INDUCTION OF FELINE ACQUIRED-IMMUNE-DEFICIENCY-SYNDROME BY FELINE LEUKEMIA-VIRUS - ALTERATION IN RESPONSE TO HORMONES IN THE HYPOTHALAMIC-PITUITARY-GONADAL SYSTEM
Sw. Wang et Cs. Teng, INDUCTION OF FELINE ACQUIRED-IMMUNE-DEFICIENCY-SYNDROME BY FELINE LEUKEMIA-VIRUS - ALTERATION IN RESPONSE TO HORMONES IN THE HYPOTHALAMIC-PITUITARY-GONADAL SYSTEM, Proceedings of the Society for Experimental Biology and Medicine, 208(4), 1995, pp. 404-412
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.