INDUCTION OF FELINE ACQUIRED-IMMUNE-DEFICIENCY-SYNDROME BY FELINE LEUKEMIA-VIRUS - ALTERATION IN RESPONSE TO HORMONES IN THE HYPOTHALAMIC-PITUITARY-GONADAL SYSTEM

Male kittens who were infected with the feline leukemia virus (FeLV) w ere found at various times after exposure to contain a sequence of dys function in their hypothalamic-pituitary-gonadal (HPG) system. To unde rstand whether the involved endocrine glands in this system were damag ed by FeLV, the hypothalamus, pituitary, and testes were tested for ho rmonal responsiveness in vivo and in vitro. The infected cats were adm inistered with luteinizing hormone-releasing hormone (LHRH) and human chorionic gonadotropin (hCG). Their response to the treatment was stud ied, and they were then compared with untreated control cats. Normal r esponse to LHRH for the synthesis of follicle stimulating hormone (FSH ), luteinizing hormone (LH), and testosterone were found in the infect ed cats prior to 10 weeks of infection. After 10 weeks, the response w as reduced by 25%, 38%, end 42%, respectively. Twelve weeks after infe ction, the response to hCG for testosterone synthesis was drastically reduced. The control cats, however, demonstrated normal prolonged biph aslc patterns of response to hCG. The in vivo administration of the tr opic hormones had no effect on the titer of FeLV gs antigen in the blo od of the infected cats. The medial basal hypothalamus (MBH) from the control cats and cats in their 13th week of infection were cultured in vitro, with the presence of high K+ ion (60 mM). The control MBH resp onded to K+ ion stimulation for LHRH release. The K+-stimulated releas e of LHRH in the control MBH was 99% higher than that of the infected MBH. In contrast, the amount of unreleased LHRH in the infected MBH wa s 74% higher than that of the control MBH. In in vitro culture, the co ntrol pituitary gland responded markedly higher to LHRH stimulation fo r the release of gonadotropins (FSH and LH) than that of the infected one (140% compared with 56% for FSH, and 70% compared with 28% for LH, respectively). Whereas, the amount of unreleased FSH and LH in the in fected pituitary gland were 59% and 31%, higher than that of the contr ol gland. These results suggest that (i) the progressive development o f neuroendocrine glands' dysfunction is related to viral replication t ime; (ii) the in vivo and In vitro responses to tropic hormones in the infected endocrine glands are drastically reduced; and (iii) this red uction in hormonal response may be caused by defective regulation of p eptide hormonal secretion.