Inactivation at various temperatures of bovine viral diarrhea virus in beef derived from persistently infected cattle.

Bovine viral diarrhea virus (BVDV) is a pestivirus that is enzootic in most cattle populations throughout the world. This virus is present throughout the body of persistently infected (PI) cattle. Previous research has not assessed the cooking temperature at which BVDV in meat from PI cattle can be inactivated. Therefore, muscle tissue from 6 PI cattle was harvested, refrigerated, frozen, and heated to various internal temperatures. The concentration of virus present was determined by virus isolation. Average cell culture infective doses (50% endpoint; CCID(50)) of BVDV per gram of frozen, uncooked meat from PI cattle were 10(5.85) CCID(50)/g of whole cuts and 10(6.02) CCID(50)/g of ground meat. The virus in whole and ground meat was consistently inactivated when cooked to temperatures greater than or equal to 75°C. A second objective of this research was to thoroughly reassess if Vero cells were permissive to BVDV infection in our laboratory to provide further indication of whether primates, including humans, might be susceptible to BVDV. Vero cells were not permissive to infection with any of 43 different strains of BVDV that readily replicated in Madin Darby bovine kidney cells. In conclusion, this bovine pathogen, which is not considered to be a human pathogen, can be inactivated by cooking ground or whole cuts of meat to 75°C or higher. Care should be taken to ensure that susceptible hosts such as pigs are not fed improperly cooked meat, meat by-products, or waste food originating from PI cattle.

Role of estrogen and prolactin in the growth and receptor levels of N-nitrosomethylurea-induced rat mammary tumors.

Forty-eight of 81 (59%) of N-nitrosomethylurea-induced rat mammary tumors regressed in average to almost one-half of the original size 10 days after ovariectomy (ovax) (hormone responsive), while 33 remained essentially unchanged (hormone resistant). AT 20 days after ovax, further decline in hormone-responsive tumors was observed when the rats were treated daily with 0.9% NaCl solution on the tenth day after ovax. Treatment for the same length of time with estrogen either alone or in combination with bromocryptine (to effectively suppress serum prolactin level) prevented tumor regression in hormone-responsive tumors. A similar effect was observed when rats were treated with perphenazine (to stimulate endogenous prolactin secretion) either alone or in combination with the antiestrogen tamoxifen. Estrogen receptors (ERs) significantly declined after ovax. Treatment with estrogen or perphenazine did not have any significant effect on ER level. Progesterone receptors (PGRs) became virtually undetectable after ovax. Treatments with estrogen, estrogen plus bromocryptine, and perphenazine plus tamoxifen but not perphenazine alone were able to partially restore PGRs although this effect was of borderline statistical significance. ER and PGR levels were not significantly different between hormone-responsive and -resistant tumors within each group. We conclude that both estrogen and prolactin play a role in the growth of the N-nitrosomethylurea-induced rat mammary tumor. Changes in ER and PGR levels did not correlate with tumor growth under the present experimental conditions.

Hormone dependency in N-nitrosomethylurea-induced rat mammary tumors.

The majority (87%) of N-nitrosomethylurea-induced rat mammary tumors regressed within 1 week after hypophysectomy (hypox). After a hypox-induced tumor regression, ovine PRL (oPRL), and 17 beta-estradiol (E2) were administered separately or in combination in order to define the individual role of these hormones in regulating tumor growth and influencing estrogen (E), progesterone (Pg), and PRL receptor (R) levels. Administration of E2 (2.5 micrograms twice daily) or oPRL (20 IU daily, started 5 days after hypox and continued for 10 days, resulted in stabilization of tumor growth. Simultaneous administration of E2 and oPRL resulted in a synergistic effect and reactivation of tumor growth. ER levels in mammary tumors were significantly lower than those in the control 15 days after hypox (P less than 0.01). Treatment with E2, oPRL, or both simultaneously had no significant effect on ER levels. A significant decline in PgR levels was noted at both 5 and 15 days after hypox. Whereas treatment with oPRL had no significant effect on PgR levels, E2 administration either alone or in combination with oPRL restored PgR levels to control values. PRLR levels were unchanged from control values at 5 days, but significantly declined (P less than 0.005) 15 days after hypox. Treatment with E2, oPRL, or both hormones simultaneously partially maintained PRLR and prevented the decline to the extremely low level noted in the untreated group. We conclude that the growth of nitrosomethylurea-induced rat mammary tumors is dependent on both E2 and PRL. There was a synergistic effect between E2 and PRL on tumor growth but not on ER, PgR, or PRLR. Neither E2 nor PRL had any significant effect on ER after hypox. PgR is under E2 control. Either E2 or PRL or both hormones were able to maintain PRLR in mammary tumors after hypox.