the leukocyte DNA was used as template in a polymerase chain reaction procedure that targeted a 235-base pair, highly conserved domain of the BIV pol gene. The target sequence was amplified from the seminal leukocyte DNA of 9 of the specimens (82%), and nucleotide sequencing confirmed the BIV specificity of the fragment. This finding provides evidence that stud bull semen may serve as an important reservoir of BIV, suggesting the possibility that artificial insemination of dairy cows may have a major role in transmission and wide-spread dissemination of this bovine lentivirus.