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) were found at various times after exposure to contain a sequence of dysfunction in their hypothalamic-pituitary-gonadal (HPG) system. To understand whether the involved endocrine glands in this system were damaged by FeLV, the hypothalamus, pituitary, and testes were tested for hormonal responsiveness in vivo and in vitro. The infected cats were administered with luteinizing hormone-releasing hormone (LHRH) and human chorionic gonadotropin (hCG). Their response to the treatment was studied, and they were then compared with untreated control cats. Normal response to LHRH for the synthesis of follicle stimulating hormone (FSH), luteinizing hormone (LH), and testosterone were found in the infected cats prior to 10 weeks of infection. After 10 weeks, the response was reduced by 25%, 38%, and 42%, respectively. Twelve weeks after infection, the response to hCG for testosterone synthesis was drastically reduced. The control cats, however, demonstrated normal prolonged biphasic patterns of response to hCG. The in vivo administration of the tropic hormones had no effect on the titer of FeLV gs antigen in the blood 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 responded to K+ ion stimulation for LHRH release. The K(+)-stimulated release 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 was 74% higher than that of the control MBH. In in vitro culture, the control pituitary gland responded markedly higher to LHRH stimulation for the release of gonadotropins (FHS 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 infected pituitary gland were 59% and 31%, higher than that of the control gland. These results suggest that (i) the progressive development of neuroendocrine glands' dysfunction is related to viral replication time; (ii) the in vivo and in vitro responses to tropic hormones in the infected endocrine glands are drastically reduced; and (iii) this reduction in hormonal response may be caused by defective regulation of peptide hormonal secretion.